Prabhakar Nanduri R, Dick Thomas E, Nanduri Jayasri, Kumar Ganesh K
Department of Physiology & Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44109, USA.
Exp Physiol. 2007 Jan;92(1):39-44. doi: 10.1113/expphysiol.2006.036434. Epub 2006 Nov 23.
Patients with recurrent apnoeas exhibit autonomic abnormalities manifested as persistent increase in sympathetic nerve activity (SNA). Several studies suggest that chronic intermittent hypoxia (CIH) resulting from recurrent apnoeas is a major stimulus for evoking autonomic morbidity. Although it has been proposed that CIH, by way of activating the chemoreceptor reflex, leads to sympathetic excitation, the underlying mechanisms are incompletely understood. Studies on experimental models have provided new insights into the mechanisms associated with CIH-evoked sympathoexcitation. The purpose of this article is to highlight recent information on systemic, cellular and molecular analysis of the effects of CIH on chemoreceptor-mediated sympathoexcitation. Chronic intermittent hypoxia exerts two major effects on the chemoreceptor reflex: (a) augmentation of the carotid body and sympathetic effector responses to acute hypoxia; and (b) induction of long-lasting activation of both the sensor and the effector that persists several hours after termination of CIH. Available evidence indicates that CIH may facilitate processing of chemoreceptor afferent information at the central nervous system. Recent studies suggest that reactive oxygen species-mediated signalling is a major cellular mechanism, and transcriptional activation by hypoxia-inducible factor-1 is one of the critical molecular mechanisms underlying chemoreceptor-mediated sympathoexcitation by CIH.
复发性呼吸暂停患者表现出自主神经异常，表现为交感神经活动（SNA）持续增加。多项研究表明，复发性呼吸暂停导致的慢性间歇性缺氧（CIH）是引发自主神经病变的主要刺激因素。尽管有人提出CIH通过激活化学感受器反射导致交感神经兴奋，但其潜在机制尚未完全明确。对实验模型的研究为与CIH诱发的交感神经兴奋相关的机制提供了新的见解。本文的目的是强调关于CIH对化学感受器介导的交感神经兴奋作用的系统、细胞和分子分析的最新信息。慢性间歇性缺氧对化学感受器反射有两个主要影响：（a）增强颈动脉体和交感效应器对急性缺氧的反应；（b）诱导传感器和效应器的长期激活，这种激活在CIH终止后持续数小时。现有证据表明，CIH可能促进中枢神经系统对化学感受器传入信息的处理。最近的研究表明，活性氧介导的信号传导是主要的细胞机制，缺氧诱导因子-1介导的转录激活是CIH介导化学感受器交感神经兴奋的关键分子机制之一。
