[呼吸及其睡眠相关疾病的调节]。

Sbornik lekarsky Pub Date : 2002-01-01
Z Tomori, V Donic, R Benacka, M Kuchta, S Koval, J Jakus
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引用次数: 0

摘要

本文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、内外感受反射和超尿素影响)及其与睡眠有关的疾病。中枢化学感受器对二氧化碳敏感性的降低和睡眠期间上呼吸道阻力的增加导致生理状态下的低通气和轻度低氧血症。睡眠时,呼吸力代偿性增加,同时抑制咽扩张器,可减少上呼吸道管腔,表现为打鼾、上呼吸道阻力综合征和阻塞性睡眠呼吸暂停。由此产生的低氧血症可引起明显的心血管、神经精神、内分泌代谢和行为障碍。增加的通气努力和低氧血症引起呼吸道的反射性扩张和从睡眠中唤醒,刺激交感神经-肾上腺系统,从而通过喘息引起自我复苏,防止致命的窒息。这种自我复苏机制的失败似乎会导致小岛屿发展中国家。无论是呼吸中枢病变引起的Ondine's诅咒,还是中枢化学感受器不足引起的先天性中枢性低通气综合征,由于睡眠而消除自主呼吸都会导致呼吸衰竭和死亡。夜间发作的支气管和心脏哮喘,肺水肿和其他后果的肺充血也进行了讨论。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病理机制。SAS的严重心血管后果可急性表现为心绞痛、心肌梗死。心律失常,短暂性缺血发作,甚至中风或心源性猝死。OSAS还可能导致高血压、中枢性肥胖、糖尿病、勃起功能障碍、抑郁症和各种行为障碍。
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[Regulation of respiration and its sleep-related disorders].

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.

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