Journal of Applied Physiology
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J Appl Physiol 92: 962-966, 2002. First published October 12, 2001; doi:10.1152/japplphysiol.00616.2001
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Vol. 92, Issue 3, 962-966, March 2002

Nitric oxide mediates hypoxia-induced cerebral vasodilation in humans

Annette H. M. Van Mil1, Aart Spilt2, Mark A. Van Buchem2, Edward L. E. M. Bollen3, Luc Teppema4, Rudi G. J. Westendorp1, and Gerard J. Blauw1

Departments of 1 General Internal Medicine, Section of Gerontology and Geriatrics, 2 Radiology, 3 Neurology, and 4 Physiology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands

Nitric oxide (NO) plays a pivotal role in the regulation of peripheral vascular tone. Its role in the regulation of cerebral vascular tone in humans remains to be elucidated. This study investigates the role of NO in hypoxia-induced cerebral vasodilatation in young healthy volunteers. The effect of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) on the cerebral blood flow (CBF) was assessed during normoxia and during hypoxia (peripheral O2 saturation 97 and 80%, respectively). Subjects were positioned in a magnetic resonance scanner, breathing normal air (normoxia) or a N2-O2 mixture (hypoxia). The CBF was measured before and after administration of L-NMMA (3 mg/kg) by use of phase-contrast magnetic resonance imaging techniques. Administration of L-NMMA during normoxia did not affect CBF. Hypoxia increased CBF from 1,049 ± 113 to 1,209 ± 143 ml/min (P < 0.05). After L-NMMA administration, the augmented CBF returned to baseline (1,050 ± 161 ml/min; P < 0.05). Similarly, cerebral vascular resistance declined during hypoxia and returned to baseline after administration of L-NMMA (P < 0.05 for both). Use of phase-contrast magnetic resonance imaging shows that hypoxia-induced cerebral vasodilatation in humans is mediated by NO.

cerebrovasculature; vascular reactivity; NG-monomethyl-L-arginine; magnetic resonance imagery


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