慢性间歇低氧所致高血压的中枢调控机制研究进展

Research progress on the neurogenic mechanisms of hypertension caused by chronic intermittent hypoxia

睡眠呼吸暂停综合征可以引起持续性的血压升高,但其引起血压升高的机制尚不完全清楚。目前认为中枢调控的交感神经放电活性增强在高血压形成过程中发挥重要作用。间歇低氧动物模型研究结果显示间歇低氧可以快速及持续的激活包括孤束核、终板及下丘脑室旁核在内的中枢环路影响交感神经放电活性。本文将对孤束核、终板及下丘脑室旁核在间歇低氧所致交感神经放电活性增强及高血压中的作用做一综述,进一步探讨间歇低氧所致高血压的中枢调控机制。

Obstructive sleep apnea hypopnea syndrome can lead to persistent hypertension, but the mechanisms are still poorly understood. The central regulation of sympathetic nerve discharge activity plays an important role in the formation process of hypertension. Related research results of models of nocturnal intermittent hypoxia(IH) indicate that IH rapidly and persistently activates a central circuit that includes the nucleus of the solitary tract(NTS), forebrain lamina terminalis and the hypothalamic paraventricular nucleus(PVN), which can influence the sympathetic nerve discharge.This brief review will focus on the findings related to the role of regions in the central nervous system that are proposed to play major roles in the sympatho-excitatory response to IH: the NTS, the lamina terminalis and the PVN.