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, 23 (2), 60-66

Human Heart as a Shock Organ in Anaphylaxis


Human Heart as a Shock Organ in Anaphylaxis

Gianni Marone et al. Allergo J Int.


Anaphylaxis is a potentially fatal, immediate hypersensitivity reaction. Mast cells and basophils, by elaborating vasoactive mediators and cytokines, are the main primary effector cells of anaphylaxis. Mast cells have been identified in human heart between myocardial fibers, perivascularly, in the adventitia, and in the arterial intima. Mast cells isolated from human heart tissue (HHMC) of patients undergoing cardiac transplantation express high affinity immunglobulin E (IgE) receptors (FcεRI), C3a, C5a, and kit receptors (KIT). Anti-IgE, anti-FcεRI, and immunoglobulin superallergens induce in vitro secretion of preformed mediators (histamine, tryptase, chymase, and renin) and the de novo synthesis of cysteinyl leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) from HHMC. Complement is activated and anaphylatoxin forms during anaphylaxis. C5a and C3a cause the in vitro release of histamine and tryptase from HHMC. Therapeutic (general anesthetics, protamine, etc.) and diagnostic agents (radio contrast media, etc.), which can cause anaphylactoid reactions, activate HHMC in vitro. Low concentrations of histamine and cysteinyl leukotrienes given to subjects undergoing diagnostic catheterisation caused significant systemic and coronary hemodynamic effects. These data indicate that human heart mast cells and their mediators play a role in severe anaphylactic reactions.

Keywords: Anaphylaxis; heart; histamine; leukotrienes; mast cells; tryptase.


Fig. 1
Fig. 1
Electron micrograph of a mast cell in human heart tissue. The cytoplasm contains numerous secretory granules. The mast cell is adjacent to a coronary blood vessel. (Stained with uranyl acetate and lead citrate; original magnification 9,000×; reprinted with permission from [13].) © G. Marone
Fig. 2
Fig. 2
HHMC express the high affinity receptor (FcɛRI) for IgE, the C3a, the C5a, and the Kit receptors. Activation of the IgE receptors on HHMC can be induced by antigens, immunoglobulin superantigens (superallergens), anti-IgE, and anti-FcɛRI autoantibodies. IgE crosslinking and activation of C3aR or C5aR on HHMC induces the release of preformed mediators (histamine, chymase, renin, etc.), of cytokines (TNF-α, SCF, etc.), and the de novo synthesis of lipid mediators (PGD2, LTC4, PAF). Not shown in this figure is a variety of nonimmunological stimuli used for diagnostic (contrast media, etc.) or therapeutic purposes (general anesthetics, protamine, etc.) that can induce the release of mediators from HHMC. © G. Marone

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