Resultado da pesquisa (5)

Termo utilizado na pesquisa myenteric plexus

#1 - A new experimental model of intrinsic denervation in ileum from wistar rats through intramural microinjections of benzalkonium chloride

Abstract in English:

Extensive literature is available about the intrinsic denervation of segments of the digestive tube through the application of CB in the serosa of the viscera. However, this technique has some disadvantages like causing peritonitis, flanges and high mortality, limiting its use in humans. The aim of the present study was to evaluate the feasibility of benzalkonium chloride (CB) to induce intrinsic chemical denervation, through applications of CB in the intramural ileum of wistar rats, as well as deepen the knowledge about the evolution of neuronal injury caused in the process. We used 40 rats, divided into two groups (control-GC and benzalkonium GB) of 20 animals each, divided into four sub-groups according to the time of postoperative assessment of 24, 48 hours, 30 and 90 days. The animals were submitted to intramural microinjections of sterile saline solution 0.9% (GC) or benzalkonium chloride (GB) in ileal portion, and subsequent histopathological analysis and immunohistochemistry for evaluation of neuronal injury. A significant decrease (p<0.05) was found of the neuronal myenteric count over time in groups, GB3, GB4 and GB2. The specific positive immunolabeling for H2AX and Caspase-3 confirmed the results obtained in the histopathological evaluation, denoting the ignition of irreversible cell injury in 24 hours, evolving into neuronal apoptosis in 48 hours after application of the CB 0.3%. Under the conditions in which this work was conducted, it can be concluded that the application of CB 0.3% by means of microinjections intramural in the ileal wall is able to induce intrinsic chemical denervation of the diverticulum of wistar rats and that the main mechanism of neuronal death is induction of apoptosis.

Abstract in Portuguese:

Existe vasta literatura sobre a desnervação intrínseca de segmentos do tubo digestório através da aplicação de CB na serosa da víscera. Entretanto, essa técnica tem a desvantagem de causar peritonite, formação de bridas e alta mortalidade, não sendo factível para eventuais utilizações em humanos. O objetivo do presente estudo foi avaliar a viabilidade do Cloreto de benzalcônio (CB) induzir desnervação química intrínseca, por meio de aplicações intramurais em íleo de ratos wistar, além de aprofundar o conhecimento sobre a evolução da lesão neuronal causada neste processo. Foram utilizados 40 ratos, distribuídos em dois grupos (controle- GC e benzalcônio GB) de 20 animais cada, subdivididos em quatro subgrupos de acordo com o tempo de avaliação pós-operatória de 24, 48 horas, 30 e 90 dias. Os animais foram submetidos à microinjeções intramurais de solução salina estéril 0,9% (GC) ou de cloreto de benzalcônio (GB) em porção ileal, e posterior análise histopatológica e imuno-histoquímica, para avaliação da lesão neuronal. Houve diminuição significativa (p<0,05) na contagem neuronal mientérica ao longo do tempo nos grupos GB2, GB3 e GB4. A imunomarcação específica positiva para H2AX e Caspase-3 confirmou os resultados obtidos na avaliação histopatológica, denotando início da lesão celular irreversível em 24 horas, evoluindo para apoptose neuronal em 48 horas após a aplicação do CB 0,3%. Nas condições em que este trabalho foi conduzido, é possível concluir que a aplicação de CB 0,3% por meio de microinjeções intramurais na parede ileal é capaz de induzir desnervação química intrínseca da porção ileal de ratos wistar e que o principal mecanismo de morte neuronal é a indução de apoptose.


