CEREBRAL MICROCIRCULATION IN EXPERIMENTAL HYPERTENSION

实验性高血压的脑微循环

• 批准号: 3485756
• 负责人: HERMES A KONTOS
• 金额: $ 26.05万
• 依托单位: VIRGINIA COMMONWEALTH UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1990
• 资助国家: 美国
• 起止时间: 1990-07-01 至 1995-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3485756
• 关键词: angiotensin /renin /aldosterone hypertension; arterioles; blood viscosity; brain circulation; cats; eicosanoid metabolism; fatty acid biosynthesis; free radical oxygen; laboratory rabbit; microcirculation; oxygen consumption; oxygenases; platelet aggregation; reactive hyperemia; renal hypertension; vascular endothelium permeability; vascular resistance; vascular smooth muscle

The long-range objective of these studies is to clarify the mechanisms of the responses of cerebral arterioles to changes in intravascular and transmural pressure. The main areas will be explored: The mechanisms of the sustained cerebral arteriolar dilation and associated functional, morphological and metabolic alterations from acute severe arterial hypertension and the mechanisms of the adjustments in cerebral caliber from alterations in blood pressure in the so-called autoregulatory range. We will explore the hypothesis that the cerebral vascular changes from acute severe hypertension are due to the release of oxygen radicals from the vessel wall into the extracellular space. These radicals are generated in the course of increased metabolism of arachidonate by cyclooxygenase. Their production is mediated by the release of VIP and is calcium dependent. The second objective is to explore the mechanism of the adjustments in cerebral arteriolar caliber in response to moderate changes in arterial blood pressure. We will investigate the participation of both myogenic and metabolic mechanisms. The participation of the former will be investigated by bringing about changes in transmural pressure without a primary change in blood flow via alterations in the external pressure applied to the entire body, while the brain is maintained at atmospheric pressure. The response of cerebral arterioles to metabolic mechanisms will be investigated by bringing about changes in blood flow without alterations in transmural pressure via changes in blood viscosity induced by administration of hypertonic solutions. These solutions cause biphasic changes, initially a decrease in viscosity and hyperemia, and subsequently an increase in viscosity and reduction in blood flow. Further, the mediation of metabolic changes via adenosine will be explored.

这些研究的长期目标是阐明 脑小动脉对血管内和脑内微循环变化的反应 透壁压 将探讨的主要领域： 持续的脑小动脉扩张和相关的功能， 急性重度动脉粥样硬化性心脏病的形态和代谢改变 高血压与高血压脑血管调节的机制 在所谓的自动调节范围内的血压变化。 我们 将探讨脑血管从急性 严重的高血压是由于氧自由基的释放， 血管壁进入细胞外间隙。 这些自由基产生于 环氧合酶促进花生四烯酸代谢的过程。 其产生由VIP的释放介导，并且是钙依赖性的。 第二个目标是探索调整的机制， 脑小动脉口径对动脉中度变化的反应 血压. 我们将研究肌源性和 代谢机制 将对前者的参与情况进行调查 通过引起跨壁压的变化而不引起主要变化， 通过改变施加在血管上的外部压力来影响血流 整个身体，而大脑保持在大气压下。 的 脑小动脉对代谢机制的反应将是 通过改变血流而不改变 通过血液粘度的变化引起的跨壁压 给予高渗溶液。 这些溶液引起双相 变化，最初是粘度降低和充血，随后 粘度增加和血流减少。 此夕h 将探索通过腺苷介导代谢变化。