EFFECTS OF HYPERTROPHY AND HYPERTENSION ON INFARCTION

我实验室以前的研究表明，压力诱导的左 心肌肥厚显著改变动物冠脉循环 还有男人。当患有肾性高血压和左心室的狗 肥厚的人会受到冠状动脉突然闭塞的影响， 猝死增加三倍，梗塞面积增加 基本上是这样的。如果此模型中的高血压在治疗前或治疗后缓解 关于冠状动脉闭塞的时间，猝死的发生率回升 来控制和控制梗塞面积。这项提议的目标是 在这一领域继续深造。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 再灌注时间与心肌梗死面积的关系 处于危险中的区域的百分比。我们假设左心室 肥厚和高血压可能会加速坏死的速度 在突然冠脉闭塞后进展到危险区域。如果 就是这样，旨在改变脑梗塞病程的干预措施 高血压和左心室肥厚的存在将必须 在冠状动脉闭塞后很早就实施了。第二，我们计划 确定在多大程度上依赖于时间的缓解 肾性高血压和左心室高血压犬的高血压 冠脉突然闭塞导致的肥厚。我们之前的研究 已经证明，如果在高血压缓解之前或大约 冠脉闭塞时间与心肌梗死病程 被有利地改变。因为病人几乎从来没有到过医务室 设施足够快，可以在发病后几分钟内得到治疗 对于冠状动脉闭塞，重要的是确定给药的时间有多晚 治疗方案是可以实施的，并且仍然具有良好的效果。 所有研究都将在长期使用仪器的清醒动物身上进行 肾性高血压与左心室肥厚及其临床意义 控制。这些研究应该会提供重要的新信息 关于高血压与左心室的相互作用 肥厚和心肌梗死。

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.