PURPOSE: The aim of this study was to investigate in rats with peritonitis the effect of CO2 insufflation on behavior of bacteria, including antibiotic resistance, and the systemic and regional host response. METHODS: Inbred weaned Wistar albino rats were used. Escherichia coli ATCC 25922 was used to induce peritonitis. Rats with peritonitis were allocated to 4 groups: group 1, control; group 2, laparotomy; group 3, laparoscopy; group 4, laparoscopy + laparotomy and were killed at the end of the second hour of peritonitis. Serum, peritoneal fluid, and intraabdominal organs were taken for microbiological (biochemical markers-urease, citrate, indole; virulence factors-biofilm, protease, gelatinase, adherence), systemic immunologic (interleukin 1 [IL-1]alpha, IL-1beta, tumor necrosis factor alpha, IL-6), and regional histopathologic evaluations. Isolated strains were tested against minimum inhibitory concentrations (MICs) and sub-MICs of amikacin and amoxicillin. RESULTS: Regional inflammatory response was the highest in group 2 but the lowest in group 4. Systemic IL-1alpha level was significantly higher in group 2, and TNF-alpha level was higher in group 3. After the peritonitis process, Escherichia coli began to use citrate and urea in control groups (without antibiotic treatment). In groups 2 and 4, amoxicillin resistance developed. CONCLUSIONS: In peritonitis, in all experimental groups, Escherichia coli used different metabolic pathways other than in normal atmospheric conditions. Amoxicillin resistance developed in open surgery groups. Further kinetic microbiological and immune response studies are needed concerning the early and late effects of CO2 insufflation on various strains of bacteria and mixed infections.
PURPOSE: The aim of this study was to investigate in rats with peritonitis the effect of CO2 insufflation on behavior of bacteria, including antibiotic resistance, and the systemic and regional host response. METHODS: Inbred weaned Wistar albino rats were used. Escherichia coli ATCC 25922 was used to induce peritonitis. Rats with peritonitis were allocated to 4 groups: group 1, control; group 2, laparotomy; group 3, laparoscopy; group 4, laparoscopy + laparotomy and were killed at the end of the second hour of peritonitis. Serum, peritoneal fluid, and intraabdominal organs were taken for microbiological (biochemical markers-urease, citrate, indole; virulence factors-biofilm, protease, gelatinase, adherence), systemic immunologic (interleukin 1 [IL-1]alpha, IL-1beta, tumor necrosis factor alpha, IL-6), and regional histopathologic evaluations. Isolated strains were tested against minimum inhibitory concentrations (MICs) and sub-MICs of amikacin and amoxicillin. RESULTS: Regional inflammatory response was the highest in group 2 but the lowest in group 4. Systemic IL-1alpha level was significantly higher in group 2, and TNF-alpha level was higher in group 3. After the peritonitis process, Escherichia coli began to use citrate and urea in control groups (without antibiotic treatment). In groups 2 and 4, amoxicillin resistance developed. CONCLUSIONS: In peritonitis, in all experimental groups, Escherichia coli used different metabolic pathways other than in normal atmospheric conditions. Amoxicillin resistance developed in open surgery groups. Further kinetic microbiological and immune response studies are needed concerning the early and late effects of CO2 insufflation on various strains of bacteria and mixed infections.