Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia - a mechanism for promoting hypertension in obstructive sleep apnoea
Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia - a mechanism for promoting hypertension in obstructive sleep apnoea
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DOI：
10.1113/jphysiol.2005.094151
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发表时间：
2005-10-15
影响因子：
5.5
通讯作者：
Hainsworth, R
中科院分区：
文献类型：
--
作者：
Cooper, VL;Pearson, SB;Hainsworth, R
阻塞性睡眠呼吸暂停时发生的窒息会改变压力感受器反射，这可能导致高血压。我们最近报道，呼吸窒息性气体会使压力感受器-血管阻力反射向更高的压力方向复位。本研究旨在确定这种效应是否是由氧张力降低引起的，主要影响外周化学感受器，或由二氧化碳增加引起的，主要作用于中枢化学感受器。我们研究了年龄在20至55岁之间的11名健康志愿者受试者（6名男性）。颈动脉压力感受器的刺激使用施加到颈部腔室的-40至+60 mmHg的分级压力来改变。根据血压（Finapres）的变化评估前臂血管阻力的反应，并根据RR间期和心率的变化评估肱动脉血流速度（多普勒）和心脏反应。刺激-反应曲线在（i）空气呼吸，（ii）缺氧（12%O-2/N-2）和（iii）高碳酸血症（5%CO2/95%O-2）期间定义。在低氧或高碳酸血症之前和之后评估空气呼吸期间的反应。我们将S形函数或三阶多项式应用于曲线，并确定最大微分（相当于峰值灵敏度）和相应的颈动脉窦压力（相当于“设定点”）。缺氧导致心率增加，但平均血压或血管阻力无显著变化。然而，有一个增加的血管阻力在刺激后的时期。缺氧对压力反射敏感性或RR间期、心率或平均动脉压控制的“设定点”没有显著影响。血管阻力对压力感受器刺激的峰值敏感性从-2.5 +/-0.4单位显著降低到-1.4 +/-0.1单位（P < 0.05），并且在刺激后恢复到-2.6 +/-0.5单位。另一方面，对“设定点”高碳酸血症没有影响，导致心率降低，在刺激后阶段保持降低，平均血压显著升高。基线血管阻力显著增加，然后在控制后阶段进一步增加。与低氧一样，高碳酸血症对RR间期、心率或平均动脉压的压力反射控制没有影响。血管阻力反应的灵敏度也没有显著变化，但是，“设定点”从74.7 +/- 4 mmHg显著增加到87.0 +/- 2 mmHg（P < 0.02）。在刺激后控制期，这未完全恢复到刺激前控制水平（82.2 +/- 3 mmHg）。这些结果表明，缺氧窒息的组成部分降低压力感受器血管阻力反射敏感性，而高碳酸成分是负责增加血压和反射“设定点”。高碳酸血症似乎在去除刺激后具有持久的影响。因此，外周和中枢化学感受器对压力反射功能的影响可能有助于促进阻塞性睡眠呼吸暂停患者的高血压。
Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor-vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied I I healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of -40 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus-response curves were defined during (i) air breathing, (ii) hypoxia (12% O-2 in N-2), and (iii) hypercapnia (5% CO2 in 95% O-2). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to 'set point'). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post-stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or 'set point' for the control of RR interval, heart rate or mean arterial pressure. Peaksensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from - 2.5 +/- 0.4 units to - 1.4 +/- 0.1 units (P < 0.05) and this was restored in the post-stimulus period to -2.6 +/- 0.5 units. There was no effect on 'set point' Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post-stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post-control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, 'set point' was significantly increased from 74.7 +/- 4 to 87.0 +/- 2 mmHg (P < 0.02). This was not completely restored to pre-stimulus control levels in the post-stimulus control period (82.2 +/- 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex 'set point'. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemoreceptors on baroreflex function may contribute to promoting hypertension in patients with obstructive sleep apnoea.