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J Appl Physiol (October 12, 2001). doi:10.1152/japplphysiol.00616.2001
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Articles in PresS, published online ahead of print October 12, 2001
J Appl Physiol, 10.1152/jap.00616.2001
Submitted on June 14, 2001
Accepted on October 8, 2001

Nitric oxide mediates hypoxia induced cerebral vasodilation in humans

Annette H Van Mil1, Aart Spilt2, Mark A Van Buchem2, Edward L Bollen3, Luc Teppema4, Rudi G Westendorp1, and Gerard Jan Blauw1*

1 Internal Medicine, Section of Gerontology & Geriatrics, Leiden University Medical Center, Leiden, Netherlands
2 Radiology, Leiden University Medical Center, Leiden, Netherlands
3 Neurology, Leiden University Medical Center, Leiden, Netherlands
4 Physiology, Leiden University Medical Center, Leiden, Netherlands

* To whom correspondence should be addressed. E-mail: gerardblauw{at}compuserve.com.

Nitric oxide (NO) plays a pivotal role in the regulation of peripheral vascular tone. It's 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 L-NMMA on the cerebral blood flow (CBF) was assessed during normoxia (SpO2 97%) and during hypoxia (SpO2 80%). Subjects were positioned in a MR-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) using phase contrast Magnetic Resonance Imaging (pcMRI) techniques. Administration of L-NMMA during normoxia did not affect CBF. Hypoxia increased CBF from 1049 ± 113 to 1209 ± 143 ml/min (P<0.05). After L-NMMA administration, the augmented CBF returned to baseline (1050 ± 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). Using pcMRI, it is shown that hypoxia induced cerebral vasodilatation in humans is mediated by NO.




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