【摘要】 本实验用离体大鼠心脏Langendorff灌流模型,观察缺血及缺血——再灌注对大鼠心肌肌浆网[SR]钙转运功能的影响。结果表明:缺血25min引起SR钙摄取初速率下降,摄取量降低;缺血40min,使其进一步加重。缺血25min后再灌注15min,SR的钙转运功能进一步降低,与缺血40min后果类似;同时SR上的Ca²⁺-ATPase活性也显著降低。用不同pH的灌流液进行再灌注,对SR钙转运功能的障碍无显著影响。这提示:心肌缺血可引起SR的钙转运功能障碍,并随缺血时间的延长而加重;再灌注加重缺血造成的SR功能的损伤。偏酸或偏碱的K-H液再灌注均不能改善SR钙转运功能的抑制,表明pH变化不是缺血-再灌注时引起SR功能障碍的重要因素。更多还原

【Abstract】 Using Langendorff’s perfusion model of isolated rat heart, the effect of periodof ischemia, ischemia-reperfusion and changes in perfusate pH on the function ofcalcium uptake of cardiac sarcoplasmic reticulum (SR) was observed. The in-itial rate and capacity of calcium uptake by SR decreased significantly after 25min ischemia, and were further worsened when ischemia was prolonged to 40 min.When hearts were subjected to 15 min reperfusion after 25 min ischemia, calciumuptake capacity and initial rate decreased even more in comparison with that of 40min ischemia. In addition, the calcium dependent ATPase activity of SR wasalso markedly inhibited. Reperfusion with acid (pH 6.8) or alkaline (pH 8.0)made no significant difference on the aforementioned reperfusion induced changes.The results indicated that myocardial ischemia depressed the calcium transportactivity of SR, and this depression was further aggravated with prolonging is-chemia. Reperfusion after ischemia exacerbated the ischemic injury. Reperfu-sion with either acid or alkaline Krebs-Henseleit solution could not improve thecalcium uptake function of SR, implying that the pH change does not seem to bean important factor in inducing the SR dysfunction during ischemia-reperfusion.更多还原