Change of Myocardial Endothelin-1 and Norepinephrine during Cerebral Ischemia and Reperfusion to Cause Myocardial Injury in Rat

【Objective】 In order to investigate the expression of endothelin-1 (ET-1) and norepinephrine (NE) in myocardium during cerebral ischemia and reperfusion, and research the mechanism of cerebral cardiac syndrome. 【Methods】 The rats were divided into three groups: sham control group (n = 48), ischemia group (n = 80), and ischemia / reperfusion group (n = 80). The area of cerebral ischemia, the concentration of serum CK-MB, and the concentration of myocardial NE and ET-1 were determined at 0, 6, 12, 24, 48, and 72 hours after cerebral ischemia and cerebral reperfusion,and compared at the same and different time. 【Results】 Cerebral ischemia focus might be observed after 6 hours of cerebral necrosis in cerebral ischemia group , and was the largest after 12 hours (P 0.05). The concentration of CK-MB increased gradually after cerebral ischemia, and peaked at 12 hour (P 0.05). The content of ET-1 in myocardium began to increase at 6 hours after cerebral ischemia, and peaked at 12 hours (P 0.05). The myocardial concentration of NE peaked at 6 h, and gradually decreased after 12 h (P 0.01). In ischemia / reperfusion group, all of cerebral necrosis size, CK-MB concentration and myocardial ET-1 concentration peaked at 12 hour and gradually decreased (P 0.05). The peak time of myocardial NE was not changed, but the high level of NE was delayed over 48 h. Compared with ischemia group, the size of cerebral necrosis reduced obviously at 24 h, 48 h, and 72 h in cerebral ischemia / reperfusion group (P 0.05). The concentration of CK-MB in ischemia / reperfusion group was higher than in ischemia group (P 0.05). The peak of myocardial ET-1 advanced to show up in in ischemia / reperfusion group. The peak time of myocardial NE was not changed, but the high level of NE was delayed over 48 h (P 0.05). The pathological change of myocardium included inflammatory cell infiltration, endocarditis, myofibrosis, and focal necrosis. 【Conclusion】 Cerebral ischemia might cause myocardial injury. NE and ET-1 involved in the course of myocardial injury following cerebral ischemia. Though cerebral reperfusion protected brain tissue, it made myocardial injury more serious. NE and ET-1 participated in this course.