摘要
目的观察二氮嗪预处理对高钾停跳离体兔心缺血/再灌注损伤的保护作用。方法采用离体兔心Langendorff灌注实验模型,离体兔心40只随机等分成5组(n=8)。离体兔心4℃标准St.Thomas停搏液(K+16mmol/L)至心脏停跳,45 min后再灌注20 min,药物于心脏停跳前灌注15 min,观察在不同二氮嗪浓度下对再灌注后心功能及冠脉血流的影响以及再灌注末心肌超微结构、蛋白含量、脂质过氧化物丙二醛、超氧化物歧化酶、心肌酶以及腺苷酸含量的变化。结果再灌注后各浓度二氮嗪预处理的离体兔心心功能的恢复率均明显高于对照组,心肌丙二醛的含量、蛋白的漏出量明显低于对照组(P<0.05或0.01),超微结构观察结构损伤较轻。结论二氮嗪预处理和超极化停跳对离体兔心缺血/再灌注心肌具有较好的保护效果。
Objective To investigate the protective effect of mitochondrial ATP sensitive potassium （KATP） channel opener, diazoxide, in different concentrations, against the myocardial injury in isolated rabbit hearts caused by ischemia/reperfusion. Methods The experiment was performed in isolated rabbit hearts perfused on Langendorff apparatus. 40 rabbit hearts were randomly divided into five groups. The hearts were first arrested by cold cardioplegia for 45 rain before warm K - H solution was reperfused for 20 min. Diazoxide of different concentrations, 1, 30, 50 and 200 μmol/L, was perfused for 15 min before the heart stopped beating. The hemodynamic indexes were determined in the course of reperfusion. The ultrastructural and biochemical studies on the myocardium were made be the end of the experiment. Results In contrast to the findings in the control group, the recovery of myocardial contractility and heart rate was earlier in the test groups, the myocardial MDA level and the release amount of albumen were lower, the activities of creatin kinase （CK） and lactate dehydrogenase （LDH） were much lower, and also, the level of myocardial ATP was higher（ P 〈 0.05 or 0.01 ）. Conclusion The drug preconditioning with diazoxide and the hyperpolarized arrest induced by diazoxide （200 μnol/L） may offer myocardial protective effect against ischemia/ reperfusion injury.
出处
《徐州医学院学报》
CAS
2005年第6期522-525,共4页
Acta Academiae Medicinae Xuzhou
基金
徐州医学院附属医院科研资助项目(2003051)
关键词
二氮嗪
缺血/再灌注损伤
心
离体家兔
diazoxide
ischemia/reperfusion injury
heart, isolated rabbit
