RIGHT & LEFT VENTRICULAR FUNCTION DURING FETAL HYPOXEMIA

正确的

• 批准号: 3081316
• 负责人: MARK RELLER
• 金额: $ 6.7万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-09-30 至 1991-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3081316
• 关键词: blood flow measurement; blood pressure; cardiac output; catecholamines; disease /disorder model; embryo /fetus disorder; heart ventricle; hemodynamics; hormone regulation /control mechanism; hypertension; myocardial ischemia /hypoxia; newborn animals; nitroferricyanide; renin; sheep; vasopressins

Hypoxemia is a major problem with significant adverse effects on both the fetus and the newborn infant. The accepted experimental model for the investigation of fetal hypoxemia has been to reduce the inspired oxygen concentration in the maternal ewe. Using this model, fetal hypoxemia is frequently associated with reduced cardiac output due to reduced stroke volume and arterial hypertension. Previous investigations have demonstrated that myocardial oxygen delivery increases during fetal hypoxemia primarily by increased coronary blood flow accomplished by coronary vasodilation. A proposed mechanism for the reduction in combined ventricular output in the fetus with hypoxemia is that stroke volume drops due to an associated increase in arterial pressure. Previous investigations from this laboratory have demonstrated that the two fetal ventricles have distinctly different sensitivities to arterial pressure--that is, increases in arterial pressure result in significant reductions in right ventricular stroke volume, while left ventricular stroke volume remains constant. Hypoxemia, when associated with fetal arterial hypertension would, by itself, be expected to produce a substantial reduction in right ventricular output. The purpose of this investigation is to determine the mechanism(s) for the reduction in fetal cardiac output with hypoxemia. The plan is to test the hypotheses that: 1) stroke volume sensitivity to increased arterial pressure, or 2) inadequate coronary blood flow with hypoxemia and increased arterial pressure, reduces cardiac output. To accomplish these goals, we plan the following specific aims in the chronically Instrumented near term fetal lamb: a) generate biventricular function curves before and during fetal hypoxemia, and during hypoxemia after normalization of arterial pressure, b) generate biventricular stroke volume-arterial pressure relationship curves during hypoxemia, c) determine the arterial pressure at which myocardial blood flow limits biventricular performance during normoxemia and during hypoxemia. These specific aims integrate the principal investigator's long-term interest and commitment to the understanding of the pathophysiology of fetal and neonatal hypoxemia with a laboratory possessing expertise in fetal hemodynamics and ventricular function.

低氧血症是一个主要的问题， 胎儿和新生儿。 接受实验 研究胎儿低氧血症的模型已经减少 母母羊的吸入氧气浓度。 使用此 模型，胎儿低氧血症经常与减少 心输出量由于每搏输出量和动脉 高血压 以前的调查表明， 胎儿低氧血症时心肌氧输送增加 主要是通过增加冠状动脉血流量， 血管舒张 一项拟议的减少联合国 低氧血症胎儿的心室输出量 由于动脉压相关升高，容量下降。 该实验室以前的研究表明， 两个胎儿心室具有明显不同的敏感性 也就是说，动脉压的升高 导致右心室卒中显著减少 左心室每搏输出量保持不变。 低氧血症，当与胎儿动脉高压相关时， 本身，预计将产生实质性的减少权利， 心室输出量 本研究的目的是确定机制 低氧血症导致胎儿心输出量减少 该计划 是为了检验以下假设：1）每搏输出量对 动脉压升高，或2）冠状动脉血流不足 低氧血症和动脉压升高，降低心脏 输出. 为了实现这些目标，我们计划采取以下具体措施： 目的是在长期仪器化的近期胎羊中：a） 在胎前和胎中生成双心室功能曲线 低氧血症，以及在动脉正常化后的低氧血症期间 压力，B）生成双心室搏出量-动脉压 低氧血症期间的关系曲线，c）确定动脉 心肌血流限制双心室的压力 在常氧血症和低氧血症期间的性能。 这些具体 目标整合了主要研究者的长期利益， 致力于了解胎儿的病理生理学， 新生儿低氧血症，实验室拥有胎儿 血流动力学和心室功能。