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To exploit the potential of explanted cardiac cells as a model to study drug actions it is recommended that (a) the preparation be characterized with electrophysiological methods and (b) the preparation of explanted cardiac cells be selected so that it facilitates the solution of a well-defined pharmacological problem. <\/jats:p>","DOI":"10.1139\/y81-068","type":"journal-article","created":{"date-parts":[[2017,10,15]],"date-time":"2017-10-15T14:49:00Z","timestamp":1508078940000},"page":"443-467","source":"Crossref","is-referenced-by-count":16,"title":["Explanted cardiac cells: a model to study drug actions?"],"prefix":"10.1139","volume":"59","author":[{"given":"O. F.","family":"Schanne","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G.","family":"Bkaily","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"fr","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y81-068","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T16:23:38Z","timestamp":1578241418000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y81-068"}},"issued":{"date-parts":[[1981,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1981,5,1]]}},"alternative-id":["10.1139\/y81-068"],"URL":"https:\/\/doi.org\/10.1139\/y81-068","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1981,5,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T21:17:17Z","timestamp":1649107037108},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"9","license":[{"start":{"date-parts":[[1988,9,1]],"date-time":"1988-09-01T00:00:00Z","timestamp":589075200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1988,9,1]]},"abstract":"<jats:p> The relationship between transmural potential difference (PD) and smooth muscle electrical and mechanical activity was investigated in the rabbit ileum in vitro. Transmural PD was monitored using agar salt bridge electrodes connected via calomel half cells to an electrometer. Force displacement transducers recorded predominantly longitudinal smooth muscle activity. Concurrently, predominantly circular muscle activity was recorded at three sites using intraluminal pressure probes. At the same sites, suction electrodes monitored electrical activity of the smooth muscle. In all experiments, fluctuations in transmural PD were temporally linked to smooth muscle mechanical and electrical activity. The frequency of PD oscillations, electrical slow waves, and cyclic pressure changes were identical within each segment. Adrenaline abolished smooth muscle electrical spiking, all mechanical activity, and transmural fluctuations in PD. However, the slow waves were not abolished, though their frequency was increased. Phentolamine but not propranolol reversed the effects of adrenaline, thus slow wave frequency is influenced by \u03b1-adrenergic stimulation in the rabbit ileum. In conclusion, oscillations in transmural PD are unrelated to the ionic processes associated with the slow wave. However, they are in some way linked to smooth muscle contractile activity, possibly via an intrinsic neural mechanism as observed in the guinea pig. <\/jats:p>","DOI":"10.1139\/y88-191","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T20:54:14Z","timestamp":1303592054000},"page":"1161-1165","source":"Crossref","is-referenced-by-count":1,"title":["Relationship between transmural potential difference and smooth muscle slow waves and contractility in the rabbit small intestine <i>in vitro<\/i>"],"prefix":"10.1139","volume":"66","author":[{"given":"Beverley","family":"Greenwood","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan D.","family":"Huizinga","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edwin","family":"Chow","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wylie J.","family":"Dodds","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y88-191","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T15:16:17Z","timestamp":1578237377000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y88-191"}},"issued":{"date-parts":[[1988,9,1]]},"references-count":0,"journal-issue":{"issue":"9","published-print":{"date-parts":[[1988,9,1]]}},"alternative-id":["10.1139\/y88-191"],"URL":"https:\/\/doi.org\/10.1139\/y88-191","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1988,9,1]]}},{"indexed":{"date-parts":[[2025,3,5]],"date-time":"2025-03-05T07:40:09Z","timestamp":1741160409894,"version":"3.38.0"},"reference-count":41,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[1999,9,1]],"date-time":"1999-09-01T00:00:00Z","timestamp":936144000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1999,9,1]]},"abstract":"<jats:p>Administration of the antineoplastic doxorubicin to rodents causes depression of hepatic cytochrome P450 (CYP) dependent biotransformation, an effect that has been partially attributed to the ability of doxorubicin to stimulate microsomal lipid peroxidation. Since doxorubicin can be bioactivated by the CYP\/NADPH-CYP reductase system to products that bind covalently to microsomal protein, we hypothesized that doxorubicin functions as a mechanism-based inactivator of hepatic microsomal CYPs and (or) NADPH-CYP reductase under conditions in which doxorubicin-stimulated NADPH-dependent lipid peroxidation is minimized. In vitro studies were conducted with hepatic microsomes isolated from untreated and phenobarbital-treated male rats. Unlike the positive control carbon tetrachloride, doxorubicin (10 \u00b5M) did not stimulate NADPH-dependent lipid peroxidation in microsomal incubations containing EDTA (1.5 mM). Doxorubicin did not cause NADPH-dependent loss of microsomal CYP, heme, or