Leprán I, Lefer A M
Circ Shock. 1985;15(2):79-88.
Products of the lipoxygenase pathway of arachidonate metabolism, including hydroperoxides, free radicals, and leukotrienes, are thought to mediate ischemic damage during acute myocardial ischemia (MI). Propyl gallate (1 mg/kg/h) was infused in anesthetized cats 0.5 h after coronary artery occlusion. Propyl gallate did not influence mean arterial blood pressure (MABP), heart rate (HR), or the product of these, the pressure-rate index. Treatment of MI with propyl gallate significantly reduced the plasma accumulation of creatine kinase (CK). This was confirmed by reduced CK loss in biopsies from the ischemic region of the heart, indicative of a protective effect. Propyl gallate also reduced the loss of compounds containing amino-nitrogen groups from the ischemic region, although it did not significantly reverse the S-T segment elevation in the electrocardiogram. These results are consistent with the concept that inhibition of formation of lipoxygenase products protects the myocardium from ischemic damage. This study also helps explain the work of others demonstrating that combined cyclooxygenase-lipoxygenase inhibitors or depletion of leukocytes is beneficial in MI.
花生四烯酸代谢的脂氧合酶途径的产物，包括氢过氧化物、自由基和白三烯，被认为在急性心肌缺血（MI）期间介导缺血性损伤。在冠状动脉闭塞0.5小时后，将没食子酸丙酯（1毫克/千克/小时）注入麻醉的猫体内。没食子酸丙酯不影响平均动脉血压（MABP）、心率（HR）或它们的乘积——压力-心率指数。用没食子酸丙酯治疗MI可显著减少肌酸激酶（CK）的血浆蓄积。心脏缺血区域活检中CK损失的减少证实了这一点，表明其具有保护作用。没食子酸丙酯还减少了缺血区域含氨基氮基团化合物的损失，尽管它没有显著逆转心电图中的ST段抬高。这些结果与脂氧合酶产物形成的抑制可保护心肌免受缺血性损伤这一概念一致。这项研究也有助于解释其他人的研究结果，即联合使用环氧化酶-脂氧合酶抑制剂或消耗白细胞对MI有益。
