EFFECTS OF HYPERTROPHY AND HYPERTENSION ON INFARCTION

我实验室以前的研究表明， 心室肥大显著改变动物冠状动脉循环 当患有肾性高血压和左心室肥厚的狗 心肌肥厚者冠状动脉突然闭塞， 猝死增加三倍，梗死面积增加 实质上。 如果该模型中的高血压在给药前或给药后缓解， 大约在冠状动脉闭塞的时间，猝死的发生率恢复到 来控制梗死面积。 这项建议的目的是 在这方面继续深造。 首先，我们计划确定 肾性高血压和左心室肥厚的存在改变了 再灌注时间和梗死面积之间的关系表示为 %的地区处于危险之中。 我们假设左心室 肥大和高血压可能会加快坏死的速度， 在冠状动脉突然闭塞后跨越危险区进展。 如果 因此，旨在改变脑梗死进程的干预措施， 高血压和左心室肥大的存在必须 在冠状动脉闭塞后非常早实施。 第二，我们计划 确定如何依赖于时间的问候效果救济的 犬肾性高血压和左室高血压 冠状动脉突然闭塞导致的肥大。 我们以前的研究 已经证明，如果高血压在大约 冠状动脉闭塞的时间、心肌梗死的病程可以 有利地改变。 由于病人几乎从不去医院， 在发病后几分钟内就能得到治疗 冠状动脉闭塞，重要的是要确定如何晚任何给定的 可以实施治疗方案并且仍然具有良好的效果。 所有研究都将在慢性仪器清醒动物中进行， 肾性高血压和左室肥厚，并适当 对照 这些研究应该提供重要的新信息 关于高血压、左心室 肥大和心肌梗塞。

Previous studies in my laboratory have shown that pressure-induced left ventricular hypertrophy markedly alters the coronary circulation in animals and man. When dogs with renal hypertension and left ventricular hypertrophy are subjected to sudden coronary occlusion, the incidence of sudden death increases three-fold and infarct size increases substantially. If hypertension in this model is relieved prior to or at about the time of coronary occlusion, the incidence of sudden death returns to control and so does infarct size. The objectives of this proposal are to pursue further studies in this area. First, we plan to determine if the presence of renal hypertension and left ventricular hypertrophy alters the relationship between time of reperfusion and infarct size expressed as a percent of the area at risk. We postulate that left ventricular hypertrophy and hypertension may accelerate the rate at which necrosis progresses across the risk zone following sudden coronary occlusion. If this is so, interventions aimed at altering the course of infarction in the presence of hypertension and left ventricular hypertrophy will have to be implemented very early following coronary occlusion. Second, we plan to determine how time dependent are the salutatory effects of relief of hypertension in dogs with renal hypertension and left ventricular hypertrophy subjected to sudden coronary occlusion. Our previous studies have demonstrated that if the hypertension is relieved prior to or at about the time of coronary occlusion the course of the myocardial infarction can be favorably altered. Since patients almost never arrive at the medical facility soon enough to be treated within minutes of the time of the onset of coronary occlusion, it is important to determine how late any given therapeutic regimen can be implemented and still have salutatory effects. All studies will be pursued in chronically-instrumented awake animals with renal hypertension and left ventricular hypertrophy and appropriate controls. These studies should provide important new information concerning the interaction between hypertension, left ventricular hypertrophy and myocardial infarction.