羟苯氨酮对实验性心肌缺血的治疗作用

目的研究强心扩血管新药羟苯氨酮(oxyphenamone)对心肌缺血的治疗作用。方法用多导生理记录仪和电磁流量计测定心脏血流动力学参数，观察药物对阻断冠脉致急性心肌梗死猫心脏生理功能的影响。形成异丙肾上腺素致大鼠心肌缺血坏死模型，从心肌酶学及病理形态学方面评价药效。结果羟苯氨酮(2-8 mg·kg^-1,iv)可剂量依赖性地降低心梗猫的心率、血压、血管阻力与张力时间指数(TTI)，轻度增加心肌收缩力与心输出量，不影响左室压与心脏作功。羟苯氨酮(4-8 mg·kg^-1,ip)可明显减轻异丙肾上腺素致大鼠心肌肌酸磷酸激酶(CPK)、丙二醛(MDA)与血清谷草转氨酶(GOT)活性变化与病理形态学损伤。结论羟苯氨酮对心肌缺血性损伤有明显治疗作用。

Effects of oxyphenamone on myocardial ischemia in cats and rats

AIM: To study the therapeutic effects of oxyphenamone, a novel inodilator, on myocardial ischemia. METHODS: The cardiac hemodynamic variables in cats with acute myocardial infarction induced by occlusion of the left anterior descending coronary artery (LAD) were recorded with a physiological polygraph and electromagnetic flowmeter. A model of myocardial necrosis induced by subcutaneous injection of isoproterenol was used for evaluating the effects of drugs on myocardial enzymes and morphological change. RESULTS: Intravenous injection of oxyphenamone (2 - 8 mg x kg(-1)) dose-dependently decreased heart rate, mean arterial pressure, vascular resistance and the parameters of myocardial oxygen consumption (tension time index, TTI) in cats with myocardial infarction. It increased myocardial contractile force and cardiac output transiently but showed no influence on the left ventricular pressure and cardiac work. The changes of myocardial morphology, creatine phosphate kinase (CPK), malodialdehyde (MDA) and serum glutamic-oxaloacetic transaminase (GOT) induced by isoproterenol in rats were diminished by intraperitoneal injection of oxyphenamone (4 - 8 mg x kg(-1)). CONCLUSION: By the examination of the cardiac hemodynamics, myocardial enzymes and morphology, it showed that the myocardial damage induced by ischemia or beta-agonist can be antagonized markedly by oxyphenamone, indicating that oxyphenamone may be beneficial for the treatment of myocardial infarction.