steroid hydroxylation activities selective for CYP2A, CYP2B, CYP2C11, and CYP3A. The positive control 1-aminobenzotriazole caused marked NADPH-dependent decreases in all of these parameters. Neither doxorubicin nor 1-aminobenzotriazole caused NADPH-dependent loss of NADPH-CYP reductase activity, and neither compound altered the immunoreactive protein levels of CYP2B, CYP2C11, CYP3A, and NADPH-CYP reductase. These results indicate that a pharmacologically relevant concentration of doxorubicin does not cause direct mechanism-based inactivation of hepatic microsomal CYPs or NADPH-CYP reductase, suggesting that the ability of doxorubicin to depress hepatic CYP-mediated biotransformation in vivo is due to lipid peroxidation mediated heme destruction, altered heme metabolism, and (or) decreased expression of selected CYP enzymes.Key words: doxorubicin, cytochrome P450, mechanism-based inactivation, lipid peroxidation.<\/jats:p>","DOI":"10.1139\/y99-053","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T09:33:07Z","timestamp":1303637587000},"page":"589-597","source":"Crossref","is-referenced-by-count":4,"title":["Lack of mechanism-based inactivation of rat hepatic microsomal cytochromes P450 by doxorubicin"],"prefix":"10.1139","volume":"77","author":[{"given":"Johnny Di","family":"Re","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chunja","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David S","family":"Riddick","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"p_1\/p_1_1","first-page":"150","volume":"74","author":"Afsar A.","year":"1996","journal-title":"Can. 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Toxicol."}],"container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y99-053","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,5]],"date-time":"2025-03-05T07:20:36Z","timestamp":1741159236000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y99-053"}},"issued":{"date-parts":[[1999,9,1]]},"references-count":41,"journal-issue":{"issue":"8","published-print":{"date-parts":[[1999,9,1]]}},"alternative-id":["10.1139\/y99-053"],"URL":"https:\/\/doi.org\/10.1139\/y99-053","ISSN":["0008-4212","1205-7541"],"issn-type":[{"type":"print","value":"0008-4212"},{"type":"electronic","value":"1205-7541"}],"published":{"date-parts":[[1999,9,1]]}},{"indexed":{"date-parts":[[2023,9,26]],"date-time":"2023-09-26T08:10:45Z","timestamp":1695715845004},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"11","license":[{"start":{"date-parts":[[1973,11,1]],"date-time":"1973-11-01T00:00:00Z","timestamp":120960000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1973,11,1]]},"abstract":"<jats:p> The molecular size of immunoreactive human growth hormone (IR-HGH) in serum and the relationship of IR-HGH to sulfation factor (SF) require further investigation. Sera obtained from normal volunteers, patients with Laron-type dwarfism, and hypopituitary patients with gigantism were fractionated on large columns of Sephadex. The IR-HGH in normal serum was found in a molecular size range similar to extracted pituitary HGH (epHGH), as well as in a larger and a smaller molecular size. Laron dwarf plasma had a similar molecular size IR-HGH distribution when compared with normal serum. Sera from hypopituitary patients with gigantism showed an increased relative amount of small IR-HGH compared with normal serum. SF activity was recovered in normal serum but not in other sera fractions. SF activity appeared mainly in the molecular size range less than 17\u2002000 and another peak was noted in the molecular size area greater than 55\u2002000.This study further supports the existence of IR-HGH in a large and a small molecular size in normal serum. IR-HGH in Laron dwarf serum appears similar in molecular size to normal serum IR-HGH. The relative increase in small IR-HGH in hypopituitary patients with gigantism requires further investigation. SF activity appears in a molecular size different from epHGH in normal serum, the main peak being in a smaller molecular size area, with a lesser peak in a larger size area. <\/jats:p>","DOI":"10.1139\/y73-129","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T20:43:38Z","timestamp":1303591418000},"page":"845-852","source":"Crossref","is-referenced-by-count":8,"title":["Fractionation Studies on Plasma of Normals and Patients with Laron Dwarfism and Hypopituitary Gigantism"],"prefix":"10.1139","volume":"51","author":[{"given":"R. M.","family":"Bala","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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The results presented indicate that under these conditions of in vivo exposure and in vitro assay, hyperbaric oxygen does not affect permanently the activities of the enzymes which were examined. <\/jats:p>","DOI":"10.1139\/y69-072","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T16:38:07Z","timestamp":1303576687000},"page":"400-402","source":"Crossref","is-referenced-by-count":3,"title":["Investigations on the effects of hyperbaric oxygen on enzyme activity"],"prefix":"10.1139","volume":"47","author":[{"given":"Nicole","family":"B\u00e9gin-Heick","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Hochstein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gale B.","family":"Hill","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y69-072","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T11:18:06Z","timestamp":1578223086000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y69-072"}},"issued":{"date-parts":[[1969,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1969,4,1]]}},"alternative-id":["10.1139\/y69-072"],"URL":"https:\/\/doi.org\/10.1139\/y69-072","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1969,4,1]]}},{"indexed":{"date-parts":[[2024,3,2]],"date-time":"2024-03-02T07:52:09Z","timestamp":1709365929262},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol.","Rev. can. physiol. pharmacol.","Revue