The effect of cimetidine on platelet function: a study involving gastric fluid measurements

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Abstract
Gastric fluid samples were aspirated 30 and 60 minutes after the ingestion of two 200 mg tablets of cimetidine. The concentration of cimetidine in these samples was measured and their effect on platelet aggregation assessedin vitro. Gastric fluid samples significantly inhibited adrenaline- and ADP-induced platelet aggregationin vitro. In a further series of experiments, cimetidine solutions, at concentrations found in gastric fluid, inhibited platelet aggregation and thromboxane A2 (TXA2) release,in vitro. Ranitidine, another H2-receptor antagonist, was a more potent inhibitor of platelet aggregation than cimetidine. Since ranitidine is also the more potent H2-receptor antagonist which, unlike cimetidine, does not include an imidazole group (which is known to inhibit TXA2 synthesis) in its structure, we conclude that H2 blockade mediates the observed inhibition of aggregation. This platelet anti-aggregatory effect may be relevant to haemostatic mechanisms involved in bleeding peptic ulcers or gastric erosions exposed to high local concentrations of H2-receptor antagonists.