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

研究重复性高碳酸血症对大鼠动脉血压、心率、血红蛋白浓度及RV/(LV+S)的影响。将32只雄性Sprague-Dawley大鼠分为4组：对照组、3周、4周和5周暴露组。使用定时电磁阀，将CO2和N2的混合物冲入腔内1min，将FIO2降至7%，将FICO2提高至8%；然后冲洗空气，使气体馏分恢复到环境水平3分钟。每个周期重复6小时/天。测量是在有意识的休息状态下进行的。在所有组中，高碳酸血症缺氧使Pao2降低至44-46 Torr，使Paco2升高至48-49 Torr。各组间基线血压、心率、血红蛋白浓度和动脉血气无显著差异。然而，在高碳酸血症缺氧期间，动脉血压明显升高，心率明显下降，且在5周暴露组的变化幅度最大。暴露组血红蛋白浓度在高碳酸血症缺氧期间短暂升高。RV/(LV+S)随暴露时间的增加而增加。酚妥拉明可降低急性血压升高，阿托品可消除高碳酸血症缺氧时的心动过缓。结果表明，这种水平的重复性高碳酸血症缺氧不会产生永久性高血压和红细胞增多症，但会引起急性血压升高、心动过缓和心室肥大，这取决于暴露时间。血红蛋白浓度在高碳酸血症缺氧时短暂升高。交感神经和副交感神经张力的增加似乎在高碳酸血症缺氧时心血管变化的发展中起主要作用。除缺氧外，二氧化碳潴留可能在睡眠呼吸暂停综合征患者心血管变化的发展中起重要作用。

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.