CONTROL OF ILIAC ARTERY VASOACTIVITY

髂动脉血管活性的控制

• 批准号: 3471177
• 负责人: MARK j YOUNG
• 金额: $ 7.37万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-07-01 至 1992-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3471177
• 关键词: artery stenosis; autonomic reflex; blood lipoprotein; dietary lipid; hypercholesterolemia; vascular endothelium; vasoconstriction; vasodilation; vasospasm

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.

损伤血管内皮细胞，高血清胆固醇， 动脉粥样硬化和血流速度的变化是 改变血管反应性。 然而，很少有研究系统地 研究了这种血管活性改变的机制。 此外，大多数关于内皮细胞作用的先前工作 和胆固醇水平升高的血管控制已经进行了， 隔离的血管或麻醉的动物，因此， 这表明了完整的有意识的动物的控制机制。 这 研究建议将系统地评估变化的影响， (1)髂动脉血流，（2）去除内皮，（3）急性和（4）慢性 血清胆固醇和血浆脂蛋白的饮食升高 控制清醒犬的大髂动脉直径。 具体 将注意这些干预措施对肾上腺素能的影响， 和胆碱能自主血管收缩和血管舒张， 受体亚型参与这些机制。 我们亦会研究 去除内皮和急性或慢性胆固醇的影响 髂血管壁的弹性特性升高。 中央 该建议假设是去除髂动脉内皮 细胞，或血浆胆固醇水平升高，将降低对 自主血管扩张刺激，同时增强对自主神经的反应， 血管收缩刺激。 这些变化的累积效应可能 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 澄清造成改变的机制 血管活性将产生大动脉控制的基础知识 有意识的动物中的机制。