INTERMITTENT HYPOXIA NEUROCIRCULATORY RESPONSE TO CHEMOREFLEX & EXERCISE REFLEX

对化学反射的间歇性缺氧神经循环反应

• 批准号: 7951302
• 负责人: URS A LEUENBERGER
• 金额: $ 0.23万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-04-01 至 2010-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7951302
• 关键词: Blood Vessels; Blood flow; Clinical Research; Computer Retrieval of Information on Scientific Projects Database; Exercise; Funding; Goals; Grant; Human; Hypoxia; Institution; Reflex action; Regulation; Research; Research Personnel; Resources; Role; Source; Stress; Sympathetic Nervous System; Training; United States National Institutes of Health; Vasoconstrictor Agents; Vasodilation; Work; 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. The goal of this study is to determine the role of hypoxic stress on the regulation of sympathetic activity and blood flow in healthy humans. Transient hypoxia acutely increases sympathetic activity and evokes vasodilation while intermittent hypoxia tends to evoke sustained sympathoexcitation and enhanced chemoreflex sensitivity. The working hypothesis of this study is that intermittent hypoxia compared to transient hypoxia will excite the sympathetic nervous system, alter sympathetic reflex function and evoke compensatory adaptations of vascular function that oppose sympathetic vasoconstrictor tone during hypoxia. Further, exercise training will reduce this effect.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 本研究的目的是确定低氧应激对健康人交感神经活动和血流调节的作用。 短暂缺氧会急剧增加交感神经活动并引起血管舒张，而间歇性缺氧往往会引起持续的交感神经兴奋并增强化学反射敏感性。本研究的工作假设是，与短暂性缺氧相比，间歇性缺氧会兴奋交感神经系统，改变交感神经反射功能，并引起血管功能的代偿性适应，从而在缺氧期间对抗交感血管收缩张力。 此外，运动训练将减少这种影响。