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.
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