Background and Aims: Experimental peritonitis causes gut intramucosal acidosis indicating intramucosal ischemia. However, tissue acidosis may reflect other conditions than ischemia. An increased mucosal-arterial Pco2difference (Pco2-gap) is suggested to be a more adequate measure of tissue ischemia than intramucosal pH (pHi). This study was performed to elucidate whether keeping cardiac index (Cl) and splanchnic blood flow normal or supranormal by administration of colloids and an inotropic drug could prevent the acidosis as well as reduce the Pco2-gap. A secondary aim was to study to what degree the low pHiin peritonitis really reflects ischemia.Subjects: 24 anesthetized pigs (18–27 kg) divided into four groups.Models: A Swan-Ganz catheter, transonic flow meters and catheters for blood sampling were applied. pHiwas calculated using tonometry. Standardized fecal peritonitis was induced, except in controls. One peritonitis group was given dextran (Group PDEX) and another in addition dobutamine (Group PDOB) to keep Cl normal or supranormal, respectively. Results: After 4 h, a significant drop in pHiwas found in all peritonitis groups, most pronounced in untreated peritonitis (to 7.09 ± .02). Corresponding values in Group PDEXand Group PDOBwere 7.22 ± .03 and 7.22 ± .01, respectively, and in controls 7.30 ± .02. The Pco2-gap and the mucosal-arterial [H+] difference ([H+]-gap) increased significantly in untreated peritonitis but did not increase in groups given dextran and dextran + dobutamine.Conclusion: Maintaining Cl in peritonitis attenuated the reduction in pHiand prevented the increased Pco2- and [H+]-gap. It seems justified from these data to conclude that the somewhat reduced pHiin treated peritonitis groups did not reflect tissue ischemia.