CORONARY BLOOD FLOW IN SUB CORONARY AORTIC STENOSIS

冠状动脉瓣下狭窄的冠状动脉血流

• 批准号: 3352302
• 负责人: BLASE A CARABELLO
• 金额: $ 7.69万
• 依托单位: MEDICAL UNIVERSITY OF SOUTH CAROLINA
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-12-01 至 1986-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3352302
• 关键词: aortic valve stenosis; heart circulation; heart contraction; heart dimension /size; intracardiac pressure; ventricular hypertrophy

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.

人的主动脉狭窄，产生压力超负荷肥大 左心室，通常与心绞痛相关。 这暗示着 心肌缺血，即使在正常冠状动脉的情况下也会发生 动脉。 与之相关的冠状动脉血流异常 已经提出肥大是这种缺血的原因。 实验 压力超负荷冠状动脉血流的研究 心室表现出降低的心脏心脏血流。 这些 但是，实验使用上次体带技术来模拟 主动脉狭窄。 这些模型产生严重的压力超负荷肥大 心室的，但与真正的主动脉狭窄不同，因为 冠状动脉暴露于高于正常收缩压。 冠状动脉 高血压可能影响冠状动脉血流。 确实，解剖学 冠状动脉模型中冠状动脉的改变已经 显示。 这种改变对未知血流的影响。 这是 实验性上主动脉主动脉主动脉的血液流量的变化可能 狭窄可能无法反映出亚心下主动脉狭窄中的狭窄 患者。 某些主动脉患者可能会抑郁收缩功能 狭窄。 动物中此问题的实验研究已经产生 结果矛盾。 冲突的一种来源是大多数实验性 模型在心室施加了突然的压力超负荷。 这是 不类似于逐渐发生的压力超负荷人类主动脉 狭窄并可能损害心肌。 因此，对结果的解释 从突然的压力超负荷模型获得的情况很难评估。 在主动脉中了解冠状动脉血流和肌肉收缩功能 狭窄将通过研究次生体的模型来提高狭窄 狭窄产生逐渐但严重的压力超负荷肥大。 这 将消除冠状动脉收缩期的混杂影响 在胸膜上以及可能的心肌中看到的高血压 突然施加的压力超负荷造成的损害。 我们建议学习 狗的冠状血流和心室肌肉收缩功能 逐渐应用亚肾上腺主动脉狭窄的模型。