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Potential role of mononuclear cells infiltration on the autoimmune myocardial dysfunction.

In autoimmune myocarditis significant alterations in contractility when the heart is studied in vitro could be demonstrated. The isolated atria from mice hyperimmunized with heart exhibited tachycardia, decrease in contractility and dysrhythmia. Spleen lymphocytes from mice with autoimmune myocarditis, can react in vitro with spontaneously beating normal atria inducing dysrhythmias and negative inotropic effect. The alterations in contractility of normal atria induced by immune cells, resemble those observed in atria from animals with autoimmune myocarditis. The use of pharmacologic inhibitors strongly suggests that the cardiac dysfunction is generated by the release of endogenous SRS-A as a result of the hyperimmunization with heart. The possibility that autoimmune lymphocyte can influence the contractile behavior of the heart is interesting and could provide some evidence for the role of lymphocytic infiltration in the mechanism operating in primary and specific myocarditis.