canadienne de physiologie et pharmacologie"],"published-print":{"date-parts":[[2000]]},"DOI":"10.1139\/cjpp-78-12-1003","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:53:53Z","timestamp":1027767233000},"page":"1003-1012","source":"Crossref","is-referenced-by-count":2,"title":["Factors controlling ovarian apoptosis"],"prefix":"10.1139","volume":"78","author":[{"given":"C.V.","family":"Andreu-Vieyra","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.R.","family":"Habibi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"deposited":{"date-parts":[[2015,4,10]],"date-time":"2015-04-10T00:36:47Z","timestamp":1428626207000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrc.ca\/cgi-bin\/cisti\/journals\/rp\/rp2_abst_e?cjpp_y00-101_78_ns_nf_cjpp78-00"}},"issued":{"date-parts":[[2000]]},"references-count":0,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2000]]}},"URL":"https:\/\/doi.org\/10.1139\/cjpp-78-12-1003","ISSN":["1205-7541","0008-4212"],"issn-type":[{"value":"1205-7541","type":"electronic"},{"value":"0008-4212","type":"print"}],"published":{"date-parts":[[2000]]}},{"indexed":{"date-parts":[[2023,11,4]],"date-time":"2023-11-04T20:02:09Z","timestamp":1699128129942},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[1969,8,1]],"date-time":"1969-08-01T00:00:00Z","timestamp":-13219200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1969,8,1]]},"abstract":"<jats:p> Central vasomotor effects of (\u2212)-N-(1-phenylethyl)guanidine, a potent adrenergic neuron blocking agent, were studied. The compound was localized in the central sites by intracerebroventricular injection, topical application on the vasomotor center, intra-arterial (vertebral) injection, and intrathecal injection. It potentiated the carotid occlusion response, response to anoxia, spinal compression vasomotor response, and the threshold and optimal vasomotor responses to direct electrical stimulation of the medullary vasomotor center without affecting the peripheral norepinephrine pressor response and the nictitating membrane response. The peak effect was obtained in 15\u201320\u2002min, and recovery occurred in 80\u201390\u2002min. The compound probably made catecholamines unavailable to the vasomotor neurons, making them more excitable. <\/jats:p>","DOI":"10.1139\/y69-123","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T16:39:07Z","timestamp":1303576747000},"page":"725-729","source":"Crossref","is-referenced-by-count":1,"title":["Analysis of the central vasomotor effects of (\u2212)-<i>N<\/i>-(1-phenylethyl)guanidine, a new adrenergic neuron blocking agent"],"prefix":"10.1139","volume":"47","author":[{"given":"S. K.","family":"Bapat","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. N.","family":"Dhawan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. C.","family":"Srimal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y69-123","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T11:18:08Z","timestamp":1578223088000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y69-123"}},"issued":{"date-parts":[[1969,8,1]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[1969,8,1]]}},"alternative-id":["10.1139\/y69-123"],"URL":"https:\/\/doi.org\/10.1139\/y69-123","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1969,8,1]]}},{"indexed":{"date-parts":[[2023,11,4]],"date-time":"2023-11-04T20:07:04Z","timestamp":1699128424860},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"5","license":[{"start":{"date-parts":[[1967,9,1]],"date-time":"1967-09-01T00:00:00Z","timestamp":-73699200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1967,9,1]]},"DOI":"10.1139\/y67-107","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T08:48:12Z","timestamp":1303634892000},"page":"915-918","source":"Crossref","is-referenced-by-count":40,"title":["THE EFFECT OF ETHANOL ON THE CONCENTRATION OF \u03b3-AMINOBUTYRIC ACID IN THE RAT BRAIN"],"prefix":"10.1139","volume":"45","author":[{"given":"Ellen R.","family":"Gordon","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y67-107","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T16:10:05Z","timestamp":1578240605000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y67-107"}},"issued":{"date-parts":[[1967,9,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1967,9,1]]}},"alternative-id":["10.1139\/y67-107"],"URL":"https:\/\/doi.org\/10.1139\/y67-107","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1967,9,1]]}},{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T13:25:41Z","timestamp":1775654741335,"version":"3.50.1"},"reference-count":16,"publisher":"Canadian Science Publishing","issue":"9","license":[{"start":{"date-parts":[[2003,9,1]],"date-time":"2003-09-01T00:00:00Z","timestamp":1062374400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2003,9,1]]},"abstract":"<jats:p>Thyroid hormones are known to influence various processes of cell differentiation. Recently, it was reported that hypothyroidism reduces the sensitivity to Ca<jats:sup>2+<\/jats:sup>-channel antagonists in the rat uterus. We examined the sensitivity to dihydropyridines of the uterus from mice that had reduced thyroid hormone levels. Isradipine relaxed with the same potency precontracted uterine muscle strips from control and hypothyroid mice, independently from a pseudo-pregnant state. These results demonstrate that hypothyroidism does not change dihydropyridine sensitivity (i.e., the pattern of Ca<jats:sup>2+<\/jats:sup>-channel expression) in the murine uterus.Key words: uterus, smooth muscle, Ca<jats:sup>2+<\/jats:sup>channel, isradipine.