Tomori Z, Donic V, Benacka R, Kuchta M, Koval S, Jakus J
Ustav patofyziológie Lekárskej fakulty Univerzity P.J. Safárika, Tr. SNP 1, 040 66 Kosice, Slovak Republic.
Sb Lek. 2002;103(1):65-71.
Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
分析了呼吸的四种基本控制机制（脑干呼吸中枢、外周和中枢化学感受器、内感受和外感受反射以及脑桥上影响）及其与睡眠相关的紊乱。睡眠期间中枢化学感受器对二氧化碳的敏感性降低以及上呼吸道阻力增加，在生理状态下就会导致通气不足和轻度低氧血症。睡眠期间呼吸努力的代偿性增加与咽部扩张肌的同步抑制，会使上呼吸道管腔变窄，表现为打鼾、上呼吸道阻力综合征和阻塞性睡眠呼吸暂停（OSA）。由此产生的低氧血症可能会导致明显的心血管、神经精神、内分泌代谢和行为紊乱。增强的呼吸努力和低氧血症会引起气道反射性扩张和从睡眠中觉醒，刺激交感 - 肾上腺系统，通过喘息引发自动复苏以防止致命性窒息。这种自动复苏机制的失败似乎会导致婴儿猝死综合征（SIDS）。无论是在呼吸中枢病变引起的翁丁氏诅咒中，还是在中枢化学感受器不足导致的先天性中枢性通气不足综合征中，睡眠时自主呼吸的消除都会导致呼吸衰竭和死亡。还讨论了夜间支气管和心脏哮喘发作、肺水肿以及肺充血的其他后果。还分析了白天极度嗜睡、慢性疲劳以及记忆、认知和其他脑功能障碍的发病机制。睡眠呼吸暂停综合征（SAS）严重的心血管后果可能会急性表现为心绞痛、心肌梗死、心律失常、短暂性脑缺血发作，甚至中风或心源性猝死。阻塞性睡眠呼吸暂停低通气综合征（OSAS）也可能导致高血压、中心性肥胖、糖尿病、勃起功能障碍、抑郁症以及各种行为障碍。
