EFFECT OF SYMP NEURAL BLOCKADE ON REACTIVE HYPEREMIA & RESPONSES IN OSA

SYMP 神经阻滞对反应性高血症的影响

• 批准号: 7378463
• 负责人: URS A LEUENBERGER
• 金额: $ 1.72万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7378463
• 关键词: EFFECT; SYMP; NEURAL; BLOCKADE; REACTIVE

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 purpose of this study is to better understand the role the sympathetic nervous system plays in the regulation of vascular tone in patients with obstructive sleep apnea (OSA). The specific aims of this protocol are to determine: 1) the maximal vasodilator capacity (reactive hyperemic blood flow response, RHBF); 2) the effects of sympathetic vasoconstrictor tone on RHBF; and 3) the effect of sympathetic vasoconstrictor tone on hypoxia-induced vasodilation in OSA. Based on preliminary data, we postulate that in OSA mechanisms of vasodilation are impaired. We further postulate that the reduced response to vasodilator stimuli is due to enhanced sympathetic tone. These aims will be addressed in 3 separate studies that employ similar techniques. In Study I we will determine RHBF in the arm and leg in OSA and in controls. In Study II we will determine the effect of regional forearm sympathetic blockade (Bier block, see below) on RHBF in OSA and in controls. In Study III we will determine the effect of the Bier block on forearm vasodilation induced by systemic hypoxia in OSA and in controls. Only one of the 3 studies will be performed in each subject on a given day. However, the subject may be invited to return on another day to participate in one of the other studies described above. To determine whether OSA therapy reverses vascular dysfunction, OSA patients will participate in the same study after 1-6 months of OSA treatment with continuous positive airway pressure therapy (CPAP).

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。本研究的目的是更好地了解交感神经系统在阻塞性睡眠呼吸暂停（OSA）患者血管张力调节中的作用。本方案的具体目的是确定：1）最大血管舒张能力（反应性充血血流反应，RHBF）; 2）交感血管收缩张力对RHBF的影响; 3）交感血管收缩张力对OSA中缺氧诱导的血管舒张的影响。基于初步的数据，我们推测，在阻塞性睡眠呼吸暂停的血管舒张机制受损。我们进一步假设，对血管扩张刺激的反应降低是由于交感神经张力增强。这些目标将在采用类似技术的3项单独研究中进行阐述。在研究I中，我们将测定OSA和对照组手臂和腿部的RHBF。在研究II中，我们将确定区域前臂交感神经阻滞（比尔阻滞，见下文）对OSA和对照组RHBF的影响。在研究III中，我们将确定Bier阻滞对OSA和对照组中全身缺氧诱导的前臂血管舒张的影响。在给定的一天，每例受试者仅进行3项研究中的1项。 但是，受试者可能会被邀请在另一天返回参加上述其他研究之一。为了确定OSA治疗是否逆转血管功能障碍，OSA患者将在使用持续气道正压通气治疗（CPAP）进行OSA治疗1-6个月后参加相同的研究。