#2 - Effects of infection with Toxoplasma gondii oocysts on the intestinal wall and the myenteric plexus of chicken (Gallus gallus), 30(9):787-792

Abstract in English:

ABSTRACT.- Bonapaz R.S., Hermes-Uliana C., Santos F.N., Silva A.V., Araújo E.J.A. & Sant’Ana D.M.G. 2010. Effects of infection with Toxoplasma gondii oocysts on the intestinal wall and the myenteric plexus of chicken (Gallus gallus). Pesquisa Veterinária Brasileira 30(9):787-792. Laboratório de Neurogastroenterologia Experimental, Universidade Paranaense, Praça Mascarenhas de Moraes 4282, Centro, Umuarama, PR 87506-140, Brazil. E-mail: debora@unipar.br This paper aims to analyze the effects of the Toxoplasma gondii infection in the intestinal wall and myenteric plexus of chicken (Gallus gallus). Ten 36-day-old chickens were separated into two groups: control and experimental, orally inoculated with oocysts of the T. gondii strain M7741 genotype III. After 60 days the birds were submitted to euthanasia and had their duodenum removed. Part of the intestinal segments was submitted to histological routine, HE staining, PAS histochemical technique, and Alcian Blue. Qualitative analysis of the intestinal wall and comparative measurements among the groups with respect to total wall thickness, muscle tunic, mucosa, and tunica mucosa were carried out. Caliciform cells were quantified. The other part of the intestinal segments was fixed in formol acetic acid and dissected having the tunica mucosa and the tela submucosa removed. Neurons were stained with Giemsa, counted, and measured. Chickens from the experimental group presented diarrhea and inflammatory infiltrates in the tunica mucosa, thickness reduction of all the parameters assessed in the intestinal wall, and an increase of the number of caliciform cells. There was a ~70% reduction regarding the intensity of myenteric neurons; and the remaining cells presented a reduction of ~2.4% of the perikarion and ~40.5% of the nucleus (p<0.05). Chronic infection induced by T. gondii oocysts resulted in intestinal wall atrophy, mucin secretion increase, death and atrophy of chicken myenteric plexus neurons. Death and atrophy of myenteric plexus neurons may be related with the causes of diarrhea observed in chickens with toxoplasmosis.

Abstract in Portuguese:

RESUMO.- Bonapaz R.S., Hermes-Uliana C., Santos F.N., Silva A.V., Araújo E.J.A. & Sant’Ana D.M.G. 2010. Effects of infection with Toxoplasma gondii oocysts on the intestinal wall and the myenteric plexus of chicken (Gallus gallus). [Efeitos da infecção por oocistos de Toxoplasma gondii sobre a parede intestinal e o plexo mientérico de Gallus gallus.] Pesquisa Veterinária Brasileira 30(9):787-792. Laboratório de Neurogastroenterologia Experimental, Universidade Paranaense, Praça Mascarenhas de Moraes 4282, Centro, Umuarama, PR 87506-140, Brazil. E-mail: debora@unipar.br O objetivo deste trabalho foi analisar os efeitos da infecção pelo Toxoplasma gondii sobre a parede intestinal e o plexo mientérico de Gallus gallus. Dez galinhas de 36 dias de idade separadas em dois grupos: controle e experimental inoculado com oocistos da cepa M7741 de T. gondii (genótipo III) pela via oral. Após 60 dias os animais foram submetidos à eutanásia e o duodeno coletado. Parte dos segmentos intestinais foi submetida à rotina histológica, coloração por HE e técnica histoquímica de PAS e Alcian Blue. Realizou-se uma avaliação qualitativa da parede intestinal e medidas comparativas entre os grupos da espessura da parede total, túnica muscular, muscular da mucosa e túnica mucosa. As células caliciformes foram quantificadas. Outra parte dos segmentos intestinais foi fixada em formol acético e dissecada retirando-se a túnica mucosa e a tela submucosa. Os neurônios foram corados pela técnica de Giemsa, contados e mensurados. Os animais do grupo experimental apresentaram diarréia e infiltrados inflamatórios na túnica mucosa, redução da espessura de todos os parâmetros avaliados da parede intestinal e aumento do número das células caliciformes. Houve uma redução de ~70% da densidade dos neurônios mientéricos e as células remanescentes sofreram redução de ~2,4% do pericário e ~40,5% do núcleo (p<0,05). A infecção crônica induzida por oocistos de T. gondii levou a atrofia da parede intestinal, aumento da secreção de mucinas, morte e atrofia dos neurônios do plexo mientérico de galinhas. A morte e atrofia dos neurônios do plexo mientérico podem estar envolvidas na causa da diarréia observada em galinhas com toxoplasmose.


