Navegando por Palavras-chave "Hypertension, Portal"
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- ItemAcesso aberto (Open Access)Esplenoportografia transparietal: seu valor na identificação da síndrome de hipertensão portal (por bloqueio pré e intrahepático), avaliação de sua intensidade e suas possibilidades para a comprovação de varizes esofagogástricas(Universidade Federal de São Paulo (UNIFESP), 1962) Vilela, Moacyr Pádua [UNIFESP]; Universidade Federal de São Paulo [UNIFESP]
- ItemEmbargoEstudo da translocação bacteriana em um modelo experimental de hipertensão porta aguda e crônica(Universidade Federal de São Paulo (UNIFESP), 2009-09-30) Toma, Ricardo Katsuya [UNIFESP]; Koh, Ivan Hong Jun [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Portal Hypertension (PH) is a Syndrome that clinically manifests with ascites, portosystemic encephalopathy and esophageal variceal hemorrhage, and is often associated with bacterial infections leading to death. Given the predominance of enteric bacterial origin in these infections, the causal factor has been attributed to the bacterial translocation (BT) phenomena. The aim of this study was to evaluate the role of the acute and chronic portal hypertension (APH and CPH) state on the BT process. Methods: Wistar EPM rats (n=62) were randomly distributed in 3 groups: BT, APH and CPH, with or without BT induction on the post-operative days 2 and 14, by oroduodenal inoculation [10 ml E. Coli R6, 107 or 1010 colony-forming units (CFU/ml)], which were confined in the small bowel for 2 hours period. Control groups (Sham groups) were injected with saline. The PH was induced by calibrated portal vein stenosis. Portal vein flow and spleen weight were monitored. Mesenteric lymph node (MLN), liver, spleen, lung, blood and peritoneal fluid (PF) samples were cultured. Results: When the APH factor was associated to the high inoculum BT induction (1010CFU/mL), both higher positive percentage and bacterial recovery index were seen at the extra-intestinal sites as well as to the lung and peritoneal fluid, sites usually free of BT-event. Besides, usually BT-negative low inoculum (107CFU/mL) was able to provoke translocation. In the CPH period, lower translocation-index was seen as compared to the APH phase with both inoculum. However, the translocation susceptibility to the peritoneal fluid persisted at the CPH period. Conclusion: 1) PH factor modified the intensity, threshold and pattern of bacterial allocation to the extraintestinal compartments under this BT-model. 2) The acute PH state favored BT-process as well as the lung and peritoneal cavity susceptibility to bacterial allocation. 3) The chronic PH state was less susceptible for BT-process as compared to acute PH phase, although, peritoneal cavity susceptibility to bacterial allocation persisted. 4) BT process differences between acute and chronic PH phases seemed to have relation with the time dependent hemodynamic adaptation.