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咳嗽增强的实验模型与机制

Experimental models and mechanisms of enhanced coughing.

作者信息

Bolser Donald C

机构信息

Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, P.O. Box 100144, Gainesville, FL 32610-0144, USA.

出版信息

Pulm Pharmacol Ther. 2004;17(6):383-8. doi: 10.1016/j.pupt.2004.09.016.

Abstract

Enhanced coughing can be produced in a variety of animal models, including the guinea pig, cat, dog and pig. Typically, airway inflammation has been produced by sensitization, exposure to cigarette smoke, sulphur dioxide or angiotensin-converting enzyme inhibitors. In some of these models, inflammatory mediators such as bradykinin and tachykinins have been shown to contribute to the enhanced coughing. While most of these studies have focussed on peripheral mechanisms, increases in central excitability of the cough reflex have been shown to occur as a result of airway inflammation. As such, we propose that enhanced coughing in pathological conditions is the result of plastic changes in both peripheral and central neural elements. Furthermore, we present a modified model of the neurogenesis of cough that takes into account peripheral and central plasticity induced by mediators of inflammation.

摘要

在多种动物模型中均可诱发咳嗽增强,包括豚鼠、猫、狗和猪。通常,气道炎症是通过致敏、暴露于香烟烟雾、二氧化硫或血管紧张素转换酶抑制剂而产生的。在其中一些模型中,已证实缓激肽和速激肽等炎症介质会导致咳嗽增强。虽然这些研究大多集中在外周机制上,但已表明气道炎症会导致咳嗽反射的中枢兴奋性增加。因此,我们认为病理状态下咳嗽增强是外周和中枢神经元件可塑性变化的结果。此外,我们提出了一种咳嗽神经发生的改良模型,该模型考虑了炎症介质诱导的外周和中枢可塑性。

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