维生素C对抗外源性溶血磷脂酰胆碱所致的离体大鼠工作心脏类缺血再灌注损伤作用

目的 :观察维生素C的对抗外源性溶血磷脂酰胆碱(LPC)所致的离体大鼠工作心脏类缺血再灌注损伤作用。方法 :利用麻醉SD大鼠 ,制备离体大鼠工作心脏模型。C组 :用正常K H液连续灌注 35min ;L组 :用含 5 μmolLPC的K H液灌注 5min ,正常K H液再灌注 30min ;V组 :先用含 10 0 μmol维生素C的K H液灌注 5min ,再用含 5μmolLPC的K H液灌注 5min ,用含 15 0 μmol维生素C的K H液再灌注 30min。结果 :与C组相比 ,再灌后L组心功能指标均明显下降 ,室颤发生率提高 ,灌注液中乳酸脱氢酶(LDH)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。L组相比 ,V组心功能指标均明显升高 ,无室颤发生 ,灌注液中LDH和MDA含量明显降低 ,心肌组织中SOD活力变化不明显。结论 :维生素C对LPC所致的心肌类缺血再灌注损伤有明显的对抗作用。

Effect of Vitamine C on Ischemia-Reperfusion-Like Effect of Exogenous Lysophosphatidylcholin on Isolated Working Rat Hearts

Objective: To observe the effect of vitamine C on ischemia-reperfusion-like effect of exogenous Lysophosphatidylcholin(LPC) in isolated working rat heart models. Method: Established isolated working rat heart models and divided into three groups: C group: The hearts were perfused with normal K-H buffer for 35 min; L group: The hearts were perfused with K-H buffer contaning 5 μmol LPC, and reperfused with normal K-H buffer for 30 min; V group: The hearts were perfused first with buffer containing 100 μmol vitamine C for 5 min, and LPC buffer for 5 min, and again with vitamine C buffer for 30 min. Results: Reperfusion in L group caused acardiac dysfunction and an increase in the release of lactic dehydrogenase(LDH) and malondialdehyde(MDA), and an increase in incidence of ventricular fibrillation(VF), and significant decrease of the activity of superior dismutase(SOD). Vitamine C antagonized the effect of LPC, improved the recovery of cardiac function, reduced LDH and MDA release and VF incidence. Conclusion: Vitamine C has protective effect on ischemia-reperfusion-like injuries of exogenous LPC.