大鼠脑缺血/再灌注致心肌损伤中心肌内皮素和去甲肾上腺素的表达  

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

作　　者：王吉文[1] 丘宇茹[1] 符少萍[1] 陈玉成[1] 黄子通[1] 

机构地区：[1]中山大学附属第二医院急诊科,广东广州510120

出　　处：《中山大学学报（医学科学版）》2008年第6期695-700,共6页Journal of Sun Yat-Sen University:Medical Sciences

基　　金：中山大学第二附属医院青年人才基金项目(F00200307)

摘　　要：【目的】探讨内皮素1(ET-1)和去甲肾上腺素(NE)在脑缺血期间心肌中的表达及再灌注对其的影响,明确ET-1在脑心综合征发病机制中的作用。【方法】将大鼠随机分成假手术组(n=48)、缺血组(n=80)、再灌注组(n=80),测定脑缺血及再灌注0、6、12、24、48、72h的脑缺血区域面积、血清CK-MB的的浓度、心肌中ET-1、NE的含量变化,比较各指标在同一时点及不同时点间的变化。【结果】脑缺血后6h可见的缺血灶,12h达到峰值(P>0.05);CK-MB逐渐升高,12h达峰值,其后逐渐下降(P<0.05);心肌ET-1于6h开始升高,12h达峰值,而后下降(P<0.05),NE于6h达到峰值,12h开始下降(P<0.05)。再灌注组脑缺血面积、CK-MB、心肌中ET-1均于12h达到峰值,而后下降(P<0.05),心肌NE峰值不变,但至48h持续高水平状态(P<0.05)。与缺血组比较,再灌注组脑缺血面积在24、48、72h明显减少(P<0.05),CK-MB在6、12h明显降低(P<0.05),心肌ET-1峰值前移,在12、48h显著性降低(P<0.05),NE在6、12、72h较缺血组显著增高(P<0.05)。心肌中ET-1和NE含量相关(r=0.166,P=0.036)。心肌病理表现为炎性细胞浸润、心内膜炎、肌纤维变性、灶性坏死,偶见大面积心肌坏死。【结论】较大面积的脑缺血可继发心肌损伤,ET-1、NE可能参与脑缺血后继发心肌损伤的过程;脑缺血后再灌注可明显保护脑组织,但加重继发性心肌损伤,ET-1、NE可能参与此作用。[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 c

关 键 词：脑缺血/再灌注 内皮素-1 去甲肾上腺素 心肌损伤 CK-MB 

分 类 号：R54[医药卫生—心血管疾病]