PCO2 in the large intestine of mice, rats, guinea pigs, and dogs and effects of the dietary substrate

PCO2 in the lumen and serosa of cecum and colon was measured in rats, guinea pigs, and dogs to examine the relationship between serosal PCO2 and the incidence of intestinal necrotic lesions after administration of gas-carrier contrast agents in rodents. The effects of the dietary substrate were tested in a group of mice maintained on a diet based on glucose as the only carbohydrate source. The anesthetic used was a fentanyl-fluanison-midazolam mixture (rodents) and pentobarbital (dogs). PCO2 was measured in vivo and postmortem, and the kinetics of the postmortem serosal PCO2 [transmural CO2 flux (J(CO2))] was calculated. PCO2 in the cecal serosa and lumen, respectively, was 64 +/- 4 and 392 +/- 18 Torr in rats, 67 +/- 3 and 276 +/- 17 Torr in guinea pigs, and 73 +/- 6 and 137 +/- 7 Torr in mice on glucose-based diet. In the colon serosa and lumen of dogs PCO2 was 30 6 and 523 67 Torr, respectively. Serosal PCO2 increased rapidly after death in rats and slower in guinea pigs and mice, and the slowest change was observed in dogs. Compared with dogs, serosal PCO2 and J(CO2) of rats and guinea pigs were significantly higher. Serosal PCO2 of guinea pigs was similar to that of rats, whereas the J(CO2) of guinea pigs was significantly lower. These data suggest a causal relationship between the ability of the cecal and colonic wall to act as a barrier to CO2 diffusion and the presence of characteristic gas-carrier contrast agent-induced intestinal lesions in mice and rats and their absence in guinea pigs, dogs, and other species.