#3 - Effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats, p.295-302

Abstract in English:

ABSTRACT.- Silverio S.M., Mari R.B, Clebis N.K., Scoz J.R., Germano R.M., Major J.A.A., Bombonato P.P. & Stabille S.R. 2009. The effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats. Pesquisa Veterinária Brasileira 29(4):295-302. Departamento de Cirurgia, Setor de Anatomia dos Animais Domésticos e Silvestres, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270, Brazil. E-mail: remari@usp.br The exacerbation of the oxidative stress and of the polyol pathway which impair damage myenteric plexus are metabolic characteristics of diabetes. The ascorbic acid (AA) is an antioxidant and an aldose reductase inhibitor, which may act as neuroprotector. The effects of AA supplementation on the density and cellular body profile area (CP) of myenteric neurons in STZ-induced diabetes in rats were assessed. Four groups with five animals each were formed: normoglycemic (C); diabetic (D); AA-treated diabetic (DS) and AA-treated normoglycemic (CS). Dosagen of 50mg of AA were given, three times a week, for each animal (group DS and CS). Ninety days later and after euthanasia, the ileum was collected and processed for the NADPH-diaphorase technique. There were no differences (P>0.05) in the neuronal density among the groups. The CP area was lower (P<0.05) in the DS and CS groups, with a higher incidence of neurons with a CP area exceeding 200mm2 for groups C and D. The AA had no influence on the neuronal density in the ileum but had a neuroprotective effect, preventing the increase in the CP area and allowing a higher number of neurons with a CP area with less than 200mm2.

Abstract in Portuguese:

ABSTRACT.- Silverio S.M., Mari R.B, Clebis N.K., Scoz J.R., Germano R.M., Major J.A.A., Bombonato P.P. & Stabille S.R. 2009. The effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats. Pesquisa Veterinária Brasileira 29(4):295-302. Departamento de Cirurgia, Setor de Anatomia dos Animais Domésticos e Silvestres, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270, Brazil. E-mail: remari@usp.br The exacerbation of the oxidative stress and of the polyol pathway which impair damage myenteric plexus are metabolic characteristics of diabetes. The ascorbic acid (AA) is an antioxidant and an aldose reductase inhibitor, which may act as neuroprotector. The effects of AA supplementation on the density and cellular body profile area (CP) of myenteric neurons in STZ-induced diabetes in rats were assessed. Four groups with five animals each were formed: normoglycemic (C); diabetic (D); AA-treated diabetic (DS) and AA-treated normoglycemic (CS). Dosagen of 50mg of AA were given, three times a week, for each animal (group DS and CS). Ninety days later and after euthanasia, the ileum was collected and processed for the NADPH-diaphorase technique. There were no differences (P>0.05) in the neuronal density among the groups. The CP area was lower (P<0.05) in the DS and CS groups, with a higher incidence of neurons with a CP area exceeding 200mm2 for groups C and D. The AA had no influence on the neuronal density in the ileum but had a neuroprotective effect, preventing the increase in the CP area and allowing a higher number of neurons with a CP area with less than 200mm2.


#4 - The number and profile of reactive NADH-d and NADPH-d neurons of myenteric plexus of six-month-old rats are different in the cecum portions, p.241-248

Abstract in English:

ABSTRACT.- Silva E.A., Natali M.R.M. & Prado I.M.M. 2008. The number and profile of reactive NADH-d and NADPH-d neurons of myenteric plexus of six-month-old rats are different in the cecum portions. Pesquisa Veterinária Brasileira 28(5):241-248. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, USP, Cidade Universitária, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270. E-mail: elizangela@usp.br Whole-mount preparations were prepared and submitted to NADH-diaphorase and NADPH-diaphorase histochemistry techniques. The myenteric plexus arrangement and the number of neurons were comparatively evaluated among the different portions of the cecum. The neurons from the apical and basal regions were distributed in classes at intervals of 100µm2, the means of the corresponding intervals being compared. The ganglia, in both techniques, were often connected by fine bundles, which became thicker in the mesenteric region and in the region next to the cecal ampulla. The number of positive NADH-d neurons was higher than that of NADPH-d neurons in all portions, from both regions. The numbers of reactive NADH-d e NADPH-d neurons were significantly different among the different portions of the cecum, except for the antimesenteric basal and intermediate basal regions, considering the NADH-d neurons. The profile area for the reactive NADH-d e NADPH-d neurons was higher in the apical region than in the basal area. Differences in arrangement, distribution and size of positive NADH-d e NADPH-d neurons in the different cecum portions evidenced the importance of the subdivision of the analyzed organ.

Abstract in Portuguese:

ABSTRACT.- Silva E.A., Natali M.R.M. & Prado I.M.M. 2008. The number and profile of reactive NADH-d and NADPH-d neurons of myenteric plexus of six-month-old rats are different in the cecum portions. Pesquisa Veterinária Brasileira 28(5):241-248. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, USP, Cidade Universitária, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270. E-mail: elizangela@usp.br Whole-mount preparations were prepared and submitted to NADH-diaphorase and NADPH-diaphorase histochemistry techniques. The myenteric plexus arrangement and the number of neurons were comparatively evaluated among the different portions of the cecum. The neurons from the apical and basal regions were distributed in classes at intervals of 100µm2, the means of the corresponding intervals being compared. The ganglia, in both techniques, were often connected by fine bundles, which became thicker in the mesenteric region and in the region next to the cecal ampulla. The number of positive NADH-d neurons was higher than that of NADPH-d neurons in all portions, from both regions. The numbers of reactive NADH-d e NADPH-d neurons were significantly different among the different portions of the cecum, except for the antimesenteric basal and intermediate basal regions, considering the NADH-d neurons. The profile area for the reactive NADH-d e NADPH-d neurons was higher in the apical region than in the basal area. Differences in arrangement, distribution and size of positive NADH-d e NADPH-d neurons in the different cecum portions evidenced the importance of the subdivision of the analyzed organ.


#5 - Assessment of NADPH-diaphorase stained myenteric neurons of the jejunum of diabetic rats supplemented with ascorbic acid, p.95-102

Abstract in English:

ABSTRACT.- Silverio S.M., Mari R.B., Clebis N.K., Scoz J.R., Germano R.M., Agreste F., Bombonato P.P. & Stabille S.R. 2008. Assessment of NADPH-diaphorase stained myenteric neurons of the jejunum of diabetic rats supplemented with ascorbic acid. Pesquisa Veterinária Brasileira 28(2):95-102. Departamento de Ciências Biológicas, UNIPAR, Campus-Paranavaí, Av. Huberto Brüning 360, Jardim Santos Dumont, Paranavaí, PR 87706-490, Brazil. E-mail: srstabille@wnet.com.br The relation between hyperglycemia and diabetic neuropathy has already been demonstrated in some studies. Among the theories proposed for its etiology the oxidative stress stands out. The performance of nitric oxide as a link between the metabolic and vascular neuropathogenic factors that triggers the diabetic neuropathy has already been put forward. This study aimed to assess the quantification and measurements of the cell body profile area (CBPA) of NADPH-diaphorase reactive (NADPH-dp) myenteric neurons of the jejunum of diabetic rats (induced by streptozotocin) supplemented with Ascorbic Acid (AA). These changes in the myenteric neurons seem to be related to the gastrointestinal disturbances observed in diabetes mellitus (DM). Twenty male Wistar rats (Rattus norvegicus) were distributed in 4 groups (n=5): controls (C), control supplemented (CS), diabetic (D), and diabetic suplemented (DS). DM was induced by estreptozotocin (50mg/kg body wt). One week after the induction and confirmation of the DM (glycemia exam), animals of the groups CS and DS received 50mg of AA three times a week by gavage. After 90 days of experiment, the animals were anesthetized with lethal thiopental dose (40mg/kg) and the collected jejunum processed for the histochemistry NADPH-diaphorase technique. Whole-mount preparations were obtained for quantitative and morphometric analysis of the myenteric neurons. A quantity of jejunum neurons in the Group D (96±7.5) was not different (P>0.05) from Group DS (116±8.08), C (92±9.7), and CS (81±5.4), but in Group DS the quantity was higher (P<0.05) than in Group C and CS. The CBPA of neurons from Group D (189.50±2.68µm2) and DS (195.92±3.75µm2) were lower (P<0.05) than from Group C (225.13±4.37µm2) and CS (210.23±3.15µm2). The streptozotocin-induced DM did not change the jejunum-ileum area, the jejunum myenteric plexus space organization and the density of NADPH-dp neurons. The 50g AA-supplementation, three times a week, during 90 days, did not decrease hyperglycemia; however, it had a neuroprotective effect on the myenteric neurons, minimizing the increase on the CBPA of NADPH-dp neurons and increasing the amount of NADPD-dp neurons.

