Koster J F, Slee R G, Essed C E, Stam H
J Mol Cell Cardiol. 1985 Jul;17(7):701-8. doi: 10.1016/s0022-2828(85)80069-9.
In the isolated, perfused rat heart, lipid peroxidation, induced by cumene hydroperoxide (Cum OOH), is accompanied by the release of malondialdehyde (MDA). Using a modified perfusion technique resulting in the separate collection of coronary and interstitial effluent, it can be shown that upon Cum OOH (0.5 mM) perfusion there is an immediate release of MDA in the coronary effluent and a delayed release in the interstitial fluid, indicating the susceptibility and coronary vascular tissue towards free radical-induced lipid peroxidation. Perfusion with Cum OOH leads to an initial increase of the coronary flow and a depressed contractility followed by a cardiac arrest concomitantly with the onset of MDA release in the interstitial fluid. Finally, during prolonged perfusion the coronary flow diminishes and contracture of the heart muscle ('stone heart') develops. These phenomena resemble those occurring during the 'calcium paradox'. Although the contractility diminishes immediately after the perfusion with Cum OOH the tissue ATP level and energy charge (formula; see text) remain constant. From the moment of cardiac arrest the ATP and creatine phosphate levels gradually decrease and the energy charge drops simultaneously with the appearance of MDA in the interstitial fluid. In contrast to the calcium paradox there is no simultaneous increase in the myocardial AMP level. Various mitochondrial enzymes (cytochrome c oxidase, monoamine oxidase, carnitinepalmitoyltransferase I and palmitoyl CoA synthetase) were tested and not affected by Cum OOH perfusion. During the development of contracture after 20 min of Cum OOH perfusion massive contraction band necrosis of cardiac tissue occurs. However, overall protein release is lower when compared with the protein release during the calcium paradox.(ABSTRACT TRUNCATED AT 250 WORDS)
在离体灌注的大鼠心脏中，异丙苯过氧化氢（Cum OOH）诱导的脂质过氧化伴随着丙二醛（MDA）的释放。采用一种改良的灌注技术，可分别收集冠状动脉和间质流出液，结果表明，灌注Cum OOH（0.5 mM）时，冠状动脉流出液中MDA立即释放，间质液中释放延迟，这表明冠状动脉血管组织对自由基诱导的脂质过氧化敏感。灌注Cum OOH会导致冠状动脉血流最初增加、收缩力降低，随后心脏停搏，同时间质液中开始释放MDA。最后，在长时间灌注过程中，冠状动脉血流减少，心肌出现挛缩（“石心”）。这些现象类似于“钙反常”期间发生的现象。虽然灌注Cum OOH后收缩力立即降低，但组织ATP水平和能荷（公式；见正文）保持不变。从心脏停搏时刻起，ATP和磷酸肌酸水平逐渐降低，能荷下降，同时间质液中出现MDA。与钙反常不同的是，心肌AMP水平没有同时升高。对各种线粒体酶（细胞色素c氧化酶、单胺氧化酶、肉碱棕榈酰转移酶I和棕榈酰辅酶A合成酶）进行了测试，它们不受Cum OOH灌注的影响。在Cum OOH灌注20分钟后挛缩形成过程中，心脏组织出现大量收缩带坏死。然而，与钙反常期间的蛋白质释放相比，总体蛋白质释放较低。（摘要截断于250字）
