THE VASCULAR EFFECTS OF ACUTE HYPOXIA

急性缺氧对血管的影响

• 批准号: 7718931
• 负责人: JAMES WOODROW WEISS
• 金额: $ 0.05万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7718931
• 关键词: Acute; Age; Arteries; Blood Pressure; Blood Vessels; Blood flow; Cardiovascular system; Chronic; Computer Retrieval of Information on Scientific Projects Database; Condition; Disease; Environmental air flow; Functional disorder; Funding; Glucose Intolerance; Grant; Heart Rate; Human; Hyperinsulinism; Hypoxia; Institution; Insulin; Mediating; Metabolic; Muscle; Nerve; Obstructive Sleep Apnea; Pathology; Patients; Rattus; Recruitment Activity; Reporting; Research; Research Personnel; Resources; Source; Testing; Trees; United States National Institutes of Health; Woman; Work; experience; men; relating to nervous system; respiratory; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Hypoxia experienced environmentally or as a consequence of pathology causes changes in respiratory, cardiovascular, neural, and metabolic function. In patients with obstructive sleep apnea, a disease characterized by chronic hypoxia, cardiovascular and metabolic dysfunctions are reported, hypoxia has been implicated as the main factor. Cardiovascular control is mediated locally and centrally and is different along the vascular tree. Metabolic function is dependent on cellular activity and vascular dynamics. In the humans, hypoxia has been shown to cause glucose intolerance, an indicator of metabolic dysfunction. In rats, hyperinsulinemia caused microvascular recruitment that occurred without changes in arterial flow. Hypoxia, working via similar and different mechanisms as insulin could conceivably cause heterogeneous responses of the arteries and microvasculature leading to downstream metabolic dysfunction. To test the first part of this question we will evaluate both arterial blood flow and microvascular recruitment before and after hypoxia. Muscle sympathetic nerve activity, heart rate, blood pressure, and ventilation will be collected continuously. We hypothesize that under hypoxic conditions, microvascular and arterial dynamics will be different. For this initial study, we will recruit a total of 10 healthy men and women between the ages of 18-64 yrs.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 缺氧在环境上或由于病理学而导致的呼吸道，心血管，神经和代谢功能的变化。 在阻塞性睡眠呼吸暂停的患者中，有一种以慢性缺氧为特征的疾病，据报道心血管和代谢功能障碍，缺氧已被视为主要因素。 心血管控制是在本地和集中介导的，沿血管树是不同的。 代谢功能取决于细胞活性和血管动力学。 在人类中，缺氧已被证明会导致葡萄糖不耐症，这是代谢功能障碍的指标。在大鼠中，高胰岛素血症引起的微血管募集发生，而动脉流量没有变化。通过与胰岛素相似和不同机制起作用的缺氧可能会引起动脉和微脉管系统的异质反应，从而导致下游代谢功能障碍。 为了测试这个问题的第一部分，我们将评估缺氧前后的动脉血流和微血管募集。 肌肉交感神经活动，心率，血压和通气将连续收集。 我们假设在低氧条件下，微血管和动脉动力学将有所不同。 在这项最初的研究中，我们将招募18至64岁年龄段的10名健康男人和女性。