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非特异性支气管高反应性的神经源性和肌源性机制。

Neurogenic and myogenic mechanisms of nonspecific bronchial hyperresponsiveness.

作者信息

Thomson N C

出版信息

Eur J Respir Dis Suppl. 1983;128 (Pt 1):206-12.

PMID:6578068
Abstract

Airway smooth muscle is under neurogenic and myogenic control and thus bronchial hyperresponsiveness in asthma may be related to an abnormality in one or other of these systems. Possible neurogenic mechanisms leading to hyperresponsiveness include an abnormality of vagal pathways, of alpha and beta adrenergic receptors in airway smooth muscle or of nonadrenergic noncholinergic nerves. The relative importance of these different mechanisms remains controversial, and regarding nonadrenergic noncholinergic pathway untested. The findings of some recent studies suggest that neither an alteration in vagal pathways nor of adrenergic receptors can be considered as the primary disorder accounting for nonspecific increases in bronchial responsiveness. Possible myogenic mechanisms for hyperresponsiveness include an increase in contractility of individual muscle cells or an increase in cell to cell coupling between muscle cells i.e. a shift from multi-unit to single unit behaviour. These hypotheses have only started to be tested experimentally.

摘要

气道平滑肌受神经源性和肌源性控制,因此哮喘中的支气管高反应性可能与这些系统中一个或另一个的异常有关。导致高反应性的可能神经源性机制包括迷走神经通路、气道平滑肌中的α和β肾上腺素能受体或非肾上腺素能非胆碱能神经的异常。这些不同机制的相对重要性仍存在争议,且关于非肾上腺素能非胆碱能通路尚未得到验证。一些近期研究的结果表明,迷走神经通路的改变或肾上腺素能受体的改变都不能被视为导致支气管反应性非特异性增加的主要疾病。高反应性的可能肌源性机制包括单个肌肉细胞收缩力的增加或肌肉细胞之间细胞间偶联的增加,即从多单位行为向单单位行为的转变。这些假设刚刚开始通过实验进行验证。

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