Chemoreflexes - physiology and clinical implications
Chemoreflexes - physiology and clinical implications
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DOI：
10.1046/j.1365-201x.2003.01083.x
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发表时间：
2003-03-01
期刊：
影响因子：
--
通讯作者：
Somers, VK
中科院分区：
文献类型：
--
作者：
Kara, T;Narkiewicz, K;Somers, VK
化学反射是交感神经激活的重要调节因子。位于颈动脉小体的外周化学感受器主要对低氧血症作出反应。位于脑干区域的中枢化学感受器对高碳酸血症有反应。低氧或高碳酸化学反射的激活都会引起换气过度和交感神经激活。在呼吸暂停期间，当肺传入神经拉伸的抑制作用被消除时，交感神经对缺氧和高碳酸血症的反应都增强。与中枢化学感受器激活相比，肺传入的抑制作用对交感神经外周反应的影响更为显著。动脉压力反射对化学反射也有很强的抑制作用。与中枢化学反射相比，外周化学反射的抑制作用更为明显。在高血压患者中，交感神经和呼吸系统对低氧血症的反应明显增加。在呼吸暂停期间，随着呼吸抑制影响的消除，未治疗的轻度高血压患者的交感神经反应明显大于匹配的正常血压对照组。高血压患者外周化学反射敏感性增强的部分原因可能是这些患者的压力反射功能受损。外周化学反射敏感性增强在阻塞性睡眠呼吸暂停患者中也很明显。这种外周化学反射增强不能用肥胖来解释，因为肥胖个体与瘦对照组相似，中枢化学感受器具有外周化学反射反应的选择性增强。对低氧血症的敏感性增加对经历重复性和严重低氧血症应激的阻塞性睡眠呼吸暂停患者具有重要意义。化学反射的强直性激活也可能有助于高水平的交感神经活动，即使在睡眠呼吸暂停患者白天正常清醒时也是如此。对睡眠呼吸暂停患者给予100%氧气可降低心率、血压和中枢交感神经流出量。在心力衰竭患者中，对高碳酸血症的中枢化学反射反应显着和选择性地增强。这种增加的中枢化学反射敏感性可能有助于心力衰竭患者中枢性睡眠呼吸暂停的发展。100%供氧不会降低心力衰竭患者的交感神经活动，这进一步证明了外周化学反射增强的存在。外周和中枢化学反射对健康和疾病中的交感神经活动都有强大的影响，并可能对疾病病理生理起重要作用，特别是在高血压、阻塞性睡眠呼吸暂停和心力衰竭等情况下。
The chemoreflexes are important modulators of sympathetic activation. The peripheral chemoreceptors located in the carotid bodies respond primarily to hypoxaemia. Central chemoreceptors located in the region of the brainstem respond to hypercapnia. Activation of either the hypoxic or hypercapnic chemoreflex elicits both hyperventilation and sympathetic activation. During apnoea, when the inhibitory influence of stretch of the pulmonary afferents is eliminated, there is a potentiation of the sympathetic response to both hypoxia and hypercapnia. This inhibitory influence of the pulmonary afferents is more marked on the sympathetic response to peripheral compared with central chemoreceptor activation. The arterial baroreflexes also have a powerful inhibitory influence on the chemoreflexes. This inhibition is again more marked with respect to the peripheral compared with central chemoreflexes.In patients with hypertension, there is a marked increase in the sympathetic and ventilatory response to hypoxaemia. During apnoea, with elimination of the inhibitory influence of breathing, the sympathetic response in untreated mild hypertensive patients is strikingly greater than that seen in matched normotensive controls. This potentiated peripheral chemoreflex sensitivity in hypertension may be explained in part by impaired baroreflex function in these patients. Enhanced peripheral chemoreflex sensitivity is also evident in patients with obstructive sleep apnoea. This peripheral chemoreflex enhancement is not explained by obesity, as obese individuals have a selective potentiation of the central chemoreceptors with peripheral chemoreflex responses similar to those seen in lean controls. Increased sensitivity to hypoxaemia has important implications in patients with obstructive sleep apnoea who experience repetitive and severe hypoxaemic stress. Tonic activation of the chemoreflex may also contribute to the high levels of sympathetic activity evident even during normoxic daytime wakefulness in sleep apnoea patients. Administration of 100% oxygen in patients with sleep apnoea results in reductions in heart rate, blood pressure and central sympathetic outflow.In patients with heart failure, the central chemoreflex response to hypercapnia is markedly and selectively enhanced. This increased central chemoreflex sensitivity may contribute to the development of central sleep apnoea in heart failure patients. Administration of 100% oxygen does not lower sympathetic activity in patients with heart failure, providing further evidence against any peripheral chemoreflex potentiation.The peripheral and central chemoreflexes have powerful effects on sympathetic activity in both health and disease and may contribute importantly to disease pathophysiology, particularly in conditions such as hypertension, obstructive sleep apnoea and heart failure.