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

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 在这项研究中，研究人员将研究自主神经系统在心力衰竭的热诱导血管扩张中所起的作用。将检验以下假设：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患者皮肤血管扩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；以及3)心力衰竭中出现的压力反射损害将因热应激而加剧。

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.