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CONTROL OF ILIAC ARTERY VASOACTIVITY

髂动脉血管活性的控制

基本信息

批准号：
3471178
负责人：
MARK j YOUNG
金额：
$ 8.46万
依托单位：
HARVARD MEDICAL SCHOOL
依托单位国家：
美国
项目类别：
财政年份：
1987
资助国家：
美国
起止时间：
1987-07-01 至 1989-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3471178
关键词：
adrenergic receptor artery stenosis autonomic reflex blood lipoprotein dietary lipid dogs hypercholesterolemia muscarinic receptor vascular endothelium vasoconstriction vasodilation vasospasm

项目摘要

Damage to vascular endothelial cells, high serum cholesterol, atherosclerosis, and changes in blood flow velocity, are factors which alter vascular reactivity. However, few studies have systematically studied the mechanisms responsible for this altered vasoactivity. Furthermore, most previous work concerning the role of endothelial cells and elevated cholesterol levels in vascular control has been conducted in isolated vessels or anesthetized animals and, therefore, may not be indicative of control mechanisms in the intact, conscious animal. This research proposal will systematically evaluate the effects of changes in (1) iliac blood flow, (2) removal of endothelium, (3) acute and (4) chronic dietary elevation of serum cholesterol and plasma lipoproteins on the control of large iliac artery diameter in the conscious dog. Specific attention will be paid to the effects of these interventions on adrenergic and cholinergic autonomic vasoconstriction and vasodilation, and the receptor subtypes involved in these mechanisms. We will also examine the effects of removal of endothelium and acute or chronic cholesterol elevation on the elastic properties of the iliac vessel wall. The central hypothesis of this proposal is that removal of iliac artery endothelial cells, or elevated plasma cholesterol levels, will reduce the response to autonomic vasodilator stimuli, while enhancing the response to autonomic vasoconstrictor stimuli. The cumulative effects of these alterations may account for the greater degree of vasoconstriction observed during episodes of vasospasm. Clarification of the mechanisms responsible for the altered vasoactivity will yield fundamental knowledge of large artery control mechanisms in the conscious animal.

对血管内皮细胞的损伤，高血清胆固醇，动脉粥样硬化和血流速度的变化是改变血管的反应性。然而，很少有系统的研究。研究了导致这种血管活性改变的机制。此外，以前大多数关于内皮细胞作用的工作在血管控制中升高的胆固醇水平已经在隔离的血管或麻醉的动物，因此可能不会表明了完好无损的清醒动物的控制机制。这研究提案将系统地评估以下变化的影响 (1)髂动脉血流，(2)内皮剥离，(3)急性和(4)慢性膳食中血清胆固醇和血浆脂蛋白的升高清醒犬大髂动脉内径的控制。特定的注意这些干预措施对肾上腺素能的影响胆碱能自主神经血管收缩和血管扩张，以及参与这些机制的受体亚型。我们还将研究去除血管内皮细胞与急、慢性胆固醇的影响高度对髂动脉管壁弹性性能的影响。中环这一建议的假设是去除髂动脉内皮细胞细胞，或血浆胆固醇水平升高，会降低对自主神经血管扩张剂刺激，同时增强对自主神经的反应血管收缩刺激。这些变化的累积影响可能解释了在发作期间观察到的更大程度的血管收缩血管痉挛的症状。澄清造成更改的机制血管活动将产生大动脉控制的基本知识有意识的动物的机制。