NEURAL CONTROL OF SKIN BLOOD FLOW DURING HEAT STRESS IN CONGESTIVE HEART FAILURE

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。在这项提议中，研究者将研究自主神经系统在心力衰竭热诱导血管舒张中的作用。以下假设将被检验：1)CHF患者对热应激挑战的总皮肤神经活动反应将减弱；2) CHF患者的皮肤血管舒张反应减弱是由于皮肤血管收缩活性增加和/或循环儿茶酚胺增加。3)心力衰竭患者的压力反射损伤会因热应激而加剧。

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. In this proposal, the investigators will examine the role that the autonomic nervous system plays in heat-induced vasodilation in heart failure. The following hypotheses will be tested: 1) Total skin nerve activity responses to heat stress challenges will be attenuated in CHF patients; 2) The attenuated skin vasodilation responses seen in CHF patients are due to increased skin vasoconstrictor activity and/or increased circulating catecholamines and 3) Baroreflex impairments seen in heart failure will be exaggerated by heat stress.