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J Appl Physiol (February 6, 2004). doi:10.1152/japplphysiol.01241.2003
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Submitted on November 19, 2003
Accepted on January 20, 2004

Evidence of Sustained Forearm Vasodilatation after Brief Isocapnic Hypoxia

Renaud Tamisier1*, Daniel Norman2, Amit Anand2, Yoon Choi2, and J. Woodrow Weiss2

1 Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA; Sleep laboratory, HP2 (Hypoxia PathoPhysiology) laboratory, Centre Hospitalier Universitaire, Grenoble, France
2 Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA

* To whom correspondence should be addressed. E-mail: rtamisie{at}bidmc.harvard.edu.

Healthy subjects exposed to 20 minutes of hypoxia increase ventilation and muscle sympathetic nerve activity (MSNA). After return to normoxia, although ventilation returns to baseline, MSNA remains elevated for up to an hour. Since forearm vascular resistance is not elevated after hypoxic exposure, we speculated that the increased MSNA might be a compensatory response to sustained release of endogenous vasodilators. We studied the effect of isocapnic hypoxia (mean SaO2 81.6 ± 4.1%, PetCO2 44.7 ± 6.3 mmHg) on plethysmographic forearm blood flow (FBF) in 8 healthy volunteers, while infusing intra-arterial phentolamine to block local {alpha}-receptors. The dominant arm served as control. Forearm arterial vascular resistance (FVR) was calculated as the mean arterial pressure (MAP)/FBF ratio. MAP, HR and FVR were reported at 5 min intervals at baseline, then while infusing phentolamine during room air, isocapnic hypoxia, and recovery. Despite increases in HR during hypoxia, there was no change in MAP throughout the study. By design, FVR decreased during phentolamine infusion. Hypoxia further decreased FVR in both forearms. With continued phentolamine infusion, FVR after termination of the exposure (17.47 ± 6.3) remained lower than pre-exposure baseline value (23.05 ± 8.51, p<0.05). We conclude that, unmasked by phentolamine, the vasodilation occurring during hypoxia persists for at least 30 min after the stimulus. This vasodilation may contribute to the sustained MSNA rise observed after hypoxia.




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