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心肌腺嘌呤核甙酸(AN)耗竭是限制缺血后心肌代谢和功能恢复的重要机制。大量冷停搏液(CPS)连续灌注冲去缺血期积聚的AN降解产物即AN再合成前体,势必妨碍ATP水平的恢复。本实验采用Tyer等CPS,试析多剂CPS分次灌注总量的增加对缺血后大鼠心肌恢复的影响。离体Sprague-Dawley大鼠心脏分成四组,首先灌注CPS 2分钟。A组不再灌注。B组每30分钟灌注1分钟。C组每30分钟灌注1分钟。D组每20分钟灌注2分钟。各组灌注总时间分别为2、5、7和12分
Cardiac adenosine triphosphate (AN) depletion is an important mechanism that limits myocardial metabolism and functional recovery after ischemia. A large number of cold cardioplegia (CPS) continuous perfusion rushed to the ischemic period accumulation of AN degradation products that AN re-synthesis of precursors, is bound to hinder the recovery of ATP levels. In this study, Tyer and other CPS, analysis of multi-dose CPS perfusion increase the amount of myocardial ischemia in rats after recovery. Isolated Sprague-Dawley rat hearts were divided into four groups: CPS was first perfused for 2 minutes. Group A no longer perfusion. Group B was perfused for 1 minute every 30 minutes. Group C was infused for 1 minute every 30 minutes. Group D was infused for 20 minutes every 2 minutes. The total perfusion time of each group were 2, 5, 7 and 12 respectively