CORONARY BLOOD FLOW IN SUB CORONARY AORTIC STENOSIS

男性主动脉狭窄，导致压力超负荷肥大 左心室，常与心绞痛有关。这表明 即使在冠状动脉正常的情况下也会发生心肌缺血 动脉。冠脉血流异常与 肥大被认为是导致这种缺血的原因之一。实验 压力超负荷肥厚患者冠脉血流的研究 脑室显示心内膜下血流量减少。这些 然而，实验使用了冠脉上捆绑技术来模拟 主动脉狭窄。这些模型会产生严重的压力超负荷肥大。 但与真正的主动脉狭窄不同之处在于 冠脉暴露在高于正常收缩压的环境中。冠状动脉 高血压会影响冠脉血流量。的确，解剖学 冠脉上模型中冠状动脉的改变 展示了。这种改变对血流的影响尚不清楚。它是 实验性冠脉上动脉血流变化的可能性 狭窄可能不能反映冠状动脉下动脉狭窄。 病人。 部分主动脉病患者的收缩功能可能受到抑制 狭窄。在动物身上对这一问题的实验研究已经取得了成果 相互矛盾的结果。冲突的一个来源是最具实验性的 模特们突然给脑室施加了超负荷的压力。这是 不是类似于逐渐出现的人主动脉压力超负荷 狭窄，并可能损害心肌。因此，对结果的解释 从突发性压力超载模型中得到的结果难以评价。 对主动脉冠脉血流和肌肉收缩功能的认识 通过研究冠脉下动脉狭窄的模型，可以促进狭窄的发生 狭窄导致逐渐但严重的压力超负荷肥大。这 将消除冠状动脉收缩压的混杂影响 冠脉上模型中可见的高血压以及可能的心肌 由突然施加的压力过载造成的损害。我们建议研究 犬冠脉血流量与心肌收缩功能的关系 逐步应用的冠脉下动脉狭窄模型。

Aortic stenosis in man, which produces pressure overload hypertrophy of the left ventricle, is often associated with angina pectoris. This suggests myocardial ischemia and occurs even in the presence of normal coronary arteries. An abnormality in coronary blood flow associated with hypertrophy has been proposed as a cause of such ischemia. Experimental studies of coronary blood flow in pressure overload hypertrophied ventricles have shown reduced subendocardial blood flow. These experiments, however, used supracoronary banding techniques to simulate aortic stenosis. These models produce severe pressure overload hypertrophy of the ventricle but differ from true aortic stenosis in that the coronaries are exposed to higher than normal systolic pressure. Coronary hypertension could affect coronary blood flow. Indeed, anatomic alterations of the coronary arteries in supracoronary models have been shown. The effects of such alteration on blood flow in unknown. It is possible that changes in blood flow in experimental supracoronary aortic stenosis may not reflect those seen in subcoronary aortic stenosis in patients. Contractile function may be depressed in some patients with aortic stenosis. Experimental studies of this issue in animals have yielded conflicting results. One source of conflict is that most experimental models have imposed a sudden pressure overload on the ventricle. This is not analogous to gradually occurring pressure overload ot human aortic stenosis and may damage the myocardium. Thus, interpretation of results obtained from sudden pressure overload models are difficult to evaluate. Knowledge of coronary blood flow and muscle contractile function in aortic stenosis would be advanced by study of a model in which a subcoronary stenosis produced gradual but severe pressure overload hypertrophy. This would obviate the confounding influences of coronary artery systolic hypertension seen in supracoronary models as well as possible myocardial damage created by suddenly imposed pressure overload. We propose to study coronary blood flow and ventricular muscle contractile function in a dog model of gradually applied subcoronary aortic stenosis.