THE VASCULAR EFFECTS OF ACUTE HYPOXIA

这个子项目是众多研究子项目之一

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.