己酮可可碱对大鼠离体心脏缺血/再灌注及缺钙/复钙损伤的保护作用

目的探讨己酮可可碱对缺血/再灌注引起心肌损伤的保护作用及其机制。方法首先建立心肌缺血/再灌注模型,采用Langendorff灌流装置进行20min预灌注,30min缺血,30min再灌注,70只Wistar大鼠随机分为己酮可可碱4个剂量(50、100、125、150μmol·L-1)组、缺血/再灌注组、对照组以及己酮可可碱再灌注组,持续观察己酮可可碱对血流动力学指标的影响;建立缺钙/复钙模型,将30只Wistar大鼠随机分为己酮可可碱给药组、钙反常组和对照组,离体心脏预灌注20 min,无钙灌注5min,复钙灌注30min,持续观察己酮可可碱对血流动力学指标的影响。结果缺血前及灌注期己酮可可碱100μmol·L-1给药能明显恢复大鼠的缺血/再灌注前后心脏的左室发展压(P<0.05),左心室舒张末期压亦明显下降;100μmol·L-1己酮可可碱明显改善钙反常模型钙超载引起的左心室收缩功能异常,左室发展压恢复41%(P<0.05)。结论己酮可可碱提高大鼠心肌缺血缺氧后心肌收缩力的恢复水平、增强心肌缺血缺氧的耐受性;改善心肌缺血/再灌注引起的钙超载可能是其心肌保护作用的机制之一。

The protective effect of pentoxifylline on myocardium injury induced by ischemia-reperfusion and Ca2+ paradox

Aim To observe the protective effect of pentoxifylline on myocardium injury induced by ischemia-reperfusion.Methods Heart ischemia-reperfusion model was induced in the isolated rat hearts subjected to 30 min ischemia and 30 min reperfusion.70 Wistar rats were divided randomly into seven groups: control group,ischemia-reperfusion group,four dose pentoxifylline treatment groups(50,100,125,150 μmol·L-1) and post ischemia pentoxifylline treatment group.The intracellular Ca2+-overload was induced in the isolated rat hearts subjected to 5 min Ca2+-depletion and 30 min Ca2+-repletion(Ca2+-paradox).30 Wistar rats were divided randomly into three groups(control group,Ca2+-paradox group and pentoxifylline treatment group).Hemodynamics data were recorded.Results Reperfusion of the ischemic heart resulted in impaired cardiac performance.These alterations in cardiac function were attenuated by treatment of the heart with 100 μmol·L-1 pentoxifylline(P<0.05).The Ca2+-paradox hearts exhibited a dramatic depression in left ventricular developed pressure,a marked elevation in left ventricular end diastolic pressure,All these changes due to Ca2+-paradox were significantly attenuated upon treating the hearts with 100 μmol·L-1 pentoxifylline(P<0.05).Conclusion These results indicated that the cardioprotective effect of pentoxifylline against ischemia reperfusion injury might be related to its role on decreased intracellular Ca2+-overload.