摘要
目的 :研究巴曲酶 (BAT)对狗心脏缺血 /再灌注 (I/R)损伤过程中血栓素A2 (TXA2 )水平的影响。方法 :结扎狗左冠状动脉前降支 3 0min ,恢复血流 90min ,造成I/R模型 ,于缺血前或缺血后 15min静注BAT( 1U/kg) ,测定血浆、心肌TXB2 浓度以及血浆磷酸肌酸激酶 (CK)和乳酸脱氢酶 (LDH)活性 ,并检测心脏功能 ,观察病理学变化。结果 :I/R组心肌组织及血浆TXB2 水平明显升高 ,血浆CK及LDH活性明显降低 ,心功能受损。病理学发现心肌纤维水肿、排列紊乱、线粒体水肿、嵴明显断裂、细胞核皱缩。给予BAT后 ,动物死亡率、再灌期血浆及心肌TXB2 水平、血浆CK及LDH活性以及LVEDP明显低于I/R组 ,而±dp/dtmax明显高于I/R组 ,病理学检查无明显损伤。结论 :BAT能够降低血浆及心肌TXA2 水平减轻心肌组织I/R损伤。
AIM:To investigate the effect of batroxobin on thromboxane A 2(TXA 2)level in canine heart ischemia/reperfusion (I/R) injury and the cardioprotective mechanism of batroxobin against I/R injury. METHODS: Canine heart ischemia was induced by ligation of the left anterior descending coronary artery for 30 min followed by 90 min reperfusion.Batroxobin was intravenously administered before heart ischemia and 15 min before reperfusion.The level of plasma thromboxane (TXA 2) ,creatine phosphokinase (CK), lactic dehydrogenase (LDH ) and the concentration of myocardial TXA 2 were measured. The pathological changes in I/R myocardium were observed. RESULTS: In I/R group, TXA 2 levels of both plasma and myocardium increased significantly,and myocardium was injured obviously. Myocyte cells of central zone of I/R heart showed intracellular edema, swollen and damaged mitochondria, and fragmentation of cristae and concentrated nucleus. Plasma CK and LDH level was also elevated. Both ways of batroxobin administration reduced TXA 2 level apparently and plasma CK?LDH were also reduced significantly. LVEDP lowered while +dp/dt max elevated greatly,the mortality of I/R canine reduced obviously. CONCLUSION: Batroxobin decreased TXA 2 levels of both plasma and myocardium significantly, and could afford protection from I/R injury.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第1期25-28,共4页
Chinese Journal of Pathophysiology