<\/jats:p>","DOI":"10.1139\/y03-090","type":"journal-article","created":{"date-parts":[[2003,9,11]],"date-time":"2003-09-11T19:36:16Z","timestamp":1063308976000},"page":"890-893","source":"Crossref","is-referenced-by-count":4,"title":["Hypothyroidism does not affect the dihydropyridine sensitivity of precontracted murine uterus"],"prefix":"10.1139","volume":"81","author":[{"given":"J\u00f6rg W","family":"Wegener","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Franz","family":"Hofmann","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"p_1\/p_1_1","doi-asserted-by":"crossref","first-page":"181","DOI":"10.1113\/jphysiol.1989.sp017610","volume":"412","author":"Akaike N.","year":"1989","journal-title":"J. Physiol."},{"key":"p_2\/p_2_1","doi-asserted-by":"crossref","first-page":"214","DOI":"10.1007\/BF00584774","volume":"409","author":"Binah O.","year":"1987","journal-title":"Pflugers Arch."},{"key":"p_3\/p_3_1","doi-asserted-by":"crossref","first-page":"626","DOI":"10.1016\/0002-9343(90)90530-Q","volume":"88","author":"Dillmann W.H.","year":"1990","journal-title":"Am. J. Med."},{"key":"p_4\/p_4_1","doi-asserted-by":"crossref","first-page":"147","DOI":"10.1111\/j.1476-5381.1986.tb10166.x","volume":"87","author":"Granger S.E.","year":"1986","journal-title":"Br. J. Pharmacol."},{"key":"p_5\/p_5_1","doi-asserted-by":"crossref","first-page":"47","DOI":"10.1254\/jjp.41.47","volume":"41","author":"Ishii K.","year":"1986","journal-title":"Jpn. J. Pharmacol."},{"key":"p_6\/p_6_1","doi-asserted-by":"crossref","first-page":"88","DOI":"10.1172\/JCI113068","volume":"80","author":"Kim D.","year":"1987","journal-title":"J. Clin. 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Chem."},{"issue":"1","key":"p_12\/p_12_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1111\/j.1600-0773.1989.tb01116.x","volume":"65","author":"Wibo M.","year":"1989","journal-title":"Pharmacol. Toxicol."},{"issue":"8","key":"p_13\/p_13_1","doi-asserted-by":"crossref","first-page":"1731","DOI":"10.1016\/S0022-2828(95)90887-0","volume":"27","author":"Wibo M.","year":"1995","journal-title":"J. Mol. Cell. Cardiol."},{"issue":"8","key":"p_14\/p_14_1","doi-asserted-by":"crossref","first-page":"2787","DOI":"10.1016\/S0021-9258(17)40528-X","volume":"252","author":"Williams L.T.","year":"1977","journal-title":"J. Biol. Chem."},{"issue":"2","key":"p_15\/p_15_1","doi-asserted-by":"crossref","first-page":"473","DOI":"10.1006\/bbrc.1996.0084","volume":"218","author":"Xu C.","year":"1996","journal-title":"Biochem. Biophys. Res. 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Rev."}],"container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y03-090","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,10]],"date-time":"2021-06-10T18:05:43Z","timestamp":1623348343000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y03-090"}},"issued":{"date-parts":[[2003,9,1]]},"references-count":16,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2003,9,1]]}},"alternative-id":["10.1139\/y03-090"],"URL":"https:\/\/doi.org\/10.1139\/y03-090","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[2003,9,1]]}},{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:05:47Z","timestamp":1757541947891},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"11","license":[{"start":{"date-parts":[[1987,11,1]],"date-time":"1987-11-01T00:00:00Z","timestamp":562723200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1987,11,1]]},"abstract":"<jats:p> We investigated whether the pressor effects of systemically administered angiotensin II (AII) influence ACTH secretion. Adrenalectomized barbiturate-anesthetized mongrel dogs with constant low resting cortisol concentrations due to slow constant cortisol infusion received either bolus injections (2.5\u2002\u03bcg\u2002kg<jats:sup>\u22121<\/jats:sup>) or 15-min i.v. infusions of a low dose (12.5\u2002ng\u2002kg<jats:sup>\u22121<\/jats:sup>\u2002min<jats:sup>\u22121<\/jats:sup>) of AII during which blood samples were taken for ACTH and cortisol determinations. In sequential continuous experiments in each dog, blood pressure was allowed to increase in response to AII administration or was controlled by means of concurrent i.v. injections or infusions of the hypotensive drug papaverine, or by blood withdrawal from the vena cava. When the arterial pressure rise induced by AII was substantially attenuated or prevented by papaverine administration or blood withdrawal, mean ACTH secretion rates increased 400\u2013800% and mean ACTH concentrations increased by 280\u2013500%. On the other hand, AII administration alone caused large increases in mean arterial blood pressure but did not increase ACTH secretion significantly above control levels. These data suggest that when endogenous AII levels are elevated without a concurrent increase in blood pressure, as occurs during hypovolemia or sodium depletion, AII may have a significant influence on ACTH secretion. <\/jats:p>","DOI":"10.1139\/y87-366","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T08:55:27Z","timestamp":1303635327000},"page":"2308-2312","source":"Crossref","is-referenced-by-count":3,"title":["Pressor inhibition of angiotensin-induced ACTH