Brown A F
Department of Emergency Medicine, Royal Brisbane Hospital, Queensland, Australia.
J Accid Emerg Med. 1995 Jun;12(2):89-100. doi: 10.1136/emj.12.2.89.
This paper reviews the mechanisms of anaphylactic shock in terms of the immunoglobulin and non-immunoglobulin triggering events, and the cellular events based on the rise in intracellular cyclic AMP and calcium that release preformed granule-associated mediators and the rapidly formed, newly synthesized mediators predominantly based on arachidonic acid metabolism. These primary mediators recruit other cells with the release of secondary mediators that either potentiate or ultimately curtail the anaphylactic reaction. The roles of these mediators in the various causes of cardiovascular collapse are examined. The treatment of anaphylactic shock involves oxygen, adrenaline and fluids. The importance and safety of intravenous adrenaline are discussed. Combined H1 and H2 blocking antihistamines and steroids have a limited role. Glucagon and other adrenergic drugs are occasionally used, and several new experimental drugs are being developed.
本文从免疫球蛋白和非免疫球蛋白触发事件方面综述了过敏性休克的机制，以及基于细胞内环磷酸腺苷（cAMP）和钙升高所引发的细胞事件，这些事件会释放预先形成的颗粒相关介质以及主要基于花生四烯酸代谢快速形成的新合成介质。这些主要介质通过释放二级介质招募其他细胞，二级介质要么增强要么最终抑制过敏反应。本文还研究了这些介质在各种心血管虚脱病因中的作用。过敏性休克的治疗包括给氧、使用肾上腺素和补液。文中讨论了静脉注射肾上腺素的重要性和安全性。联合使用H1和H2阻断性抗组胺药及类固醇的作用有限。偶尔会使用胰高血糖素和其他肾上腺素能药物，并且正在研发几种新的实验性药物。
