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The possible mediator role of the products of the cyclo-oxygenase and lipoxygenase pathways (namely the endoperoxides, prostaglandins and thromboxane A2, and leukotrienes respectively), in cardiac anaphylaxis are discussed. A cyclo-oxygenase product would appear to be responsible for the early fall in coronary blood flow and leukotrienes C4 and D4 for the late fall in coronary blood flow and for the prolonged contractile failure observed in cardiac anaphylaxis. A model for the role of histamine and arachidonate metabolites in cardiac anaphylaxis is presented at the end of the summary and conclusions.
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