Efeito da solução de Carolina Rinse na injúria de isquemia e reperfusão experimental no intestino delgado de coelhos

• Ano de defesa: 2011
• Autor(a) principal: BRANDSTETTER, Luciana Ramos Gaston
• Orientador(a): ARAÚJO, Eugênio Gonçalves de
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Goiás
• Programa de Pós-Graduação: Doutorado em Ciência Animal
• Departamento: Ciências Agrárias
• País: BR
• Palavras-chave em Português: intestino delgado; MAPK; necrose
• Palavras-chave em Inglês: small intestine; MAPK; necrosis
• Área do conhecimento CNPq: CNPQ::CIENCIAS AGRARIAS::MEDICINA VETERINARIA::PATOLOGIA ANIMAL
• Link de acesso: http://repositorio.bc.ufg.br/tede/handle/tde/1135

Mechanic obstruction of blood vessels that irrigate the intestine leads to ischemia and intense reduction of oxygenation and tissue perfusion. If oxygenated blood flow returns abruptly to tissues before cellular death reperfusion injury occurs; this can be initiated by several mechanisms resulting in inflammatory response. Intestinal ischemia/reperfusion (I/R) injury has been widely associated to cell necrosis, although another distinct biochemical and morphological type of cell death, called apoptosis, is involved. Such conditions are mediated by signaling molecules in cellular surface, which lead to long term changes in gene expression. In the majority of cells, MAP (Mitogen Activated Protein) kinases (MAPK), which are part of a group of cytoplasmic enzymes, will transmit mitogenic and cell differentiation signs. Three MAPK that have been identified in mammalian cells participate in the signaling pathway: ERK, p38 and JNK. Activated p38 and JNK are usually related to apoptosis, while activated ERK 1/2 (P44/42) have a protection function inhibiting apoptosis. With the purpose of minimizing reperfusion injury after liver transplant, Carolina Rinse Solution (CRS) was designed by North Carolina University, USA. Although this solution has been used in horses to attenuate I/R injury in horse intestine, little is known about the eventual tissue protection mechanism. The present study aimed to investigate the effects of topical and intraluminal CRS in I/R injury, and the activation profile of p38 and ERK 1/2 MAPK, in rabbit jejunum. Fifteen New Zealand rabbits were allocated to three groups: Sham-operated (A), Ischemia and reperfusion (B) and CRS (C). Groups B and C were subjected to one hour of jejunal ischemia and two hours of reperfusion. In group C, ten minutes prior to reperfusion, the bowel lumen was filled with CRS, and the segment was immersed in CRS until reperfusion onset. Changes such as degeneration, necrosis, edema, hemorrhage, PMN infiltration and margination were not significantly different between groups B and C, showing that topical and intraluminal CRS did not attenuate deleterious effects of I/R in small intestinal of rabbits. I/R stimulated the phosphorylation of p44/42 MAPK and p38 MAPK pathways in some layers of jejunum. Progressive activation of p44/42 MAPK was chiefly localized to the crypts of Lieberkühn, circular and longitudinal muscle layers, whereas p38 MAPK was prominently activated in myenteric plexus and both muscle layers. All layers that did respond to I/R insult with activation increase of ERK 1/2 and p38, in all groups, showed low baseline phosphorylation levels as compared to those that did not react to the insult. The results of this work indicate that topical and intraluminal CRS does not interfere in ERK 1/2 and p38 activation profile in rabbit jejunum subjected to I/R.