European Heart Journal Advance Access originally published online on November 18, 2005
European Heart Journal 2006 27(3):338-343; doi:10.1093/eurheartj/ehi655
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Impaired skin blood flow response to environmental heating in chronic heart failure
1School of Human Movement and Exercise Science, The University of Western Australia, Crawley 6009, Nedlands, Western Australia
2Advanced Heart Failure and Cardiac Transplant Services, Royal Perth Hospital, Perth, Western Australia
3School of Medicine and Pharmacology, The University of Western Australia, Crawley 6009, Nedlands, Western Australia
4Department of Human Physiology, University of Oregon, OR, USA
5Cardiothoracic Surgery, Royal Perth Hospital, Perth, Western Australia
Received 22 June 2005; revised 7 October 2005; accepted 27 October 2005; online publish-ahead-of-print 18 November 2005.
* Corresponding author. Tel: +61 8 9380 2361; fax: +61 8 9380 1039. E-mail address: brevis{at}cyllene.uwa.edu.au
Aims We examined the thermoregulatory response to heat exposure in patients with chronic heart failure.
Methods and results Skin blood flow (SkBF) was measured in HF subjects and matched controls. Cutaneous vascular conductance (CVC) was calculated from laser-Doppler SkBF and blood pressure. To assess the nitric oxide contribution to thermoregulatory responses, subcutaneous microdialysis membranes were placed beneath the laser-Doppler probes to infuse NG-nitro-L-arginine methyl ester (L-NAME), or Ringer's solution. Core (TC) and skin temperatures (five sites, TSk) were continuously recorded. Subjects were studied during normothermia then at 38°C, 50%RH within a climate chamber. TC and TSk did not differ between HF and controls during normothermia and heating induced similar increases in both groups. During heating, CVC rose in both groups, but significantly less so in HF (HF 43.9±7.8 vs. controls 58.0±7.5% CVCmax, P<0.05). L-NAME attenuated SkBF responses in the control (58.0±7.5 vs. 34.6±5.1% CVCmax, P<0.001) and HF subjects (43.9±7.8 vs. 27.0±2.2% CVCmax, P<0.005), with a larger effect evident in the controls (P<0.05).
Conclusion HF patients exhibit impaired thermoregulatory responses to heat exposure. Lower SkBF in HF, which defends blood pressure during heat exposure, also predisposes these subjects to heat intolerance.
Key Words: Heart failure • Endothelium-derived factors • Regional blood flow • Nitric oxide • Physiology
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