Non-potentiation of myocardial lesions by isoproterenol in T. cruzi-infected rats.
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 a relative 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 and T. 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 and T. 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 in T. cruzi-infected rats.
D000783:Aneurysm / Q000209:etiology; D000818:Animals; D014355:Chagas Disease / Q000150:complications / Q000473:pathology*; D003327:Coronary Disease / Q000209:etiology; D006321:Heart / Q000187:drug effects*; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000473:pathology*; D051381:Rats
D007545:Isoproterenol