secretion"],"prefix":"10.1139","volume":"65","author":[{"given":"John","family":"Kucharczyk","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Cowan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ross","family":"Layberry","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y87-366","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T15:17:49Z","timestamp":1578237469000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y87-366"}},"issued":{"date-parts":[[1987,11,1]]},"references-count":0,"journal-issue":{"issue":"11","published-print":{"date-parts":[[1987,11,1]]}},"alternative-id":["10.1139\/y87-366"],"URL":"https:\/\/doi.org\/10.1139\/y87-366","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1987,11,1]]}},{"indexed":{"date-parts":[[2023,8,20]],"date-time":"2023-08-20T18:50:09Z","timestamp":1692557409074},"reference-count":24,"publisher":"Canadian Science Publishing","issue":"10","license":[{"start":{"date-parts":[[1995,10,1]],"date-time":"1995-10-01T00:00:00Z","timestamp":812505600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1995,10,1]]},"abstract":"<jats:p> The present study compares the hemodynamic effects and mechanisms of action of angiotensin II (AngII) antagonists, angiotensin converting enzyme (ACE) inhibitors, and renin inhibitors in the guinea pig, an animal with high similarity to primates in terms of in vitro and in vivo responses to several human renin inhibitors. Animals were anesthetized with urethane and ketamine. The carotid artery was catheterized for monitoring blood pressure and heart rate. After 30\u2002min stabilization, drug (or vehicle) effects were monitored for 1\u2002h following each increasing dose (i.v. bolus injection). Drugs tested include losartan, an AngII receptor antagonist; two renin inhibitors, BILA 2157 BS and PD-134672; and captopril, an ACE inhibitor. All drugs dose dependency decreased blood pressure. Diastolic blood pressure was reduced more than systolic blood pressure, suggestive of vasodilation. The maximum decrease (32\u2002\u00b1\u20026%, p\u2002&lt;\u20020.05\u2002vs. vehicle) in mean arterial blood pressure (MABP) by losartan was achieved with a dose of 1\u2002mg\/kg. A similar decrease in MABP was observed with renin inhibitors at a dose of 3\u2002mg\/kg, without affecting heart rate. A further increase in the dose of renin inhibitors (6\u2002mg\/kg) decreased not only blood pressure but also heart rate. Captopril decreased MABP with a maximum of 48\u2002\u00b1\u20023% (p\u2002&lt;\u20020.05\u2002vs. vehicle, losartan, and PD-134672). In the presence of HOE-140, a bradykinin antagonist, the MABP decrease by captopril was only 35\u2002\u00b1\u20024%, (p\u2002&lt;\u20020.05\u2002vs. captopril alone). Bilateral nephrectomy reduced the peak MABP effect of PD-134672 by 67%, while the effects of captopril on MABP were affected to a lesser degree (57%). Therefore, captopril remains more effective in reducing MABP (p\u2002&lt;\u20020.05\u2002vs. that of PD-134672). These results suggest that renin inhibitors and AngII antagonists act more specifically on the rennin\u2013angiotensin system cascade, while captopril acts partially by a bradykinin-dependent mechanism. The small animal model described provides a novel tool for the comparative pharmacologic assessment of different rennin\u2013angiotensin system inhibitors.Key words: blood pressure, guinea pig, rennin\u2013angiotensin system, rennin\u2013angiotensin system inhibition. <\/jats:p>","DOI":"10.1139\/y95-209","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T09:00:14Z","timestamp":1303635614000},"page":"1512-1518","source":"Crossref","is-referenced-by-count":2,"title":["Comparative studies on differential inhibition of the rennin\u2013angiotensin system in the anesthetized guinea pig"],"prefix":"10.1139","volume":"73","author":[{"given":"J.","family":"Duan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Jaramillo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. L.","family":"Jung","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. L.","family":"McLeod","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. H.","family":"Fernandas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Mathis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"p_3\/p_3_1","doi-asserted-by":"crossref","first-page":"1089","DOI":"10.1161\/01.HYP.8.11.1089","volume":"8","author":"Bentos A.","year":"1986","journal-title":"Hypertension (Dallas)"},{"key":"p_4\/p_4_1","first-page":"S53","volume":"1","author":"Bmwner H.R.","year":"1993","journal-title":"J. Hypertens. Ib(Supp"},{"key":"p_5\/p_5_1","doi-asserted-by":"crossref","first-page":"75","DOI":"10.1097\/00004872-199301000-00011","volume":"11","author":"Clozel J.-P.","year":"1993","journal-title":"Hypertens."},{"key":"p_6\/p_6_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1161\/01.HYP.16.1.1","volume":"16","author":"Corvo H, P.","year":"1990","journal-title":"Hypertension (Ddlas)"},{"key":"p_7\/p_7_1","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1097\/00005344-199308000-00010","volume":"22","author":"El Amrani A.-I.K.","year":"1993","journal-title":"Cardiovasc. Phamacol."},{"key":"p_8\/p_8_1","first-page":"75","volume":"20","author":"Fossa A.A.","year":"1992","journal-title":"Cardiovasc. Phamacol."},{"key":"p_9\/p_9_1","first-page":"S25","volume":"12","author":"Fouad-Tarazi F.M.","year":"1994","journal-title":"J. Hypertens."},{"key":"p_10\/p_10_1","doi-asserted-by":"crossref","first-page":"683","DOI":"10.1111\/j.1476-5381.1994.tb13130.x","volume":"112","author":"Feletou M.","year":"1994","journal-title":"Br. J. Pharmacol."},{"key":"p_11\/p_11_1","first-page":"873","volume":"34","author":"Ffishman W.H.","year":"1994","journal-title":"J. Clin. Phamacol."},{"key":"p_12\/p_12_1","doi-asserted-by":"crossref","first-page":"1020","DOI":"10.1038\/ki.1992.383","volume":"42","author":"Gavras I.","year":"1992","journal-title":"Kidney Hnt."