CEREBRAL MICROCIRCULATION IN EXPERIMENTAL HYPERTENSION

实验性高血压的脑微循环

• 批准号: 3485754
• 负责人: HERMES A KONTOS
• 金额: $ 22.68万
• 依托单位: VIRGINIA COMMONWEALTH UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-01-01 至 1990-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3485754
• 关键词: angiotensin /renin /aldosterone hypertension; arterioles; blood viscosity; brain circulation; calcium transporting ATPase; cats; eicosanoid metabolism; fatty acid biosynthesis; free radicals; 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.

这些研究的远程目标是阐明 脑小动物对血管内和血管变化的反应 透壁压力。 将探讨主要区域：机制 持续的大脑小动脉扩张和相关功能， 急性严重动脉的形态和代谢改变 高血压和调整的机制 所谓的自动调节范围内的血压改变。 我们 将探讨以下假设：急性变化大脑血管 严重的高血压是由于从 容器壁进入细胞外空间。 这些激进分是在 环氧合酶对蛛网膜酸盐代谢增加的过程。 它们的生产是由VIP的释放介导的，并且取决于钙。 第二个目标是探索调整的机制 脑小动脉口径响应中等动脉变化 血压。 我们将研究肌原性和 代谢机制。 前者的参与将进行调查 通过带来透壁压力的变化而没有主要变化 在血流中通过施加的外部压力的改变 整个身体，而大脑保持在大气压下。 这 大脑动脉对代谢机制的反应将是 通过带来血流变化而没有改变的调查 传播压力通过诱导的血液粘度的变化 高渗解决方案的给药。 这些解决方案引起双相 变化，最初降低粘度和充血，随后 粘度和血流减少的增加。 此外， 将探索腺苷的代谢变化的介导。