外源性溶血磷脂酰胆碱和缺血预处理对离体大鼠工作心脏的作用

The effect of exogenous lysophosphatidylcholine and ischemic preconditioning to isolated working rat hearts

目的 :观察外源性溶血磷脂酰胆碱 (L PC)对离体大鼠工作心脏的损伤作用及缺血预处理 (IP)对离体大鼠心脏的保护作用。方法 :制备离体大鼠工作心脏模型。随机分为 4组 :C组 :用 K- H液连续灌注 35 min; 组 :停灌注 40 m in,再灌注 30 m in;L 组 :用含 5 μmol/L L PC的 K- H液灌注 5 min,再用正常 K- H液灌注 30 min;P组 :停灌注 5 m in后再灌注 5 min,重复 3次 ,然后重复 L 组全过程。结果 :再灌后 ,L 组和 I组心功能均明显下降 ,室颤发生率提高 ,灌注液中乳酸脱氢酶 (L DH)和丙二醛 (MDA)含量明显升高 ,心肌组织中超氧化物歧化酶 (SOD)活力明显降低。与 L 组相比 ,P组心功能指标明显升高 ,L DH和 MDA含量明显降低 ,SOD活力较高 ,无室颤发生。结论 :L PC可导致与经典方法类似效果的类缺血再灌注损伤作用 ,IP对 L PC损伤有保护作用。

AIM:To observe the ischemia reperfusion like effect of exogenous lysophosphatidylcholine(LPC) and the protective effect ischemic preconditioning(IP) in isolated working rat hearts. METHODS:Established isolated working rat heart models,and divided into four groups:C group:the hearts were perfused with K H buffer for 35 min;I group:stop perfusion for 40 min,and then reperfusion for 30 min;L group:the hearts were perfused with K H buffer containing 5 μmol/L LPC for 5 min, reperfused for 30 min;P group:first,the hearts were in three cycle of 5 min of ischemia and 5 min of reperfusion,and then prefused as the L group. RESULTS:Reperfusion in L and I group both caused a cardiac dysfunction and an increase in the release of lactic dehydrogenase (LDH) and malondialdeyde (MDA),and an increase in incidence of ventricular fibrillation (VF),the activity of superoxide dismutase (SOD) were significantly decreased. There is no significant difference between L and I group. IP can improve the recovery of cardiac function and SOD activity,reduced LDH and MDA release and VF incidence. CONCLUSION:Exogenous LPC can cause ischemia reperfusion like changes,IP has protective effect to LPC injury.