Foi realizado um estudo quantitativo e qualitativo dos plexos deAndrade caracterizou bem a fase aguda e a forma indeterminada da cardiopatia chagásica no cão1 . Lana inoculando a cepa Be78 em cães caracterizou m uito bem a card io p atia chagásica crônica fibrosame, com quadro clínico e eletrocardiográfico muito semelhante a forma cardíaca humana". Pelo que sabemos, até o m o m en to , não se d o cu m en to u claramente a forma digestiva (megaesôfago e megacólon) experimental. Também nao se tem notícias de estudos sistematizados dos neurônios dos plexos de Auerbach e Meissner do esôfago na trip a n o so m ía se cruzi experimental. Por estas razões realizamos o presente trab a lh o , no p re s su p o s to de encontrar prováveis lesões neuronais do esôfago na infecção chagásica experimental canina.
Qualitative and quantitative aspects o f the superficial and profound cardiac plexus o f dogs experimentally infected with The pathogenesis of chagasic cardiopathy has been studied by several authors1211. Many factors seem to be involved: inflammation, autoimmunity, fibrosis and denervation18 19. For example, denervation has an important role in the pathology of the disease but is not always the main factor1314. Based on personal experience, mainly with dogs, although it has been found that chagasic cardiopathy is not counterbalanced in the acute and chronic phases, intense systematic lesions are not observed in the intracardial nervous system, mainly in its numerical reduction11.The aims of this paper are: a) to study the inflammatory phenomena, lesions and parasitism of the superficial and profound cardiac plexus of dogs experimentally infected with Be-62 and Be-78 strains of T. cruzi ', b) to carry out a quantitative study of ganglia and neuron bodies of these plexus in infected and control dogs. maintained in the laboratory, were used. Before inoculation, each animal was examined to exclude the possibility of prior T. cruzi infection. Two groups, each of four dogs, were inoculated intraperitoneally with 2000 blood trypomastigotes/ kg body weight, respectively, with Be-6217 and Be-7810 T. cruzi strains. Both strains were isolated, on different occasions, from Berenice, accepted to be the first known human patient of Chagas' disease6. Inocula were obtained from albino mice in the acute phase of infection and counted according to Brener (1962). Four normal dogs were used as controls. MATERIAL AND METHODSDogs were maintained on an ad libitum diet and observed daily. Parasitemia was assessed according to Brener4. Dogs were sacrificed about the 37th day of infection and necropsied. The atria were removed and fixed in totum in buffered formalin at pH 7.2, dehydrated, cleared and infiltrated with paraffin with the vessels in a basal position. Semi-serial sections (1:10), 4fim thick, were stained with HE and Gomori's thricromic.Ganglia were analysed in each section to determine the following aspects: inflammatory reactions, lesions and parasitism. Inflammation was classified as discreet (+ ), moderate (+ +) or intense (+ 4-+) according to the degree of cellular infiltration. Each ganglion and its neurons (normal and degenerated) were counted systematically. The number of neuron bodies per ganglia of infected dogs were compared with control dogs by Student "t" test.13
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