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组胺诱导的人支气管平滑肌等长张力增加是由局部迷走神经介导的。

Histamine-induced increase in isometric tension of smooth muscle is mediated by local vagus nerve in human bronchus.

作者信息

Aizawa H, Inoue H, Miyazaki N, Hara N

机构信息

Clinical Research Institute, National Fukuoka-Higashi Hospital, Koga, Japan.

出版信息

Respiration. 2000;67(6):652-6. doi: 10.1159/000056295.

Abstract

BACKGROUND

The vagus nerve is reported to play an important role in the regulation of airway responsiveness.

OBJECTIVE

In the present study, we investigated the role of the local vagus nerve in the changes in isometric tension of smooth muscle induced by histamine in the human airway.

METHODS

Eight human lung tissue specimens were obtained at thoracic surgery, and 24 bronchial smooth muscle strips were used for isometric tension recording. The changes in isometric tension were induced by histamine in the presence or absence of physostigmine (10(-6) M), atropine (10(-6) M), and/or tetrodotoxin (10(-6) M).

RESULTS

We found that: (1) histamine induced a dose-dependent increase in the isometric tension in human bronchial smooth muscle; (2) physostigmine (10(-6) M) significantly potentiated the amplitude of the histamine-induced increase in isometric tension; (3) atropine (10(-6) M) significantly suppressed the histamine-induced increase in isometric tension; (4) tetrodotoxin (10(-6) M), did not affect the histamine-induced increase in isometric tension of smooth muscle, and (5) in the presence of tetrodotoxin, atropine significantly suppressed the histamine-induced increase in isometric tension.

CONCLUSION

These findings suggest that the histamine-induced increase in isometric tension is mediated partly by acetylcholine, presumably released by the direct action of histamine on the vagus efferent nerve terminals without the central reflex via vagus nerve.

摘要

背景

据报道,迷走神经在气道反应性调节中起重要作用。

目的

在本研究中,我们调查了局部迷走神经在组胺诱导的人气道平滑肌等长张力变化中的作用。

方法

在胸外科手术中获取8个人类肺组织标本,使用24条支气管平滑肌条进行等长张力记录。在存在或不存在毒扁豆碱(10⁻⁶ M)、阿托品(10⁻⁶ M)和/或河豚毒素(10⁻⁶ M)的情况下,用组胺诱导等长张力变化。

结果

我们发现:(1)组胺诱导人支气管平滑肌等长张力呈剂量依赖性增加;(2)毒扁豆碱(10⁻⁶ M)显著增强组胺诱导的等长张力增加幅度;(3)阿托品(10⁻⁶ M)显著抑制组胺诱导的等长张力增加;(4)河豚毒素(10⁻⁶ M)不影响组胺诱导的平滑肌等长张力增加,且(5)在存在河豚毒素的情况下,阿托品显著抑制组胺诱导的等长张力增加。

结论

这些发现表明,组胺诱导的等长张力增加部分由乙酰胆碱介导,推测是组胺直接作用于迷走神经传出神经末梢释放乙酰胆碱,而不通过迷走神经的中枢反射。

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