},{"key":"p_13\/p_13_1","doi-asserted-by":"crossref","first-page":"173","DOI":"10.1002\/med.2610100203","volume":"80","author":"Greenlee W.J.","year":"1990","journal-title":"Med. Res. Rev."},{"key":"p_14\/p_14_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1097\/00004872-199004000-00009","volume":"8","author":"Hall J .","year":"1990","journal-title":"J. Hypertens."},{"key":"p_15\/p_15_1","doi-asserted-by":"crossref","first-page":"1155","DOI":"10.1097\/00004872-199311000-00001","volume":"11","author":"Husain A.","year":"1993","journal-title":"J. Hypertens."},{"key":"p_16\/p_16_1","first-page":"81","volume":"31","author":"Keeton T.K.","year":"1981","journal-title":"Phamacol. Rev."},{"key":"p_17\/p_17_1","first-page":"281","volume":"43","author":"Eindpaintner K.","year":"1993","journal-title":"Dmg Res."},{"key":"p_19\/p_19_1","doi-asserted-by":"crossref","first-page":"721","DOI":"10.1097\/00004872-198712000-00015","volume":"5","author":"Neisius D.","year":"1987","journal-title":"J. Hypertens."},{"key":"p_20\/p_20_1","first-page":"14","volume":"1","author":"Opie L.H.","year":"1994","journal-title":"Am. Sci. Med."},{"key":"p_21\/p_21_1","doi-asserted-by":"crossref","first-page":"239","DOI":"10.1016\/0160-5402(90)90052-M","volume":"23","author":"Pails D.T.","year":"1990","journal-title":"J. Phamacol. Methods"},{"key":"p_24\/p_24_1","doi-asserted-by":"crossref","first-page":"112","DOI":"10.1097\/00041552-199401000-00016","volume":"3","author":"Smith R.D.","year":"1994","journal-title":"Curr. Opin. Nephrol. Hypertens."},{"key":"p_25\/p_25_1","doi-asserted-by":"crossref","first-page":"150","DOI":"10.1161\/01.HYP.9.2.150","volume":"9","author":"Smith S.G.","year":"1987","journal-title":"Hypertension"},{"key":"p_26\/p_26_1","first-page":"285","volume":"45","author":"Wong P.C.","year":"1993","journal-title":"Pharmacol. Rev."},{"key":"p_27\/p_27_1","doi-asserted-by":"crossref","first-page":"146","DOI":"10.1093\/cvr\/28.2.146","volume":"28","author":"Unger T.","year":"1994","journal-title":"Cardiovasc. Res."},{"key":"p_28\/p_28_1","doi-asserted-by":"crossref","first-page":"255","DOI":"10.1161\/01.HYP.19.3.255","volume":"19","author":"Veniant M.","year":"1992","journal-title":"Hypertension"},{"key":"p_29\/p_29_1","first-page":"337","volume":"9","author":"Wood J.M.","year":"1987","journal-title":"Clin. Exp. Hypertens. Part A"}],"container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y95-209","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T15:38:01Z","timestamp":1578238681000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y95-209"}},"issued":{"date-parts":[[1995,10,1]]},"references-count":24,"journal-issue":{"issue":"10","published-print":{"date-parts":[[1995,10,1]]}},"alternative-id":["10.1139\/y95-209"],"URL":"https:\/\/doi.org\/10.1139\/y95-209","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1995,10,1]]}},{"indexed":{"date-parts":[[2023,10,26]],"date-time":"2023-10-26T00:19:17Z","timestamp":1698279557841},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"5","license":[{"start":{"date-parts":[[1990,5,1]],"date-time":"1990-05-01T00:00:00Z","timestamp":641520000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1990,5,1]]},"abstract":"<jats:p> We examined the effects of acute and chronic treatments with naloxone on release of vasopressin and oxytocin from the hypothalamoneurohypophyseal system (HNS) in conscious, chronically instrumented Long\u2013Evans rats. Plasma concentrations of vasopressin-associated neurophysin and oxytocin-associated neurophysin were evaluated before and during an intravenous infusion of 18% saline at 100\u2002\u03bcL\u2219kg<jats:sup>\u22121<\/jats:sup> body weight\u2219min<jats:sup>\u22121<\/jats:sup> for 60\u2002min. Acute treatment with naloxone (2.75\u2002\u03bcmol\/kg, intravenous) did not measurably alter basal plasma osmolality or vasopressin-associated neurophysin concentration, but it caused a three-fold rise in basal plasma oxytocin-associated neurophysin concentration (16\u2002\u00b1\u20022 to 46\u2002\u00b1\u20023\u2002fmol\/mL, p\u2002&lt;\u20020.005). Chronic treatment with naloxone (13.75\u2002\u03bcmol\/day, subcutaneous pellets) increased plasma osmolality (292\u2002\u00b1\u20021 to 300\u2002\u00b1\u20022\u2002mosmol\/kg H<jats:sub>2<\/jats:sub>O, p\u2002&lt;\u20020.01) by day 5, but it had no measurable effects on basal vasopressin- or oxytocin-associated neurophysin concentration. There were also no significant differences in plasma sodium concentration (144.8\u2002\u00b1\u20021.1 vs. 142.2\u2002\u00b1\u20021.4\u2002mequiv.\/L) under both conditions. Acute and chronic treatments with naloxone accompanied by salt loading produced a five- and four-fold decrease in the rates that plasma concentration of vasopressin-associated neurophysin changed with plasma osmolality, compared with untreated salt-loaded control rats. For oxytocin secretion from the HNS, both treatments accompanied by salt loading substantially decreased the threshold for changes in relation to plasma osmolality; the rise in plasma concentration of oxytocin-associated neurophysin was similar at all levels of hyperosmotic stimulation. A strongly correlated relationship between plasma oxytocin-associated neurophysin and plasma osmolality (r\u2002=\u20020.739) found for control animals became poorly correlated following treatments (acute, r\u2002=\u20020.173; chronic, r\u2002=\u2002\u22120.079). Our results suggest that in conscious rats, endogenous opioid peptides enhance the secretion of vasopressin from neurones of the HNS in response