CEREBRAL MICROCIRCULATION IN EXPERIMENTAL BRAIN INJURY

实验性脑损伤中的脑微循环

• 批准号: 3399338
• 负责人: HERMES A KONTOS
• 金额: $ 12.33万
• 依托单位: VIRGINIA COMMONWEALTH UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1983
• 资助国家: 美国
• 起止时间: 1983-04-01 至 1986-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3399338
• 关键词: arterioles; blood brain barrier; brain circulation; brain injury; calcium; cerebral artery; cerebrovascular disorders; eicosanoid metabolism; electron microscopy; fatty acid biosynthesis; free radicals; hypocapnia; hypotension; microcirculation; molecular weight; respiratory oxygen; vascular endothelium permeability; vascular smooth muscle; vasoactive intestinal peptide; vasoconstriction

The objectives of these studies are to clarify the mechanism of the cerebral microcirculatory alterations following experimental percussion-type brain injury in anesthetized cats. This type of brain injury induces pial arteriolar dilation associated with reduced responsiveness to the vasoconstrictor effects of arterial hypocapnia and with reduced ability to dilate in response to arterial hypotension. The vessels which show these abnormalities have lesions in their vascular smooth muscle and discrete destructive lesions in their endothelium. These abnormalities are mediated by free oxygen radicals generated in association with increased prostaglandin synthesis. The proposed experiments will determine the timing of the generation of the free oxygen radicals. They will identify the effects of enzymatically generated free radicals on cerebral arteriolar caliber and responsiveness and on the morphology of these vessels, as well as on the permeability of the blood-brain barrier. Other studies will ascertain the time-course of the pial arteriolar changes following brain injury over a period of 24 to 48 hours after brain injury. The responses of pial arterioles to brain injury will be compared to the responses of cerebellar arterioles to identify whether or not the responses of cerebral microvessels in infratentorial areas differ from those in supratentorial areas. Also, we will examine the role of calcium and of vasoactive intestinal polypeptide in the mediation of the cerebral microcirculatory effects of brain injury.

这些研究的目的是阐明 实验性脑微循环改变 麻醉猫的冲击性脑损伤。这种类型的大脑 损伤引起的软膜小动脉扩张与减少相关 动脉低碳酸血症对血管收缩效应的反应性 对动脉低血压的反应能力减弱。这个 显示这些异常的血管在其血管中有病变 血管内皮细胞的平滑肌和离散的破坏性损伤。这些 异常是由结合过程中产生的氧自由基介导的 随着前列腺素合成的增加。拟议中的实验将 确定氧自由基产生的时间。他们 将确定酶产生的自由基对 脑小动脉口径和反应性及其形态的研究 这些血管以及血脑屏障的通透性。 其他研究将确定软膜小动脉改变的时间进程。 在脑损伤后24至48小时内。 软脑膜小动脉对脑损伤的反应将与 小脑小动脉的反应以识别是否有反应 脑微血管在幕下区域的分布与 幕上区域。此外，我们还将研究钙和钙的作用。 血管活性肠肽在脑损伤中的中介作用 脑损伤的微循环效应。