Systemic/intestinal anaphylaxis

The route of antigen administration can alter the speed of antigen access to the circulation and, thus, the systemic symptoms in anaphylaxis models. For example, allergen ingestion typically induces anaphylaxis that includes gastrointestinal symptoms, such as diarrhea [4]. These intestinal anaphylaxis models in mice are dependent on IgE-induced mast cell activation, and the release of PAF and serotonin (rather than histamine) [1,4]. 

The main varieties of adverse effects attributed to cimetidine relate to its antiandrogenic properties and its actions in sufficient concentrations on the central nervous system. There is also a spectrum of drug interactions, mainly attributable to inhibition of hepatic CYP isoforms, but they only have clinical consequences under special circumstances. Occasional adverse effects, which are generally minor, include bradycardia and conduction defects, thrombocytopenia, neutropenia, interstitial nephritis, mild hepatic dysfunction, and headache. Intestinal infection due to loss of the gastric acid barrier also occurs, and myalgia, fever, monoamine oxidase-Uke interactions, and neuropathies have been well documented occasionally. Allergic reactions, such as bronchospasm, have rarely been described. Anaphylaxis with recurrence on rechallenge is on record, as are asthma and skin effects. 

The peptidoleukotrienes play a major role in the pathophysiological sequelae of anaphylaxis by exerting profound effects on smooth muscle tone. Peptidoleukotrienes contract respiratory, vascular, and intestinal smooth muscle. Furthermore, peptidoleukotrienes have potent effects on the cardiovascular system including coronary vasoconstriction, reduced heart rate, arteriolar constriction, venule dila-... 

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