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Evidence of sustained forearm vasodilatation after brief isocapnic hypoxia

¹Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215; and ²Sleep Laboratory, Hypoxia PathoPhysiology Laboratory, Centre Hospitalier Universitaire, 38000 Grenoble, France

Submitted 19 November 2003 ; accepted in final form 20 January 2004

Healthy subjects exposed to 20 min 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. Because 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 arterial oxygen saturation 81.6 ± 4.1%, end-tidal PCO₂ 44.7 ± 6.3 Torr) on plethysmographic forearm blood flow (FBF) in eight healthy volunteers while infusing intra-arterial phentolamine to block local -receptors. The dominant arm served as control. Forearm arterial vascular resistance (FVR) was calculated as the mean arterial pressure (MAP)-to-FBF ratio. MAP, heart rate (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 mmHg·min·ml^-1·100 ml of tissue) remained lower than preexposure baseline value (23.05 ± 8.51 mmHg·min·ml^-1·100 ml of tissue; 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.

adrenergic antagonists; vascular resistance; sympathetic nervous system

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