Belluk B, Gupta M, Singal P K
Cardiovascular Sciences Division, St. Boniface General Hospital Research Center, Winnipeg, Man., Canada.
Can J Physiol Pharmacol. 1988 Aug;66(8):1087-91. doi: 10.1139/y88-177.
The role of oxygen radicals and lipid peroxidation in calcium-paradox injury in isolated perfused rat hearts was studied by examining the effects of mannitol and (or) allopurinol on this phenomenon. Myocardial changes due to calcium paradox were characterized by contractile failure, a rise in resting tension, and cell damage. These changes were also accompanied by increased lipid peroxidation, as indicated by an increase in malondialdehyde content. Mannitol (an effective quencher of hydroxyl radicals) treatment resulted in a dose-dependent decrease in lipid peroxidation but did not affect other changes due to calcium paradox. Allopurinol (an inhibitor of xanthine oxidase) neither affected lipid peroxidation nor modified any of the structure-function changes due to calcium paradox. These data demonstrate the occurrence of lipid peroxidation which, however, may not be involved in the observed structure-function changes due to calcium paradox. It is also suggested that in this experimental model, xanthine oxidase may not be the inducer of oxygen radicals or of lipid peroxidation.
通过检测甘露醇和（或）别嘌呤醇对该现象的影响，研究了氧自由基和脂质过氧化在离体灌注大鼠心脏钙反常损伤中的作用。钙反常引起的心肌变化表现为收缩功能衰竭、静息张力升高和细胞损伤。这些变化还伴随着脂质过氧化增加，如丙二醛含量升高所示。甘露醇（一种有效的羟自由基淬灭剂）处理导致脂质过氧化呈剂量依赖性降低，但不影响钙反常引起的其他变化。别嘌呤醇（一种黄嘌呤氧化酶抑制剂）既不影响脂质过氧化，也不改变钙反常引起的任何结构-功能变化。这些数据表明脂质过氧化的发生，然而，它可能与钙反常引起的观察到的结构-功能变化无关。还表明在该实验模型中，黄嘌呤氧化酶可能不是氧自由基或脂质过氧化的诱导剂。