to hyperosmotic stimulation but inhibit both basal and stimulated release of oxytocin.Key words: naloxone, vasopressin, oxytocin, neurophysin, conscious rats. <\/jats:p>","DOI":"10.1139\/y90-083","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T16:55:07Z","timestamp":1303577707000},"page":"568-574","source":"Crossref","is-referenced-by-count":3,"title":["Influence of opioid peptides on release from vasopressin and oxytocin neurones of the hypothalamoneurohypophyseal system: effects of naloxone in the conscious rat"],"prefix":"10.1139","volume":"68","author":[{"given":"Savio W. T.","family":"Cheng","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward F.","family":"O'Connor","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William G.","family":"North","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y90-083","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T10:15:48Z","timestamp":1578219348000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y90-083"}},"issued":{"date-parts":[[1990,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1990,5,1]]}},"alternative-id":["10.1139\/y90-083"],"URL":"https:\/\/doi.org\/10.1139\/y90-083","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1990,5,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T14:47:25Z","timestamp":1649170045551},"reference-count":10,"publisher":"Canadian Science Publishing","issue":"1","license":[{"start":{"date-parts":[[1966,1,1]],"date-time":"1966-01-01T00:00:00Z","timestamp":-126230400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1966,1,1]]},"abstract":"<jats:p> The effect of X-irradiation on the cell size distribution of thymus lymphocytes was studied with the aid of an electronic Coulter cell counter.In the thymus the small lymphocytes were the most radioresistant and the large lymphocytes were repopulated before the medium-sized lymphocytes. As the radiation dose was increased from 50 to 400\u2002r, there was a decrease in the large to small thymocyte ratio, and a longer time period was required for a return to the normal ratio. Single and repeated doses of X-irradiation produced much the same type of effect on the large to small ratio of both thymus and spleen lymphocytes, and it was concluded that the effects of X-irradiation on the cell size distribution of lymphocytes in the thymus and spleen were similar. <\/jats:p>","DOI":"10.1139\/y66-009","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T08:47:18Z","timestamp":1303634838000},"page":"77-87","source":"Crossref","is-referenced-by-count":3,"title":["THE EFFECT OF X-IRRADIATION ON THE CELL SIZE DISTRIBUTION OF THYMUS LYMPHOCYTES"],"prefix":"10.1139","volume":"44","author":[{"given":"P. V.","family":"Vittorio","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Blehm","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Linkletter","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"p_3\/p_3_1","first-page":"1","volume":"1","author":"Los I.","journal-title":"Itcpt."},{"key":"p_8\/p_8_1","first-page":"253","volume":"72","author":"Hi CKEA I I E","year":"1912","journal-title":"BioI. Paris"},{"key":"p_10\/p_10_1","first-page":"717","volume":"46","author":"OIKE.","year":"1935","journal-title":"Arch. Iliol."},{"key":"p_15\/p_15_1","first-page":"225","volume":"100","author":"HCE.","year":"1956","journal-title":"Strahlcitherapie"},{"key":"p_19\/p_19_1","doi-asserted-by":"crossref","unstructured":"J . I*. GKANT,hl. C. URITTOK,alld T. E. KURTZ. iliri. J. Clin. Pnthol. 33, 13%(1960).","DOI":"10.1093\/ajcp\/33.2.138"},{"key":"p_22\/p_22_1","first-page":"349","volume":"39","author":"Ii' G.","year":"1963","journal-title":"Fiathoi."},{"key":"p_24\/p_24_1","first-page":"50","volume":"141","author":"Acts I'athoi","year":"1960","journal-title":"Microbial. Scand. SuppI."},{"key":"p_27\/p_27_1","first-page":"483","volume":"5","author":"Bfriscl O C E P","year":"1956","journal-title":"Ses."},{"key":"p_28\/p_28_1","first-page":"52","volume":"5","author":"Ii S. KAPIAK.","year":"1956","journal-title":"Res."},{"key":"p_29\/p_29_1","first-page":"24","volume":"11","author":"Ba","year":"1959","journal-title":"Kes."}],"container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y66-009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T16:11:58Z","timestamp":1578240718000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y66-009"}},"issued":{"date-parts":[[1966,1,1]]},"references-count":10,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1966,1,1]]}},"alternative-id":["10.1139\/y66-009"],"URL":"https:\/\/doi.org\/10.1139\/y66-009","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1966,1,1]]}},{"indexed":{"date-parts":[[2023,3,15]],"date-time":"2023-03-15T00:31:17Z","timestamp":1678840277278},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"6","license":[{"start":{"date-parts":[[1974,12,1]],"date-time":"1974-12-01T00:00:00Z","timestamp":155088000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1974,12,1]]},"abstract":"<jats:p> CO<jats:sub>2<\/jats:sub> administration to rats anesthetized with sodium pentobarbitone caused contraction of the spleen and elevation of its cAMP content, but no rise in serum corticosterone. Studies with adrenoreceptor blockers showed that the contraction is caused by stimulation of \u03b1-receptors, whereas cAMP elevation is a \u03b2 effect. The contraction was shown to be due to circulating catecholamines released from the adrenal glands, whereas cAMP elevation was due both to circulating and to locally released catecholamines in the spleen. Theophylline prevented the CO<jats:sub>2<\/jats:sub>-induced contraction. Dibutyryl cyclic GMP caused a