Why is sleep apnea syndrome a risk factor for cardiovascular diseases in adults?

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We investigated the effects of repetitive hypercapnic hypoxia on arterial blood pressure, heart rate, hemoglobin concentration and RV/(LV+S) in rats. Thirty-two male Sprague-Dawley rats were divided into 4 groups, controls, 3 weeks, 4 weeks and 5 weeks exposure group. With the use of a timed solenoid valve, a mixture of CO2 and N2 was flushed into the chamber for 1 min, reducing FIO2 to 7% and raising FICO2 to 8%; then air was flushed allowing return of gas fractions to ambient levels for 3 min. Each cycle was repeated for 6 h/day. Measurements were carried out in the conscious resting state. In all groups, hypercapnic hypoxia decreased Pao2 to 44-46 Torr and increased Paco2 to 48-49 Torr. There was no significant, difference in baseline blood pressure, heart rate, hemoglobin concentration and arterial blood gases among groups. However, arterial blood pressure increased and heart rate decreased significantly during hypercapnic hypoxia, and the magnitude of the changes was highest in the 5 weeks exposure group. Hemoglobin concentration increased transiently during hypercapnic hypoxia in the exposure groups. RV/(LV+S) increased with an increase in the exposure period. Phentolamine attenuated acute blood pressure elevation and atropine abolished bradycardia during hypercapnic hypoxia. The results indicate that this level of repetitive hypercapnic hypoxia does not produce permanent hypertension and polycythemia but induces acute blood pressure elevation, bradycardia and RV hypertrophy which is dependent on the exposure period. Hemoglobin concentration increased transiently during hypercapnic hypoxia. An increased sympathetic and parasympathetic tone seems to play a major role in the development of cardiovascular changes during hypercapnic hypoxia. In addition to hypoxia CO2 retention might play a significant role in the development of cardiovascular changes in patients with sleep apnea syndrome.