Perez Leiros C, Sterin-Borda L, Cossio P, Bustuoabad O, Borda E
Clin Exp Immunol. 1986 Mar;63(3):648-55.
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.
在自身免疫性心肌炎中，当在体外研究心脏时，可以证明其收缩性有显著改变。用心脏进行超免疫的小鼠的离体心房表现出心动过速、收缩性降低和心律失常。患有自身免疫性心肌炎的小鼠的脾淋巴细胞在体外可与自发跳动的正常心房发生反应，诱发心律失常和负性肌力作用。免疫细胞诱导的正常心房收缩性改变与患有自身免疫性心肌炎动物的心房中观察到的改变相似。使用药理抑制剂强烈表明，心脏功能障碍是由于用心脏进行超免疫后内源性慢反应物质-A（SRS-A）的释放所产生的。自身免疫淋巴细胞能够影响心脏收缩行为的可能性很有意思，并且可以为淋巴细胞浸润在原发性和特异性心肌炎发病机制中的作用提供一些证据。
