{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T05:21:17Z","timestamp":1783660877371,"version":"3.55.0"},"reference-count":47,"publisher":"Canadian Science Publishing","issue":"2","license":[{"start":{"date-parts":[[2021,2,1]],"date-time":"2021-02-01T00:00:00Z","timestamp":1612137600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:p> This study examined the effects of ischemic preconditioning (IP) on the ischemia\/reperfusion (I\/R) induced injury in normal and hypertrophied hearts. Cardiac hypertrophy in rabbits was induced by L-thyroxine (0.5 mg\/kg\/day for 16 days). Hearts with or without IP (3 cycles of 5 min ischemia and 10 min reperfusion) were subjected to I\/R (60 min ischemia followed by 60 min reperfusion). IP reduced the I\/R-induced infarct size from 68% to 24% and 57% to 33% in the normal and hypertrophied hearts, respectively. Leakage of creatine phosphokinase in the perfusate from the hypertrophied hearts due to I\/R was markedly less than that form the normal hearts; IP prevented these changes. Although IP augmented the increase in phosphorylated p38-mitogen-activated protein kinase (p38-MAPK) content due to I\/R, this effect was less in the hypertrophied than in the normal heart. These results suggest that reduced cardioprotection by IP of the I\/R-induced injury in hypertrophied hearts may be due to reduced activation of p38-MAPK in comparison with normal hearts. <\/jats:p>","DOI":"10.1139\/cjpp-2020-0400","type":"journal-article","created":{"date-parts":[[2021,2,8]],"date-time":"2021-02-08T04:31:13Z","timestamp":1612758673000},"page":"218-223","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Modification of ischemia\/reperfusion induced infarct size by ischemic preconditioning in hypertrophied hearts"],"prefix":"10.1139","volume":"99","author":[{"given":"Mohamad","family":"Nusier","sequence":"first","affiliation":[{"name":"School of Medicine, Department of Physiology and Biochemistry, Jordan University of Science and Technology, Irbid, Jordan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad","family":"Alqudah","sequence":"additional","affiliation":[{"name":"School of Medicine, Department of Physiology and Biochemistry, Jordan University of Science and Technology, Irbid, Jordan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vijayan","family":"Elimban","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular Sciences, St. Boniface Hospital, Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naranjan S.","family":"Dhalla","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular Sciences, St. Boniface Hospital, Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21124200"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1093\/eurjhf\/hft105"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1998.0891"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200003000-00019"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.2.609"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.66.6.1146"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.584490"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-011-0199-3"},{"key":"refg9\/ref9","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.84.1.341"},{"key":"refg10\/ref10","doi-asserted-by":"publisher","DOI":"10.1002\/iub.31"},{"key":"refg11\/ref11","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(00)00078-X"},{"key":"refg12\/ref12","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200018060-00002"},{"key":"refg13\/ref13","doi-asserted-by":"publisher","DOI":"10.3390\/medsci5020008"},{"key":"refg14\/ref14","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-014-2213-1"},{"key":"refg15\/ref15","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-34879-6"},{"key":"refg16\/ref16","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.118.11125"},{"key":"refg17\/ref17","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.2001.1341"},{"key":"refg18\/ref18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.1.H331"},{"key":"refg19\/ref19","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199910213411706"},{"key":"refg20\/ref20","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2007.10.026"},{"key":"refg21\/ref21","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1997.0456"},{"key":"refg22\/ref22","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2828(95)90590-1"},{"key":"refg23\/ref23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.56.2.262"},{"key":"refg24\/ref24","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9149(94)90257-7"},{"key":"refg25\/ref25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1076-7460.2001.00002.x"},{"key":"refg26\/ref26","doi-asserted-by":"publisher","DOI":"10.1007\/s00228-011-1193-2"},{"key":"refg27\/ref27","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-010-0568-5"},{"issue":"1","key":"refg28\/ref28","first-page":"43","volume":"20","author":"Lochner A.","year":"2009","journal-title":"Cardiovas. 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