Moolman J A, Genade S, Winterbach R, Lochner A
Department of Internal Medicine, Faculty of Medicine, University of Stellenbosch, Republic of South Africa.
Cardioscience. 1994 Jun;5(2):73-80.
It has recently been shown that hypoxia and ischemia are equally effective to precondition the myocardium of the rat. A comparison of the metabolic changes caused by transient ischemia and hypoxia has not yet been made and may help to elucidate the metabolic factors involved in eliciting preconditioning. The aim of this study was to compare the changes in tissue high energy phosphates, glycogen and lactate during and after hypoxic and ischemic preconditioning in isolated perfused rat hearts. Isolated rat hearts were subjected to global ischemia of 30 minutes duration, with and without preconditioning consisting of a single episode of 5 minutes global ischemia or hypoxia (PO2 = 12kPa). The post-ischemic recovery of aortic flow of the nonpreconditioned group was significantly less than that of the two preconditioned groups: 0.5 +/- 0.5 ml/min vs. 23.3 +/- 3.4 and 20.7 +/- 3.6 ml/min for ischemic and hypoxic preconditioning respectively. The only common metabolic factor between the two preconditioned groups was the similar extent of glycogenolysis after transient ischemia or hypoxia: glycogen decreased from 22 +/- 0.8 in non-preconditioned hearts to 16 +/- 0.5 and 16 +/- 1.5 mumoles glucose per g wet tissue in ischemic and hypoxic preconditioned hearts respectively. There was also no difference in lactate production between the two groups during the sustained episode of ischemia. We conclude that oxygen deprivation, rather than other metabolic factors, is the important factor in eliciting preconditioning.
最近的研究表明,缺氧和缺血对大鼠心肌预处理的效果相同。目前尚未对短暂缺血和缺氧引起的代谢变化进行比较,而这种比较可能有助于阐明引发预处理的代谢因素。本研究的目的是比较在离体灌注大鼠心脏中,缺氧和缺血预处理期间及之后组织中高能磷酸盐、糖原和乳酸的变化。将离体大鼠心脏进行30分钟的全心缺血处理,分为有和没有预处理两组,预处理包括单次5分钟的全心缺血或缺氧(PO2 = 12kPa)。未预处理组缺血后主动脉血流的恢复明显低于两个预处理组:分别为0.5±0.5 ml/min,而缺血预处理组和缺氧预处理组分别为23.3±3.4和20.7±3.6 ml/min。两个预处理组之间唯一共同的代谢因素是短暂缺血或缺氧后糖原分解的程度相似:糖原在未预处理心脏中从22±0.8降至缺血预处理心脏和缺氧预处理心脏中的每克湿组织16±0.5和16±1.5微摩尔葡萄糖。在持续缺血期间,两组之间的乳酸生成也没有差异。我们得出结论,缺氧而非其他代谢因素是引发预处理的重要因素。