Abstract in Portuguese:

ABSTRACT.- Silverio S.M., Mari R.B., Clebis N.K., Scoz J.R., Germano R.M., Agreste F., Bombonato P.P. & Stabille S.R. 2008. Assessment of NADPH-diaphorase stained myenteric neurons of the jejunum of diabetic rats supplemented with ascorbic acid. Pesquisa Veterinária Brasileira 28(2):95-102. Departamento de Ciências Biológicas, UNIPAR, Campus-Paranavaí, Av. Huberto Brüning 360, Jardim Santos Dumont, Paranavaí, PR 87706-490, Brazil. E-mail: srstabille@wnet.com.br The relation between hyperglycemia and diabetic neuropathy has already been demonstrated in some studies. Among the theories proposed for its etiology the oxidative stress stands out. The performance of nitric oxide as a link between the metabolic and vascular neuropathogenic factors that triggers the diabetic neuropathy has already been put forward. This study aimed to assess the quantification and measurements of the cell body profile area (CBPA) of NADPH-diaphorase reactive (NADPH-dp) myenteric neurons of the jejunum of diabetic rats (induced by streptozotocin) supplemented with Ascorbic Acid (AA). These changes in the myenteric neurons seem to be related to the gastrointestinal disturbances observed in diabetes mellitus (DM). Twenty male Wistar rats (Rattus norvegicus) were distributed in 4 groups (n=5): controls (C), control supplemented (CS), diabetic (D), and diabetic suplemented (DS). DM was induced by estreptozotocin (50mg/kg body wt). One week after the induction and confirmation of the DM (glycemia exam), animals of the groups CS and DS received 50mg of AA three times a week by gavage. After 90 days of experiment, the animals were anesthetized with lethal thiopental dose (40mg/kg) and the collected jejunum processed for the histochemistry NADPH-diaphorase technique. Whole-mount preparations were obtained for quantitative and morphometric analysis of the myenteric neurons. A quantity of jejunum neurons in the Group D (96±7.5) was not different (P>0.05) from Group DS (116±8.08), C (92±9.7), and CS (81±5.4), but in Group DS the quantity was higher (P<0.05) than in Group C and CS. The CBPA of neurons from Group D (189.50±2.68µm2) and DS (195.92±3.75µm2) were lower (P<0.05) than from Group C (225.13±4.37µm2) and CS (210.23±3.15µm2). The streptozotocin-induced DM did not change the jejunum-ileum area, the jejunum myenteric plexus space organization and the density of NADPH-dp neurons. The 50g AA-supplementation, three times a week, during 90 days, did not decrease hyperglycemia; however, it had a neuroprotective effect on the myenteric neurons, minimizing the increase on the CBPA of NADPH-dp neurons and increasing the amount of NADPD-dp neurons.


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