运动引起鼻黏膜收缩的神经生理机制。

Neurophysiological mechanism of shrinkage of nasal mucosa induced by exercise.

作者信息

Konno A, Togawa K, Itasaka Y

出版信息

Auris Nasus Larynx. 1982;9(2):81-90. doi: 10.1016/s0385-8146(82)80004-7.

Abstract

Change of serum norepinephrine level and nasal patency were measured in 10 normal volunteers during exercise and effect of unilateral cervical sympathetic ganglion block on exercise-induced shrinkage of nasal mucosa was evaluated. Serum norepinephrine elevated markedly after 10-min exercise. Unilateral blocking of cervical ganglion completely inhibited mucosal shrinkage induced by exercise in 8 of 10 subjects. Mucosal shrinkage during exercise in these subjects was assumed to be mediated through cervical sympathetic ganglion, and not by increase in circulating cathecolamine. However, in 2 subjects, moderate shrinkage of the nasal mucosa was observed in 10-min after initiation of exercise. It was impossible to rule out some effect of circulating cathecolamine on the capacitance vessels of the nasal mucosa completely.

摘要

在10名正常志愿者运动期间测量血清去甲肾上腺素水平和鼻腔通畅度，并评估单侧颈交感神经节阻滞对运动诱导的鼻黏膜收缩的影响。运动10分钟后血清去甲肾上腺素显著升高。10名受试者中有8名单侧颈神经节阻滞完全抑制了运动诱导的黏膜收缩。这些受试者运动期间的黏膜收缩被认为是通过颈交感神经节介导的，而非循环儿茶酚胺增加所致。然而，在2名受试者中，运动开始10分钟后观察到鼻黏膜有中度收缩。完全排除循环儿茶酚胺对鼻黏膜容量血管的某些影响是不可能的。