Leff A R
Section of Pulmonary and Critical Care Medicine, University of Chicago, IL 60637.
Am Rev Respir Dis. 1988 May;137(5):1198-216. doi: 10.1164/ajrccm/137.5.1198.
Airway smooth muscle responses are elicited in a complex manner through a large variety of endogenous mediators. Mediators augment or inhibit bronchomotor tone at a variety of sites through numerous different mechanisms. Interactions occur among mediators and nerves, muscle, and circulating blood elements or respiratory mast cells. Airway smooth muscle tone further is regulated by postsynaptic mediator-mediator interactions. Substances may circulate through the blood from distal sites to reach their target organ, as with epinephrine in its effects on airway smooth muscle, or may be secreted directly onto airway smooth muscle, as with the secretory products of respiratory mast cells. Recent observations have indicated that some mediators elicit airway contraction at least in part by activating efferent parasympathetic nerves and/or platelets. Direct secretion of minute quantities of mediators from adjacent epithelium or from infiltrating leukocytes may be an essential component of airway hyperreactivity. Complex interactions between the complement and kallikrein cascades have been cited as possible mechanisms of airway hyperresponsiveness. Ultimately, bronchomotor tone is mediated postsynaptically by the availability of calcium to the contractile apparatus of the smooth muscle cell. A role for the phosphoinositide system in membrane transduction and for cyclic adenosine monophosphate in regulating calcium distribution for smooth muscle contraction has been implicated. Mediator-mediator interactions distal to the synaptic cleft have been shown to augment both force and duration of airway smooth muscle contraction in a synergistic fashion. The stimuli eliciting mediator and neurotransmitter secretion, their physiologic significance, and the homeostatic infrastructure of these interactions are areas of promising investigation that require further definition.
气道平滑肌反应通过多种内源性介质以复杂的方式引发。介质通过众多不同机制在多个位点增强或抑制支气管运动张力。介质与神经、肌肉以及循环血液成分或呼吸道肥大细胞之间会发生相互作用。气道平滑肌张力还受到突触后介质 - 介质相互作用的调节。物质可能从远端部位通过血液循环到达其靶器官，如肾上腺素对气道平滑肌的作用，或者可能直接分泌到气道平滑肌上，如呼吸道肥大细胞的分泌产物。最近的观察表明，一些介质至少部分地通过激活传出副交感神经和/或血小板来引发气道收缩。从相邻上皮或浸润白细胞直接分泌微量介质可能是气道高反应性的一个重要组成部分。补体和激肽释放酶级联反应之间的复杂相互作用被认为是气道高反应性的可能机制。最终，支气管运动张力在突触后由平滑肌细胞收缩装置可获得的钙来介导。磷酸肌醇系统在膜转导中的作用以及环磷酸腺苷在调节平滑肌收缩的钙分布中的作用已被提及。已表明突触间隙远端的介质 - 介质相互作用以协同方式增强气道平滑肌收缩的力量和持续时间。引发介质和神经递质分泌的刺激、它们的生理意义以及这些相互作用的稳态基础结构是有前景的研究领域，需要进一步明确。
