Chronic intermittent hypoxia impairs endothelium-dependent dilation in rat cerebral and skeletal muscle resistance arteries. Am J Physiol Heart Circ Physiol 2004 Jan;286(1):H388-93
Date
09/27/2003Pubmed ID
14512283DOI
10.1152/ajpheart.00683.2003Scopus ID
2-s2.0-0346998122 (requires institutional sign-in at Scopus site) 123 CitationsAbstract
The goal of the present study was to evaluate the effects of relatively short-term chronic intermittent hypoxia (CIH) on endothelial function of resistance vessels in the skeletal muscle and cerebral circulations. Sprague-Dawley rats were exposed to 14 days of CIH (10% fraction of inspired oxygen for 1 min at 4-min intervals, 12 h/day, n = 6). Control rats (n = 6) were housed under normoxic conditions. After 14 days, resistance arteries of the gracilis muscle (GA) and middle cerebral arteries (MCA) were isolated and cannulated with micropipettes, perfused and superfused with physiological salt solution, and equilibrated with 21% O2-5% CO2 in a heated chamber. The arteries were pressurized to 90 mmHg, and vessel diameters were measured via a video micrometer before and after exposure to ACh (10-7-10-4 M), sodium nitroprusside (10-6 M), and acute reduction of Po2 in the perfusate/superfusate (from 140 to 40 mmHg). ACh-induced dilations of GA and MCA from animals exposed to CIH were greatly attenuated, whereas responses to nitroprusside were similar to controls. Dilations of both GA and MCA in response to acute reductions in Po2 were virtually abolished in animals exposed to CIH compared with controls. These findings suggest that exposure to CIH reduces the bioavailability of nitric oxide in the cerebral and skeletal muscle circulations and severely blunts vasodilator responsiveness to acute hypoxia.
Author List
Phillips SA, Olson EB, Morgan BJ, Lombard JHMESH terms used to index this publication - Major topics in bold
AcetylcholineAnimals
Arteries
Cerebral Arteries
Chronic Disease
Endothelium, Vascular
Hypoxia
Male
Muscle, Skeletal
Nitric Oxide Donors
Nitroprusside
Oxygen
Partial Pressure
Rats
Rats, Sprague-Dawley
Sodium Chloride
Vascular Resistance
Vasodilation
