Anaphylaxis is a potentially fatal, immediate hyper-sensitivity reaction. Mast cells and basophils, by elaborating vasoactive mediators and cytokines, are
the main primary e ector cells of anaphylaxis. Mast cells have been identi ed in human heart between myocardial  bers, perivascularly, in the adventitia,
and in the arterial intima. Mast cells isolated from human heart tissue (HHMC) of patients undergo-ing cardiac transplantation express high a nity im-munglobulin E (IgE) receptors (FcεRI), C3a, C5a, and kit receptors (KIT). Anti-IgE, anti-FcεRI, and immunoglobulin superallergens induce in vitro se-cretion of preformed mediators (histamine, trypt-ase, chymase, and renin) and the de novo synthesis of cysteinyl leukotriene C4(LTC4) and prosta-glandin D2(PGD2) from HHMC. Complement is activated and anaphylatoxin forms during anaphy-laxis. C5a and C3a cause the in vitro release of his-tamine and tryptase from HHMC.  erapeutic (general anesthetics, protamine, etc.) and diagnos-tic agents (radio contrast media, etc.), which can cause anaphylactoid reactions, activate HHMC in vitro. Low concentrations of histamine and cyste-inyl leukotrienes given to subjects undergoing dia-gnostic catheterisation caused signi cant systemic
and coronary hemodynamic e ects.  ese data in-dicate that human heart mast cells and their medi-ators play a role in severe anaphylactic reactions.