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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。
Sleep apnea syndrome can cause persistent blood pressure, but its mechanism of raising blood pressure is not yet fully understood. Now that the central regulation of sympathetic nerve activity increase in the formation of hypertension play an important role. Intermittent hypoxia animal model results show intermittent hypoxia can quickly and continuously activate the central circuit including the solitary tract nucleus, the end plate and the hypothalamic paraventricular nucleus, including the impact of sympathetic nerve activity. In this paper, the effects of intermittent hypoxic nucleus, endplate and hypothalamic paraventricular nucleus on the enhancement of sympathetic nerve activity induced by intermittent hypoxia and hypertension were reviewed. The central mechanism of intermittent hypoxia-induced hypertension was also discussed.