Beneficial effects of ibuprofen in acute myocardial ischemia.
Beneficial effects of ibuprofen in acute myocardial ischemia.
复制标题
布洛芬对急性心肌缺血的有益作用。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
E. Polansky
中科院分区：
文献类型：
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作者：
A. M. Lefer;E. Polansky
在心肌缺血的早期阶段研究了非甾体类抗炎药伊诺明，以确定其是否有助于保持心肌完整性。在冠状动脉闭塞时和2.5小时后再次静脉内给予12.5 mg/kg剂量的伊诺明。Ionine可显著抑制缺血心肌组织中肌酸磷酸激酶（CPK）释放的损失。此外，该药物显著地使S-T段升高恢复到正常值，并显著地防止具有游离氨基氮基团的化合物（蛋白质水解的指标）的心肌损失。虽然布洛芬缓和增加血浆CPK活性，血浆CPK值5小时后冠状动脉闭塞高于对照值。因此，布洛芬显著防止了用于评估心肌缺血性损伤的四个指标中的三个的改变。布洛芬的保护机制可能是通过稳定细胞膜（即，溶酶体膜），并在较小程度上降低心肌需氧量。
Ibuprofen, a nonsteriodal anti-inflammatory agent, was studied in the early stages of myocardial ischemia in order to determine whether it helps preserve myocardial integrity. Ibuprofen was administered intravenously at a dose of 12.5 mg/kg at the time of coronary artery occlusion and again 2.5 h later. Ibuprofen significantly prevented the loss of myocardial creatine phosphokinase (CPK) release in ischemic cardiac tissue. In addition, this drug significantly returned S-T segment elevation toward normal values, and significantly prevented the myocardial loss of compounds having free amino nitrogen groups, an index of proteolysis. Although ibuprofen moderated the increased plasma CPK activity, plasma CPK values 5 h after coronary occlusion were above control values. Thus, ibuprofen significantly prevented alterations in three of the four indices used to assess myocardial ischemic damage. The protective mechanism of ibuprofen may be via stabilization of cellular membranes (i.e., lysosomal membranes) and to a lesser extent on reduction in myocardial oxygen demand.