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DISCUSSION

TOP

ABSTRACT

INTRODUCTION

METHODS

RESULTS

DISCUSSION

REFERENCES



The main finding of the study is that acute hypoxia induced an
increase in total CBF that could be blunted by the competitive nitric
oxide synthase inhibitor L -NMMA, providing evidence that hypoxia-induced cerebral vasodilatation is mediated by the ...







This is the first study using pcMRI to investigate hypoxia-induced
cerebral vascular reactivity in humans. To date, Doppler ultrasonography is commonly used to quantify blood flow in the common
carotid artery, internal carotid artery, and middle cere...

24, 25 ).







The normal hemodynamic response to acute hypoxia is an increase in
heart rate and a slight decrease in mean arterial pressure due to a
redistribution of blood flow to organs with a greater O 2

dependency, e.g., skeletal muscles, kidneys, intestines, and the brain
( 27 ). The mechanism underlying this hypoxia-induced vasodilatation in selective vascular beds is not fully understood. In
animal experiments, it has been demonstrated that nitri...

2, 14, 16 ). The present data are the first to show in humans
that hypoxia-induced cerebral vasodilatation is mediated by nitric
oxide, corroborating studies in the human forearm ( 4 ). Because the cerebral vascular resistance declined during hypoxia...







The fact that the end-tidal CO 2 was not influenced by
hypoxia virtually excludes the distorting influence of changes in
P CO 2 on hypoxia-induced cerebral vasodilation
in the present study ( 28 ). Normally, the hypoxic
ventilatory response consists ...







In contrast to normoxia, L -NMMA induced a small increase in
mean arterial pressure of 6% during hypoxia. This is probably caused
by inhibition of hypoxia-induced nitric oxide-mediated systemic
vasodilation by L -NMMA. The fact that L -NMMA
did not i...







An unexpected finding of this study is that basal cerebral blood flow
is significantly different between the normoxic and hypoxic conditions.
Because the study is performed in a randomized single-blind fashion,
this finding must be accidental. This i...







The present finding that nitric oxide plays a role in hypoxia-induced
cerebral vasodilatation in humans may have relevant clinical
implications. To date, data on the role of nitric oxide in
ischemic brain disease are scarce. It has been suggested tha...







In conclusion, by using pcMRI techniques measuring cerebral blood flow,
it is shown that hypoxia-induced cerebral vasodilation in humans is
mediated by nitric oxide.





ACKNOWLEDGEMENTS



The study was supported by an unrestricted grant of the
Bristol-Myers Squibb, Princeton, NJ.



FOOTNOTES




Address for reprint requests and other correspondence: G.J.Blauw, Dept. of General Internal Medicine, Section of Gerontology &Geriatrics, C1-R, Leiden Univ. Medical Center, PO Box 9600, 2300RC
Leiden, The Netherlands (E-mail: g.j.blauw{at}lumc.nl <!...




The costs of publication of this
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10.1152/japplphysiol.00616.2001







Received 14 June 2001; accepted in final form 8 October 2001.