Permeability alteration of the sarcolemmal membrane, particularly at the site of macrophage contact, in experimental chronic Trypanosoma cruzi myocarditis in mice.

Sarcolemmal membrane permeability characteristics have been investigated, particularly at the site of macrophage contact, in experimental chronic Trypanosoma cruzi myocarditis in BALB/c mice, employing ruthenium red (RR) 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. This study provided the following new information: (I) the cytoplasmic components of mononuclear cells have a very high affinity for RR. It is conceivable that mononuclear cell activation parallels a physiological change in plasma membrane permeability; (2) RR diffusely strains the sarcoplasm of cardiocytes with anomalous contraction bands, indicating leaky sarcolemmal membranes; (3) most non-degenerating cardiocytes from experimental animals appear darker with RR staining than controls. They also frequently show rows of RR-stained sub-plasmalemmal tiny vesicles. Both changes probably reflect increased membrane permeability; (4) RR 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. This observation provides insight into a role for the macrophages in myocardial cell damage in experimental chronic Trypanosoma cruzi myocarditis. An obvious consequence of increased membrane permeability is that it may cause impairment of the transmembrane ion gradients and cause loss of intracellular elements, thus contributing to cardiocyte death. Furthermore, the findings in the present study imply that one of the consequences of macrophage-mediated cytotoxicity may be alteration in the permeability of the plasma membranes of nearby target cells, possibly due to a change in the structural integrity of the membrane resulting from peroxidation of cell membrane lipids.