缺血预适应对未成熟大鼠心肌线粒体及能量代谢的影响

目的研究内源性心肌保护机制一缺血预适应（Ｉｓｃｈｅｍｉｃ－ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ，ＩＰＣ）对未成熟心肌线粒体及能量代谢的 影响，并探讨其作用机制。方法采用改良Ｌａｎｇｅｎｄｏｒｆｆ－Ｎｅｅｌｙ离体鼠心灌流装置，建立未成年大鼠（４周龄）离体心脏顺 行灌注左心作功模型。３６只大鼠随机等分为缺血对照组（ＮＣ）、Ｓｔ．ＴｈｏｍａｓⅡ晶体停搏液组（ＳＴ）、预缺血加停搏液组 （ＰＩ）。比较再灌注后各组心功能（ＬＷＳＰ，ＬＶＥＤＰ，±ｄｐ／ｄｔｍａｘ，ＣＯ）的恢复率；测定缺血前、再灌注后线粒体游离钙（Ｃａ２＋）、 丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）及心肌ＡＴＰ含量；观察再灌注后心肌及线粒体超微结构的变化。结果 ＩＰ组心 功能指标的恢复率明显好于ＳＴ组和ＮＣ组（Ｐ＜０．０５）；再灌注后ＳＴ组、ＮＣ组心肌线粒体Ｃａ２＋、ＭＤＡ含量明显增高， ＳＯＤ含量明显减少（Ｐ＜０．０５），而 ＩＰ组则无明显变化；ＩＰ组、ＳＴ组 ＡＴＰ含量无显著差别，均明显高于 ＮＣ组；ＳＴ组、ＮＣ 组心肌及线粒体超微结构破坏明显，ＩＰ组则仅有轻微改变。结论Ｓｔ．ＴｈｏｍａｓⅡ晶体停搏液能减轻未成熟心肌能量损耗， 但对心肌线粒体的保护作用较小，影响了

Protective effects of ischemic preconditioning on mitochondria and energy metabolism in immature rat myocardial cells against subsequent ischemia and reperfusion

Objective To observe the protective effects of ischemicpreconditioning on the mitochondria(Mi)and energy metabolism in immature rat myocardial cells under ischemic condition followed by reperfusion. Methods Isolated working heart models were established using 4-weed-old rats, divided into 3 groups (12 in each group). The control rats (NC group)underwent 120 min of gllobal ischemia followed by 60 min of reperfusion with Krebs-Henseleit(K-H)solution at 37 ℃. The rats subjected to cardioplegic arrest with cold (4 ℃) St.ThomasⅡ Hospital Solution before prolonged global ischemia and reperfusion served as ST group. The rats in ischemic preconditioning group (PI group) was given the same treatment as ST group after 5 min of global ischemia followed by 5 min of reperfusion at 37 ℃ with K-H solution, Malodiadehyde (MDA),free calcium(Ca2+) and superoxide dismutase(SOD) content in the mitochodria and myocardial ATP level were assessed before ischemia and during reperfusion. In addition, the cardiacfunction was measured and changes in the ultrastructures of the myocardial cells observed. Results The recovery of left ventricular function was much better in PI group than in NC and ST groups(P<0.05). MDA and Ca2+ content in the mitochondria were markedly lowered and SOD level elevated in PI group compared with those in the other 2 groups (P<0.05). The myocardial ATP content was markedly higher in PI and ST group. Slight ultrastuctural changes of the mitochondria were observed in IP group,in contrary to the condition observed in NC and ST group. Conclusion ischemic preconditioning may provide protection in addition to the effect of crystollid cardioplegic ischemia on immature myocardium against reperfusion injury.The mechanisms by which ischemic preconditioning protects the myocardium may lie in the decrease of oxgen free radical and Ca2+ overload in the mitochondria and the preservation of ATP as well as the maintance of integration of myocardial and mitochondria ultrastructure.