Piper P J
Scand J Respir Dis Suppl. 1977;98:40-6.
The antigen-antibody union initiates the release of mediators; the reactions and interactions of these mediators in the lung appear to include negative feedback mechanisms. During anaphylactic bronchoconstriction catecholamines are released from the adrenal medulla. These act as physiological antagonists and tend to reverse the bronchoconstriction. In guinea-pig and human lung fragments, catecholamines and PGs increase cyclic AMP levels and inhibit the release of histamine, SRS-A and ECF-A following antigen challenge. EFC-A is chemotactic to eosinophils which contain arylsulphatase which destroys SRS-A. Aanphylactic bronchoconstriction seems to be a defense mechanism to limit further inhalation of antigen by the animal. It then seems that a series of negative feedback mechanisms may be triggered to terminate and reverse the bronchoconstriction and prevent further release of mediators.
抗原-抗体结合引发介质的释放;这些介质在肺中的反应和相互作用似乎包括负反馈机制。在过敏性支气管收缩过程中,儿茶酚胺从肾上腺髓质释放。这些儿茶酚胺作为生理拮抗剂,倾向于逆转支气管收缩。在豚鼠和人肺组织切片中,儿茶酚胺和前列腺素会提高环磷酸腺苷水平,并在抗原攻击后抑制组胺、慢反应物质-A和嗜酸性粒细胞趋化因子-A的释放。嗜酸性粒细胞趋化因子-A对含有芳基硫酸酯酶的嗜酸性粒细胞具有趋化作用,该酶可破坏慢反应物质-A。过敏性支气管收缩似乎是一种防御机制,可限制动物进一步吸入抗原。随后似乎会触发一系列负反馈机制来终止和逆转支气管收缩,并防止介质的进一步释放。