Morphometric and Histological Analysis of the Superior Cervical Ganglion in Experimental Chagas' Disease in Rats

Camargos, Elizabeth R.S.; Machado, Conceição R. S.

doi:10.4269/ajtmh.1988.39.456

Cited by 17 publications

(20 citation statements)

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“…The rat has been proved to be a useful experimental model for studying the involvement of the autonomic ner vous system in Chagas' disease as reviewed elsewhere (Machado et al, 1987;Camargos and Machado, 1988;Machado and Ribeiro, 1989). Using this rat model, we study now the time course of the parasitism and inflammatory infitrate in adrenal tissues, especially in the medulla, using…”

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confidence: 99%

Rat adrenal gland in experimental american trypanosomiasis : immunocytochemical study of tissue parasitism

Machado

Cardoso

1990

Ann. Parasitol. Hum. Comp.

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The rat adrenal gland is poorly parasitized during the experi mental infection with Y strain of Trypanosoma cruzi. In both cortical and medullary regions, the parasitism peaked at day 10 and was characterized by the predominance of single amastigotes over nests containing 2 or more parasites. After day 10 of infec tion, the tissue parasitism dropped rapidly to become practically null at day 32 of infection. In cortical tissue, the amastigotes occurred mainly inside the endocrine cells. In the medulla, they found mainly in glial cells and non-identified stromal cells. In both cortex and medulla, inflammatory processes were found till day 20 of infection. Our data do not support the hypothesis that a corticoid rich environment would favor T. cruzi parasitism in adrenal medulla.Résumé : La glande surrénale chez le rat au cours de la trypanosomiase américaine expérimentale : étude immunocytochimique du parasitisme tissulaire.La glande surrénale est peu parasitée au cours de l'infection expérimentale avec la souche Y de Trypanosoma cruzi. Dans le cortex comme dans la médullaire, le parasitisme atteint son maximum le 10e jour d'infection et est caractérisé par une prédo minance d'amastigotes isolés sur les sites contenant deux ou plu sieurs parasites. Après le 10e jour, le nombre de parasites dans la glande tombe rapidement et devient pratiquement nul après

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confidence: 99%

Rat adrenal gland in experimental american trypanosomiasis : immunocytochemical study of tissue parasitism

Machado

Cardoso

1990

Ann. Parasitol. Hum. Comp.

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“…During the acute phase of Chagas' disease, trypomastigotes circulate in the bloodstream, being supplied by the intracellular proliferation of the parasite as amastigotes in several tissues. However, neurons have rarely been found parasitized (Koberle, 1970;Tafuri, 1979;Ribeiro dos Santos and Hudson, 1981;Camargos and Machado, 1988). In spite of that, American trypanosomiasis causes neuronal death in autonomic ganglia, especially the parasympathetic ones of the heart and myoenteric plexus, in both human and experimental animals (Koberle, 1968;Tafuri, 1979;Oliveira, 1985).…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzi infection in rats induced early lesion of the heart noradrenergic nerve terminals by a complement-independent mechanism

Machado

Oliveira

Magalhães

et al. 1994

J. Neural Transmission

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The acute phase of the experimental Chagas' disease in rats induces extensive lesion of the heart sympathetic nerve terminals. Because of evidence indicating the involvement of immune reactions in neuron destruction provoked by Chagas' disease, we tested the effects of depleting the complement system by cobra venom factor upon the sympathetic denervation. The serum hemolytic activity against sensitized sheep erythrocytes ensured the efficacy of the anticomplementary treatment. Glyoxylic acid-induced histofluorescence and electron-microscopic methods allowed the study of the heart noradrenergic nerves. T. cruzi infection caused marked rarefaction of fluorescent nerve terminals at day 10 of infection and the ultrastructural study guaranteed that this rarefaction involved lesion of noradrenergic terminals. The complement depletion failed to prevent this early heart noradrenergic denervation, excluding the participation of complement-mediated lysis as a main mechanism.

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“…Consequently, we cannot rule out the presence or absence of morphological abnormalities of the cardiac parasympathetic neurons. Nonetheless, very recent experimental studies, carried out in different animal species, have found that despite an obvious inflammatory response in the cardiac ganglia, the parasympathetic neurons were preserved from the infective process and their number was not significantly diminished 8,9,11,15,28,39 .…”

Section: Discussionmentioning

confidence: 99%

“…Early studies showed morphologic abnormalities considered to be specifically and irreversibly caused by Trypanosoma cruzi 26,36 . However, more recent studies have found that, despite an obvious inflammatory response in the cardiac ganglia, the parasympathetic neurons were preserved from the infective process 8,9,15,28 .…”

Section: Introductionmentioning

confidence: 99%

Heart rate responses to a muscarinic agonist in rats with experimentally induced acute and subacute chagasic myocarditis

Torres

Dávila

Gottberg

et al. 2000

Rev. Inst. Med. trop. S. Paulo

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SUMMARYWe administered arecoline to rats, with experimentally induced chagasic myocarditis, in order to study the sinus node sensitivity to a muscarinic agonist. Sixteen month old rats were inoculated with 200,000 T. cruzi parasites ("Y" strain). Between days 18 and 21 (acute stage), 8 infected rats and 8 age-matched controls received intravenous arecoline as a bolus injection at the following doses: 5.0, 10.0, 20.0, 40.0, and 80.0 µg/kg. Heart rate was recorded before, during and after each dose of arecoline. The remaining 8 infected animals and 8 controls were subjected to the same experimental procedure during the subacute stage, i.e., days 60 to 70 after inoculation. The baseline heart rate, of the animals studied during the acute stage (349 ± 68 bpm, mean ± SD), was higher than that of the controls (250 ± 50 bpm, p < 0.005). The heart rate changes were expressed as percentage changes over baseline values. A doseresponse curve was constructed for each group of animals. Log scales were used to plot the systematically doubled doses of arecoline and the induced-heart rate changes. The slope of the regression line for the acutely infected animals (r = -0.99, b =1.78) was not different from that for the control animals (r = -0.97, b = 1.61). The infected animals studied during the subacute stage (r = -0.99, b = 1.81) were also not different from the age-matched controls (r = -0.99, b = 1.26, NS). Consequently, our results show no pharmacological evidence of postjunctional hypersensitivity to the muscarinic agonist arecoline. Therefore, these results indirectly suggest that the postganglionic parasympathetic innervation, of the sinus node of rats with autopsy proved chagasic myocarditis, is not irreversibly damaged by Trypanosoma cruzi.

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Morphometric and Histological Analysis of the Superior Cervical Ganglion in Experimental Chagas' Disease in Rats

Cited by 17 publications

References 0 publications

Rat adrenal gland in experimental american trypanosomiasis : immunocytochemical study of tissue parasitism

Rat adrenal gland in experimental american trypanosomiasis : immunocytochemical study of tissue parasitism

Trypanosoma cruzi infection in rats induced early lesion of the heart noradrenergic nerve terminals by a complement-independent mechanism

Heart rate responses to a muscarinic agonist in rats with experimentally induced acute and subacute chagasic myocarditis

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