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METABOLIC CONTROL OF CORONARY FLOW--31P NMR SPECTROSCOPY

冠状动脉血流的代谢控制--31P核磁共振波谱

基本信息

批准号：
3087555
负责人：
GREGORY G SCHWARTZ
金额：
$ 8.92万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
依托单位国家：
美国
项目类别：
财政年份：
1988
资助国家：
美国
起止时间：
1988-09-01 至 1993-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3087555
关键词：
cellular respiration coronary occlusion /thrombosis heart circulation heart metabolism hemodynamics high energy compound nuclear magnetic resonance spectroscopy oxygen consumption phosphates phosphorus reactive hyperemia respiratory oxygen stable isotope swine ultrasound blood flow measurement vasodilation

项目摘要

Coronary blood flow (CBF) is closely coupled to myocardial oxygen requirements (MV02). However, the mechanisms which link the regulation of CBF to changes in myocardial energy metabolism remain unknown. The purpose of the proposed work is to investigate the mechanism of CBF regulation by examining the relationship between instantaneous CBF and intracellular myocardial energy state (assessed by 31P NMR spectroscopy) in the transient phases of both functional and reactive myocardial hyperemia. The following specific hypotheses will be tested: 1. The level of myocardial high energy phosphates is tightly controlled despite changes in MVO2 by means of a rapid and precise regulation of CBF, and hence oxygen delivery. 2. Myocardial reactive hyperemia (RH), with its prolonged duration and gross overpayment of blood flow debt, is related to a temporary dissociation of instantaneous CBF from myocardial energy state Open-chest, anesthetized pigs with instrumentation including an extramural Doppler coronary flow probe will be studied in a 1- meter, 2 Tesla magnetic resonance spectrometer. Hemodynamic data, including phasic CBF, and 31P NMR spectra will be obtained while the experimental system is perturbed by a step augmentation of MV02 (by paired ventricular pacing and/or aortic constriction) or a step decrease in myocardial oxygen delivery (brief coronary occlusion). The first hypothesis predicts that a step increase in MV02 will be followed by a brief decline in high energy phosphate levels, compensatory coronary vasodilation with increased 02 delivery, and a rapid restoration of high energy phosphates to control levels. The second hypothesis predicts that myocardial high energy phosphates, partially depleted during coronary occlusion, are restored to normal upon release of the occlusion sooner than RH flow returns to its baseline. This would indicate that RH flows is in excess of that required to restore myocardial metabolic conditions. These studies will provide insight into the normal metabolic regulation of CBF, and the mechanisms of functional and reactive myocardial hyperemia. Subsequent studies will examine the potential abnormalities of such regulation in experimental models of coronary artery disease, left ventricular pressure or volume overload, or in the clinical syndrome of "impaired coronary vasodilator reserve". This work may also lead to a better understanding of the myocardial metabolic consequences of brief coronary occlusion during angioplasty.

冠状动脉血流量（CBF）与心肌血流量密切相关。氧气需求（MV 02）。然而，将CBF的调节与心肌能量的变化联系起来代谢仍然未知。这项工作的目的是调查机制通过检查CBF监管之间的关系瞬时CBF和细胞内心肌能量状态（通过31 P NMR光谱评估）在功能性和反应性心肌充血。将检验以下特定假设： 1.心肌高能磷酸盐的水平尽管MVO 2发生变化，但通过快速和精确调节脑血流量，从而实现氧气输送。 2.心肌反应性充血（RH），其持续时间持续时间和血流量债务的总超额支付，与一个瞬时CBF与心肌暂时分离能量状态开胸，麻醉猪与仪器，包括将在一个1- 2特斯拉磁共振光谱仪血流动力将获得包括相位CBF和31 P NMR谱的数据当实验系统受到阶跃扰动时， MV 02增强（通过成对心室起搏和/或主动脉收缩）或心肌氧输送逐步减少（短暂冠状动脉闭塞）。第一个假设预测MV 02的阶跃增加将是接着是高能磷酸盐水平的短暂下降，随着O2输送增加的代偿性冠状血管舒张，以及快速恢复高能磷酸盐来控制程度. 第二个假设预测，心肌高能量磷酸盐，在冠状动脉闭塞期间部分耗尽，在释放闭塞后恢复正常， RH流量恢复到其基线。这表明RH 流量超过恢复心肌所需的流量代谢条件。这些研究将提供对正常代谢的深入了解，调节CBF，以及功能性和反应性的机制，心肌充血随后的研究将审查实验模型中这种调节的潜在异常冠状动脉疾病，左心室压力或容量负荷，或在临床综合征的“受损冠状动脉血管舒张储备”。这项工作也可能导致更好的了解心肌代谢的后果，冠状动脉闭塞。