Water-soluble ethylhydroxyethyl cellulose prevents bacterial translocation induced by major liver resection in the...

Enteric bacteria might act as pathogens, translocating across the intestinal barrier to extraintestinal sites after major liver resection. In the current study, water-soluble ethylhydroxyethyl cellulose (EHEC) was administered before hepatectomy to evaluate the influence on bacterial translocation induced by major liver resection, phagocytic capacity by visceral and circulating macrophages, enteric bacterial population, and bacterial adherence on the intestinal surface in rats subjected to sham operation or to 70% or 90% hepatectomy. Oral or intravenous (IV) administration of EHEC reduced the incidence of bacterial translocation to mesenteric lymph nodes (MLN) and blood after major liver resection. Oral EHEC appeared more effective than IV administration in protecting against bacterial translocation to MLN in animals with 90% hepatectomy. Ethylhydroxyethyl cellulose (oral and IV) significantly diminished intestinal macrophage uptake capacity of 125I-labeled, heat-killed Escherichia coli as compared with animals without EHEC administration. Overgrowth or colonization of enteric bacteria after major liver resection could be prevented by oral or IV EHEC. Adherence of 14C-labeled, alive E. coli on the intestinal mucosa decreased after EHEC treatment in animals subjected to major liver resection. Systemic arterial pressure and intestinal blood flow markedly decreased from 1 hour and on after 90% hepatectomy. Intravenous administration of EHEC did not improve these alterations. Bacterial hydrophobicity and surface negative charge were significantly reduced 1 hour after bacterial culture with EHEC. Thus, EHEC appears to be a potent agent preventing translocation of enteric bacteria from the gut after major liver resection, by altering the surface characters of enteric bacteria, balancing the enteric microflora, inhibiting bacterial attachment onto the intestinal surface, and blocking phagocytosis by intestinal macrophages.