ABSTRACT
We determined the effects of chronic repetitive hypoxia and hypercapnic hypoxia on systemic and pulmonary hemodynamics using an animal model simulating sleep apnea syndrome (SAS). Fifty-six rats were divided into the hypoxia (Pao2 44-46Torr) and the hypercapnic hypoxia (Pao2 44-46Torr, Paco2 48-49Torr) group. The hypoxic gas or the hypercapnic hypoxic gas was flushed into the chamber for 1 min, then air was flushed allowing return of gas fractions to ambient levels for 3 min. Each cycle was repeated 6h/day for 5 weeks. In the hypoxia group, there was no significant difference in baseline blood pressure (BP) and heart rate (HR) between controls and the exposure group. Only HR increased transiently during hypoxia in both controls and the exposure group. RV/(LV + S) did not change after 5 weeks of exposure. In the hypercapnic hypoxia group, there was no significant difference in baseline BP and HR between controls and the exposure group. However, acute BP elevation and transient bradycardia were induced during hypercapnic hypoxia, and the magnitude of the changes increased with an increase in the exposure period. RV/(LV + S) increased after 5 weeks of exposure. Phentolamine attenuated acute BP elevation and atropine abolished bradycardia, suggesting an increased sympathetic and parasympathetic tone. The results suggest that hypercapnia associated with hypoxia plays an important role in developing cardiovascular changes in SAS.
