大鼠脑缺血-再灌注后心肌内皮素-1的表达  

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

作　　者：王吉文[1] 符少萍[1] 丘宇茹[1] 黄子通[1] 

机构地区：[1]中山大学附属第二医院急诊科,广州510120

出　　处：《中华急诊医学杂志》2008年第10期1059-1062,共4页Chinese Journal of Emergency Medicine

基　　金：中山大学附属第二医院青年人才基金项目（F00200307）

摘　　要：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（220～250g）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、72h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）；血浆ET-1浓度在6h达峰值，而后逐渐下降（P〈0．05），心肌ET-1于6h开始升高，12h达峰值，而后下降（P〈0．05）。脑缺血-再灌注后脑缺血面积、CK-MB、心肌中ET-1均于12h达到峰值，而后下降（P〈0．05），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、72h明显减少（P〈0．05），CK-MB在6、12h明显降低（P〈0．05），血清ET-1无变化，心肌ET-1峰值前移，在12、48h显著性降低（P〈0．05）。结论较大面积的脑缺血可继发心肌损伤，ET-1参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，但加重心肌损伤，ET-1参与此作用。Objective To study the expression of ET-1 in myocardium during cerebral ischemia and reperfusion, 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 isehemia group （ n = 80）, cerebral isehemia/reperfusion group （ n = 80）. The area of cerebral isehemia, 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 observed at 6 h after cerebral ischemia in cerebral ischemia group, and peaked at 12 h （ P 〉 0.05）. The concentration of CK-MB increased gradually after cerebral isehmia, peaked at 12 h （P 〈 0.05）, and then gradually decreased. The serum concentration of ET- 1 peaked at 6 h and then gradually decreased. The content of ET- 1 in myocardium began to increase at 6 h after cerebral ischemia, and peaked at 12 h （ P 〈 0.05）. In cerebral ischemia/ repeffusion 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 isehemia group, the size of cerebral necrosis reduced obviously at 24 h,48 h,72 h in cerebral ischemia/repeffusion 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 isehemia. Though cerebral reperfusion can protect brain, but it make myocardial injury more serio

关 键 词：脑缺血 脑再灌注 内皮素-1 心肌损伤 CK-MB 

分 类 号：R743.3[医药卫生—神经病学与精神病学]