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.

血管内皮细胞损伤、血清胆固醇升高、 动脉粥样硬化和血流速度的变化是导致动脉粥样硬化的因素 改变血管反应性。 但很少有研究系统地 研究了导致这种血管活性改变的机制。 此外，大多数先前的工作涉及内皮细胞的作用 血管控制中胆固醇水平升高已在 隔离的血管或麻醉的动物，因此可能不会 表明完整的、有意识的动物的控制机制。 这 研究计划将系统地评估变化的影响 (1) 髂血流，(2) 内皮去除，(3) 急性和 (4) 慢性 饮食中血清胆固醇和血浆脂蛋白升高 控制清醒狗的髂大动脉直径。 具体的 将关注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，以及 参与这些机制的受体亚型。 我们还将检查 去除内皮和急性或慢性胆固醇的影响 髂血管壁弹性特性的升高。 中央 该提议的假设是，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 自主血管舒张刺激，同时增强对自主神经的反应 血管收缩刺激。 这些改变的累积效应可能 解释了发作期间观察到的更大程度的血管收缩 血管痉挛。 澄清负责改变的机制 血管活动将产生大动脉控制的基础知识 有意识的动物的机制。