CAJ | 학술논문

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30min,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。
목적：연구파곡매(BAT)대구심장결혈/재관주(I/R)손상과정중혈전소A2（TXA2）수평적영향。방법：결찰구좌관상동맥전강지30min,회복혈류90min，조성I/R모형，우결혈전혹결혈후15min정주BAT（1U/kg），측정혈장、심기TXB2농도이급혈장린산기산격매（CK）화유산탈경매（LDH）활성，병검측심장공능，관찰병이학변화。결과：I/R조심기조직급혈장TXB2수평명현승고,혈장CK급LDH활성명현강저，심공능수손。병이학발현심기섬유수종、배렬문란、선립체수종、척명현단렬、세포핵추축。급여BAT후，동물사망솔、재관기혈장급심기TXB2수평、혈장CK급LDH활성이급LVEDP명현저우I/R조，이±dp/dtmax명현고우I/R조，병이학검사무명현손상。결론：BAT능구강저혈장급심기TXA2수평감경심기조직I/R손상。
AIM:To investigate the effect of batroxobin on thromboxaneA2（TXA2）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 (TXA2) ，creatine phosphokinase (CK)， lactic dehydrogenase (LDH ) and the concentration of myocardial TXA2 were measured. The pathological changes in I/R myocardium were observed. RESULTS: In I/R group, TXA2 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 TXA2 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 TXA2 levels of both plasma and myocardium significantly, and could afford protection from I/R injury.