大鼠脑缺血-再灌注后心肌内皮素-1的表达

目的 研究内皮素-1(ET-1)在脑缺血及再灌注期间心肌中的表达,探讨脑心综合征发生的机制. 方法 将208只SD大鼠(220～250 g)随机分成假手术组(n=48)、脑缺血组(n=80)、脑缺血-再灌注组(n=80),测定线栓法制备的脑缺血及再灌注0、6、12、24、48、72 h时点的脑缺血面积、血清ET-1和CK-MB的浓度及心肌中ET-1的含量,用t检验或方差分析进行统计. 结果 脑缺血后6 h可见的缺血灶,12 h达到峰值(P>0.05);CK-MB逐渐升高,12 h达峰值,其后逐渐下降(P<0.05);血浆ET-1浓度在6 h达峰值,而后逐渐下降(P<0.05),心肌ET-1于6 h开始升高,12 h达峰值,而后下降(P<0.05).脑缺血.再灌注后脑缺血面积、CK-MB、心肌中ET-1均于12 h达到峰值,而后下降(P<0.05),血清中ET-1与脑缺血组相似(P>0.05).与脑缺血组比较,脑缺血-再灌注组脑缺血面积在24、48、72 h明显减少(P<0.05),CK-MB在6、12 h明显降低(P<0.05),血清ET-1无变化,心肌ET-1峰值前移,在12、48 h显著性降低(P<0.05). 结论 较面积的脑缺血可继发心肌损伤,ET-1参与腩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,但加重心肌损伤,ET-1参与此作用.

Expresstion of myocardial endothelin-1 after cerebral ischemia-reperfusion in rats

Objective To study the expression of EI-1 in myocardium during cerebral ischemia and reper-fusion, and to investigate the mechanism of cerebral cardiac syndrome. Method Two hundred and eight SD rats weighting 220～250 gram, were divided into three groups: sham control group (n=48), cerebral ischemia group (n=80), cerebral ischemia/reperfusion group (n=80). The area of cerebral ischemia, and the concentration of sennn ET-1 and CK-MB, and the content of myocardial ET-1 were determined in 0,6, 12,24,48,72 h after cerebral ischemia and reperfusion, and were analyzed by t-test or F-test. Results Cerebral necrosis area was ob-served at 6 h after cerebral ischemia in cerebral ischemia group, and peaked at 12 h (P>0.05). The concentra-tion of CK-MB increased gradually after cerebral ischmia, peaked at 12 h (P<0.05), and then gradually de-creased. The serum concentration of ET-1 peaked at 6 h and then gradually decreased. The content of ET-1 in my-ocardium began to increase at 6 h after cerebral ischemia, and peaked at 12 h (P<0.05). In cerebral ischemia/reperfusion group, all of cerebral necrosis size, CK-MB concentration and myocardial ET-1 concent paelced at 12 h and then gradually decreased (P<0.05). Change of ET-1 concentration in blood was similar to that in cerebral ischemia group. Compared with cerebral ischemia group, the size of cerebral necrosis reduced obviously at 24 h,48 h,72 h in cerebral ischemia/reperfusion group (P<0.05). The concentration of CK-MB in cerebral ischemia/ reperfusion group was higher than that in cerebral isehemia group (P<0.05). The peak time of myocardial ET-1 was shatened in cerebral ischemia/reperfusion group. The change of serum ET-1 was not different between two groups. Conclusions Large area of cerebral ischemia, might cause myocardial injury. ET-1 is involved in the course of myocardial injury following cerebral ischemia. Though cerebral reperfusion can protect brain,but it make myocardial injury more serious,and ET-1 might participate in this course.