Despopulação neuronal cardíaca em hamsters (Mesocricetus auratus) cronicamente infectados com o Trypanosoma cruzi

Abstract

The aim of this study was to obtain an experimental animal model of destruction of cardiac neurons in order to investigate the behavior of the cardiac nervous system of hamsters chronically infected with Trypanosoma cruzi. We counted the neuronal cells of the cardiac autonomic nervous plexus in hamsters inoculated with 35,000 blood forms of three different T. cruzi strains and killed 5, 8 and 10 months after infection. We showed for the first time severe neuronal destruction in an experimental animal model with characteristics similar to those observed in human Chagas'disease.

Insights into the clinical and functional significance of cardiac autonomic dysfunction in Chagas disease

“…Diffuse damage to the autonomic nervous system, principally of the parasympathetic branch affecting the heart and digestive tract, is a remarkable pathological feature commonly present in variable degrees and extents in the acute and all chronic forms of human Chagas disease 11,13,15,[17][18][19] and the corresponding forms of experimental Trypanosoma cruzi infection in different animal models [20][21][22][23][24] . This is a fact recognised soon after the description of the disease at the beginning of the past century.…”

“…Many autonomic components, mainly related to functional modulation of the heart and digestive viscera, including central neural structures at different levels, peripheral extrinsic and intrinsic autonomic ganglia, afferent neurons from receptors, sympathetic and parasympathetic efferent neurons and the beta-adrenergic and muscarinic cholinergic neurotransmitter cellular receptors, may be injured exclusively or in combination, and this has been demonstrated both in human and experimental Chagas disease 11,13,15,18,[20][21][22][23][26][27][28][29] .…”

“…In the isolated or associate cardiac and digestive forms of the disease, the intrinsic innervation of the heart is often more severely damaged by inflammatory and degenerative alterations. Moreover, a decrease in the number of cardiac ganglion cells and neurons has clearly been shown, and both parasympathetic and sympathetic lesions have been described 11,13,15,18,[21][22][23][24]28,30 .…”

“…In this context, it is reasonable to hypothesise that in Chagas disease, the same pathophysiological mechanism may trigger arrhythmogenesis, considering the regional heterogeneity of the lesions in the intrinsic innervation 11,13,22,30 and in ventricular myocardium 64 of the chagasic heart. Indeed, an association between regional myocardial sympathetic denervation, detected by scintigraphy with 123 I-metaiodobenzylguanidine, and the occurrence of sustained ventricular tachycardia was observed in chagasic cardiomyopathy with preserved ventricular function 64 , and sympathetic modulation was noted to be affected in the ventricular myocardial also in chagasic subjects with the indeterminate form or borderline electrocardiogram 65 .…”

Impaired autonomic control of heart interval changes to Valsalva manoeuvre in Chagas' disease without overt manifestation

“…The human and experimental indeterminate forms present less conspicuous lesions of cardiac intrinsic innervation, which are usually represented by discrete to moderate focal or zonal chronic neuroganglionitis (Lopes and Tafuri, 1983;Andrade, 1984;Oliveira, 1985;Chapadeiro et al, 1991). Cardiac autonomic damage has also been observed in acute and chronic experimental Trypanosoma cruzi infection in mice (Tafuri, 1970;Souza et al, 1996), dogs (Andrade, 1984;Machado et al, 1998), rats (Chapadeiro et al, 1991;Junqueira et al, 1992), and hamsters (Chapadeiro et al, 1999) among other animal models.…”