超前缺血对培养乳鼠心肌细胞缺血再灌注损伤保护作用的实验研究

观察超前缺血（ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇｗｉｔｈｉｓｃｈｅｍｉａ，ＰＣＩ）对培养乳鼠心肌细胞缺血再灌注（ｉｓｃｈｅｍｉａ－ｒｅｐｅｒｆｕｓｉｏｎ，Ｉ－Ｒ）损伤的影响。发现（１）心肌细胞经ＰＣＩ后，其ＡＴＰ含量及培养液ＬＤＨ无明显变化；（２）经ＰＣＩ诱导的心肌细胞，持续３ｈ缺糖、缺氧，其ＡＴＰ消耗较对照组显著减少；（３）复灌期ＰＣＩ组ＡＴＰ含量增加，ＬＤＨ下降；（４）在各时相［Ｃａ＋＋］ｉ与对照组比较无明显变化，但ＬＰＯ于复糖、复氧后显著降低。结果提示：有限次数短暂ＰＣＩ对心肌细胞代谢及膜通透性无损伤作用；ＰＣＩ能提高细胞对长时间缺氧的耐受能力，减轻缺氧心肌Ｉ－Ｒ损伤。其机理可能是：心肌细胞作为一独立的基本功能单位，经ＰＣＩ诱导，细胞内抗氧自由基系统酶的活性增加，减轻了氧自由基的损伤效应。

The Experimental Studies of the Protective Effects of preconditioning Ischemia on Ischemic Reperfusion Injury of Cultured Neonatal Rat Myocytes

This paper presents the protective effects of the preconditioning ischemia (PCI) on the ischemic reperfusion injury of the cultured neonatal rat myocytes. the results showed :(1)There was no marked change in intracelluar adenosine triphosphate(ATP) content in the myocytes or lactate dehydrogenase(LDH)release from the myocytes in PCI group.(2)APT depletion in PCI group was much less than control group, despite 3 hour anoxia and with no glucose.(3) During reperfusion, ATP content increased and LDH release decreased in PCI group as compared with control group.(4)Ca showed no significant change in either group at different intervals.(5)LPO decreased markedly after resumption of glucose and oxygen supply to the myocytes.The authors concluded PCI of limited duration produced no ill effects either on myocardial metabolism or membrane permeability of the myocytes.In fact,PCI can improve the tolerance of the myocytes to anoxia with zero glucose and thus reduce the ischemic reperfusion injury.The mechanism may be the activity of the intracelluar anti-free oxygen radical enzyme system inside of the myocytes of the rat heart can be enhanced through PCI,so as to alleviate the ischemic reperfusion inJury.