Chronic intermittent hypoxia alters vascular function and structure in skeletal muscle resistance arteries

Abstract

Exposure of rats to chronic intermittent hypoxia (CIH) impairs vasodilator and vasoconstrictor responsiveness and raises arterial pressure; however, it is unclear whether CIH also alters vascular structure. Sprague Dawley rats were exposed to CIH (10% FIO2 for 1–2 min at 4 min intervals; 12 hrs/day). Control rats (CON) were housed under normoxic conditions. Arterial pressure was monitored by telemetry. After 14 days, gracilis arteries (GA) were isolated and cannulated with glass micropipettes, perfused and superfused with physiological salt solution which was equilibrated with 21% O2 and 5% CO2 in a heated chamber. Arteries were pressurized to 80 mmHg and diameters were measured using videomicroscopy before and after exposure to acetylcholine (10−6) or sodium nitroprusside (10−4) in the superfusate. Contralateral GA were fixed for histological examination by in situ perfusion with paraformaldehyde at 80 mmHg. The vessels were excised, mounted in paraffin and stained with Verhoff-vanGieson and hemotoxylin. After 14 days, arterial pressure in CIH rats was elevated above baseline, while pressure was unchanged in CON. Acetylcholine-induced vasodilation was attenuated in CIH vs. CON; however, responses to nitroprusside were the same in CIH and CON. Internal diameter was decreased and intima-media thickness was increased in CIH vs. CON. These results suggest that 14 days of exposure to CIH raises arterial pressure and results in concomitant alterations in function and structure of skeletal muscle resistance arteries. Funded by NIH #HL074072.