{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T09:23:39Z","timestamp":1789809819145,"version":"4.0.1"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2001,3]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            \u2014Endogenous norepinephrine release induced by cerebral ischemia may lead to small areas of necrosis in normal hearts. Conversely, norepinephrine may be one of the mediators that limit myocardial infarct size by ischemic preconditioning. Because brief ischemia in kidneys or skeletal muscle limits infarct size produced by coronary artery occlusion, we investigated whether cardiac norepinephrine release during transient cerebral ischemia also elicits remote myocardial preconditioning.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            \u2014Forty-one crossbred pigs of either sex were assigned to 1 of 7 experimental groups, of which in 6 groups myocardial infarct size was determined after a 60-minute coronary occlusion and 120 minutes of reperfusion. One group served as control (no pretreatment), while the other groups were pretreated with either cerebral ischemia or an intracoronary infusion of norepinephrine.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            \u2014In 10 anesthetized control pigs, infarct size was 84\u00b13% (mean\u00b1SEM) of the area at risk after a 60-minute coronary occlusion and 120 minutes of reperfusion. Intracoronary infusion of 0.03 nmol\/kg \u00b7 min\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            norepinephrine for 10 minutes before coronary occlusion did not affect infarct size (80\u00b13%; n=6), whereas infusion of 0.12 nmol\/kg \u00b7 min\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            limited infarct size (65\u00b12%; n=7;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Neither 10-minute (n=5) nor 30-minute (n=6) cerebral ischemia produced by elevation of intracranial pressure before coronary occlusion affected infarct size (83\u00b14% and 82\u00b13%, respectively). Myocardial interstitial norepinephrine levels tripled during cerebral ischemia and during low-dose norepinephrine but increased 10-fold during high-dose norepinephrine. Norepinephrine levels increased progressively up to 500-fold in the area at risk during the 60-minute coronary occlusion, independent of the pretreatment, while norepinephrine levels remained unchanged in adjacent nonischemic myocardium and arterial plasma.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014Cerebral ischemia preceding a coronary occlusion did not modify infarct size, which is likely related to the modest increase in myocardial norepinephrine levels during cerebral ischemia. The infarct size limitation by high-dose exogenous norepinephrine is not associated with blunting of the ischemia-induced increase in myocardial interstitial norepinephrine levels.\n          <\/jats:p>","DOI":"10.1161\/01.str.32.3.767","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"767-774","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["Cardioprotection in Pigs by Exogenous Norepinephrine but not by Cerebral Ischemia\u2013Induced Release of Endogenous Norepinephrine"],"prefix":"10.1161","volume":"32","author":[{"given":"Sandra","family":"de Zeeuw","sequence":"first","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas W.","family":"Lameris","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dirk J.","family":"Duncker","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Djo","family":"Hasan","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frans","family":"Boomsma","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anton H.","family":"van den Meiracker","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pieter D.","family":"Verdouw","sequence":"additional","affiliation":[{"name":"From the Departments of Experimental Cardiology, Thoraxcenter (S. de Z., D.J.D., P.D.V.), Internal Medicine I (T.W.L., F.B., A.H. van den M.), and Neurology (D.H.), Erasmus University Rotterdam (Netherlands)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.74.5.1124"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.1999.00172.x"},{"key":"e_1_3_2_3_2","first-page":"R887","volume":"273","year":"1997","unstructured":"Pang CY, Neligan P, Zhong A, He W, Xu H, Forrest CR. 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