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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Population Health Sciences, University of Wisconsin, Madison, WI, USA
3 Department of Orthopedics and Rehabilitation, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: jlombard{at}mcw.edu.
The goal of the present study was to evaluate the effects of relatively short-term, chronic intermittent hypoxia on endothelial function of resistance vessels in the skeletal muscle and cerebral circulations. Sprague-Dawley rats were exposed to 14 days of chronic intermittent hypoxia (CIH; 10% FIO2 for 1 min at 4 min intervals; 12 hrs/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 and 5% CO2 in a heated chamber. The arteries were pressurized to 90 mm Hg and vessel diameters were measured via video micrometer before and after exposure to acetylcholine (10 -7 to 10 -4 M), sodium nitroprusside (10-6 M), and acute reduction of PO2 in the perfusate/superfusate (from 140 to 40 mmHg). Acetylcholine-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 to 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.
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