fall in the cAMP content of the spleen but no contraction. The use of CO<jats:sub>2<\/jats:sub> for the sacrifice of experimental animals is recommended where low levels of corticosteroids in blood are desirable. <\/jats:p>","DOI":"10.1139\/y74-141","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T04:49:50Z","timestamp":1303620590000},"page":"1074-1079","source":"Crossref","is-referenced-by-count":3,"title":["Changes in Spleen Weight, Cyclic-AMP Content, and Serum-Corticosterone Levels of Rats in Response to CO<sub>2<\/sub>"],"prefix":"10.1139","volume":"52","author":[{"given":"D. C.","family":"Lehotay","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. E. Pearson","family":"Murphy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y74-141","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T11:21:33Z","timestamp":1578223293000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y74-141"}},"issued":{"date-parts":[[1974,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1974,12,1]]}},"alternative-id":["10.1139\/y74-141"],"URL":"https:\/\/doi.org\/10.1139\/y74-141","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1974,12,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T17:23:09Z","timestamp":1648920189870},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"4","license":[{"start":{"date-parts":[[1981,4,1]],"date-time":"1981-04-01T00:00:00Z","timestamp":354931200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1981,4,1]]},"abstract":"<jats:p> Cold-adapted (CA) and warm-adapted (WA) rats (5 and 28 \u00b0C) were infused with noradrenaline (4\u2002\u03bcg\u2219kg<jats:sup>\u22121<\/jats:sup>\u2219min<jats:sup>\u22121<\/jats:sup>) for 15\u2002min. Blood was collected from Sulzer's vein coming from brown adipose tissue and analyzed for total carnitine, free carnitine, and \u03b2-hydroxybutyrate content, before and up to 45\u2002min after the infusion. Acylcarnitine (total minus free carnitine) levels increased more and total carnitine levels decreased more in the CA group than in the WA group. \u03b2-Hydroxybutyrate content increased to the same extent (from about 0.16 to 0.8\u2002mM) in both groups. Brown fat was found not to release carnitine into the circulation after NA infusion. Twenty minutes after the end of infusion brown fat retained both ketones and acylcarnitine in the CA rats only. <\/jats:p>","DOI":"10.1139\/y81-055","type":"journal-article","created":{"date-parts":[[2011,4,23]],"date-time":"2011-04-23T20:48:13Z","timestamp":1303591693000},"page":"351-354","source":"Crossref","is-referenced-by-count":1,"title":["Brown adipose tissue and carnitine in cold-adapted rats"],"prefix":"10.1139","volume":"59","author":[{"given":"P.","family":"Hahn","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Laury","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Portet","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","container-title":["Canadian Journal of Physiology and Pharmacology"],"language":"en","link":[{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/pdf\/10.1139\/y81-055","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,5]],"date-time":"2020-01-05T16:23:30Z","timestamp":1578241410000},"score":0.0,"resource":{"primary":{"URL":"http:\/\/www.nrcresearchpress.com\/doi\/10.1139\/y81-055"}},"issued":{"date-parts":[[1981,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1981,4,1]]}},"alternative-id":["10.1139\/y81-055"],"URL":"https:\/\/doi.org\/10.1139\/y81-055","ISSN":["0008-4212","1205-7541"],"issn-type":[{"value":"0008-4212","type":"print"},{"value":"1205-7541","type":"electronic"}],"published":{"date-parts":[[1981,4,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T13:44:07Z","timestamp":1648993447280},"reference-count":0,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[1984,9,1]],"date-time":"1984-09-01T00:00:00Z","timestamp":462844800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[1984,9,1]]},"abstract":"<jats:p> The Canadian Nuclear Fuel Waste Management Program is developing methods for the safe disposal of both used nuclear fuel and fuel recycle waste. The disposal strategy is based on interim storage of the used fuel, immobilization of either used fuel or recycle waste, and disposal, deep in a stable geological formation in the Canadian Shield. The disposal concept proposes a multibarrier system to inhibit the release of the radioactive waste from the disposal vault. The principal components of the multibarrier system are (i) the waste form in whch the radionuclides are immobilized, (ii) engineered barriers including high integrity containers, buffers and backfills designed to retard the movement of groundwaters in the disposal vault, and (iii) the natural barrier provided by the massive geological formation itself. The research programs to investigate this concept are discussed briefly. Several different waste forms are being developed for the immobilization of high-level fuel recycle waste, including glass, glass-ceramics and crystalline materials. Dissolution of these materials in groundwater is the only likely scenario that could lead to radionuclide release. The factors that influence the aqueous dissolution behaviour of these materials are reviewed. <\/jats:p>","DOI":"10.1139\/y84-166","type":"journal-article","created":{"date-parts":[[2011,4,24]],"date-time":"2011-04-24T08:53:01Z","timestamp":1303635181000},"page":"979-985","source":"Crossref","is-referenced-by-count":0,"title":["Immobilization and geological disposal of nuclear fuel waste"],"prefix":"10.1139","volume":"62","author":[{"given":"J. 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