Myocardial damage in Trypanosoma cruzi myocarditis: a role for macrophages

Sarcolemmal membrane permeability characteristics, particularly at the site of macrophage contact, were investigated in experimental chronic Trypanosoma cruzi myocarditis in BALB/c mice, employing ruthenium red as an electron tracer. The ultrastructural features of the myocardium from infected animals were similar to those previously described. Briefly, focal myocarditis was detected, with areas of myocytolytic necrosis, atrophic myofibres, an inflammatory response composed of mononuclear cells, predominantly macrophages and a few lymphocytes, and interstitial fibrosis. The immunohistochemical study confirmed that the macrophages are in fact the majority of the inflammatory cells identified in the interstitium of the myocardium, which stained positively with both monoclonal antibodies to the class II histocompatibility (Ia and Ie) antigens (cytoplasmic and plasma membrane staining), and negatively with kappa and lambda immunoglobulin chains and S-100 protein. This study provided the following new information: the cytoplasmic components of mononuclear cells in the chronic myocarditis of T cruzi-infected mice have a very high affinity for ruthenium red. It is conceivable that mononuclear cell activation parallels some physiological change of their plasma membrane permeability. Ruthenium red diffusely stains the sarcoplasm of cardiocytes with anomalous contraction bands, indicating leaky sarcolemmal membranes. Most nondegenerating cardiocytes from experimental animals appear darker with ruthenium red staining when compared to controls. They also frequently show rows of ruthenium red-stained subplasmalemmal tiny vesicles (caveolae). Both changes probably reflect increased membrane permeability. Ruthenium red intensely labels the cytoplasmic components of cardiocytes at the site of macrophage contact or close apposition, indicating areas of altered membrane with remarkably increased permeability.(ABSTRACT TRUNCATED AT 250 WORDS)