Bonsignore M R, Marrone O, Insalaco G, Bonsignore G
Istituto di Fisiopathologia Respiratoria CNR, Palermo, Italy.
Eur Respir J. 1994 Apr;7(4):786-805. doi: 10.1183/09031936.94.07040786.
Obstructive sleep apnoeas (OSA) exert immediate marked cardiovascular effects, and may favour the development of systemic and pulmonary hypertension in the long-term. As for the pathogenesis of the acute cardiovascular changes, the first studies high-lighted the role of OSA-induced hypoxia and mechanical changes. However, more recent work pointed to the role played by the arousal reaction terminating OSA, and to the activity of the autonomic nervous system during apnoea and inter-apnoeic phase. As for the pathogenesis of chronic cardiovascular changes, recent findings suggest that the link between OSA and systemic hypertension may be through an abnormal function of the carotid body and underline the importance of chronic intermittent hypoxia versus continuous hypoxia in the development of stable systemic hypertension. On the other hand, OSA do not appear to enhance strongly the development of stable pulmonary hypertension. In this review, we analyze OSA-induced cardiovascular changes with particular emphasis on to the interplay of the possible pathogenic mechanisms involved. Acute OSA-induced cardiovascular alterations during the apnoeic phase appear to result mainly from the mechanical effects of OSA, while during the interapnoeic phase they seem mostly determined by chemical factors (hypoxia, hypercapnia) and by the arousal reaction. In addition, the role of reflex changes elicited by resumption of ventilation should be reconsidered, since lung inflation seems to exert a positive effect on the cardiovascular changes occurring at the end of OSA. This would be in contrast with the inhibitory effects described as "lung inflation reflex", and deserves further study.
阻塞性睡眠呼吸暂停（OSA）会立即产生明显的心血管效应，长期来看可能会促进系统性和肺动脉高压的发展。至于急性心血管变化的发病机制，最初的研究强调了OSA诱导的缺氧和机械变化的作用。然而，最近的研究指出了终止OSA的觉醒反应所起的作用，以及呼吸暂停和呼吸暂停间期自主神经系统的活动。至于慢性心血管变化的发病机制，最近的研究结果表明，OSA与系统性高血压之间的联系可能是通过颈动脉体的异常功能，并强调了慢性间歇性缺氧与持续性缺氧在稳定系统性高血压发展中的重要性。另一方面，OSA似乎并未强烈促进稳定型肺动脉高压的发展。在这篇综述中，我们分析了OSA诱导的心血管变化，特别强调了所涉及的可能致病机制之间的相互作用。呼吸暂停期急性OSA诱导的心血管改变似乎主要源于OSA的机械效应，而在呼吸暂停间期，它们似乎主要由化学因素（缺氧、高碳酸血症）和觉醒反应决定。此外，应重新考虑通气恢复引起的反射变化的作用，因为肺扩张似乎对OSA结束时发生的心血管变化有积极影响。这与被描述为“肺扩张反射”的抑制作用相反，值得进一步研究。
