ABSTRACT
In summary the carbon tetrachloride/phenobarbital of cirrhosis in rats mimics human cirrhosis very closely, with development of ascites and SBP. This model shows us that bacterial overgrowth occurs as cirrhosis progresses and that bacterial translocation from the gut to extra-intestinal sites is part of the early pathogenesis of SBP. SID with norfloxacin dramatically reduced translocation and SBP at the expense of grampositive overgrowth and infection with gram-positives and colonization with strange gram negatives. SID with TMP-SMZ actually delayed development of ascites and prolonged survival.
Subject(s)
Animals , Rats , Ascites/microbiology , Liver Cirrhosis, Experimental/complications , Peritonitis/microbiology , Bacterial Translocation/physiology , Ascites/prevention & control , Liver Cirrhosis, Experimental/chemically induced , Liver Cirrhosis, Experimental/microbiology , Trimethoprim, Sulfamethoxazole Drug Combination/therapeutic use , Bacterial Physiological Phenomena , Carbon Tetrachloride Poisoning , Norfloxacin/therapeutic use , Peritonitis/prevention & control , Antibiotic Prophylaxis , Bacterial TranslocationABSTRACT
En la peritonitis bacteriana espontánea se plantean como mecanismo patogénico bacteremias favorecidas por la presencia de cortocircuitos vasculares extra e intrahepáticos y la migración transmural de bactérias. Establecemos un modelo experimental en ratas para futuro estudio de la posible correlación entre una técnica invasiva (enema evacuante) y la presencia de bactérias a nivel portal y/o peritoneal