Non-potentiation of myocardial lesions by isoproterenol inT.cruzi-infected rats

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Abstract
The existing controversies on the pathogenesis of Chagas' heart disease can be simplified into two theories: (1) “neurogenic” which is concerned with the denervation of the ganglion cells of the heart (chiefly parasympathetic), theoretically resulting in arelative sympathetic overdrive to the heart, and (2) “immunoallergic”, concerned with myocarditis, evoked by antibodies related to myocardial and/or parasite products. It is known that both patients and animals with Chagas' disease exhibit such serologic antibodies. Heart-specific antibodies are known to potentiate myocardial lesions caused by isoproterenol. This observation may provide clues in terms of a link between these two theories of the pathogenesis of Chagas' disease by virtue of two mutually potentiating mechanisms. To test the above hypothesis groups of control andT.cruzi-infected rats were submitted to either two s.c. injections of isoproterenol HCl (190 mg/kg) at 24 h intervals or saline solution. Ten days later, the survivors were killed, and gross heart lesions as well as a detailed histological grading of myocardial lesions were recorded. No differences were detected between control andT.cruzi-infected rats with respect to mortality, gross heart lesions, and myocardial histopathology after isoproterenol treatment. These results indicate no potentiation of myocardial lesions by isoproterenol inT.cruzi-infected rats.