Skin Sympathetic Nerve Activity Response to Heat Stress in Congestive Heart Failure

Abstract

BACKGROUND: Previous studies show that the rise in skin blood flow (SkBF) during heat stress is substantially attenuated in congestive heart failure (CHF) patients when compared to healthy subjects. However, the mechanism(s) leading to the attenuated rise in SkBF in CHF patients with heat stress is not clear. Both local mechanisms and central mechanism (i.e. skin sympathetic nerve activity, SSNA) may play a role in control of SkBF in heat stress. However, the SSNA response to heat stress in CHF has not been reported. PURPOSE: To examine the hypothesis that whole body heat stress does not cause any increase in SSNA in CHF. METHODS: We assessed SSNA (microneurography) from peroneal nerve and forearm SkBF (laser Doppler) in 7 patients with stable class II-III CHF and in healthy subjects during passive whole body heating with water perfused suit. RESULTS: Whole body heating induced a similar increase in internal temperature (∼0.7 °C) in all groups. The elevation in forearm cutaneous vascular conductance (CVC) in patients with CHF was significantly lower than that in healthy control subjects (233±37 vs. 852±176% of normothermic baseline (100%; P<0.001). Heat stress increased SSNA in CHF patients (100 to 239±29% of normothermic baseline, P<0.05) and healthy controls (100 to 369±74% of normothermic baseline, P<0.001). However, the CVC/SSNA in heat in CHF was lower than the healthy subjects (1.23±0.08 vs. 2.93±0.60, P<0.05). CONCLUSIONS: The data showed that SSNA was activated in CHF patients with whole body heating, however, lower CVC/SSNA in CHF may suggest an impaired cutaneous vasodilator response to the nerve activity. Supported by AHA 0635245 N, NIH P01 HL077670, and M01 RR010732.