Isoflurane-induced acidosis depresses basal and PGE(2)-stimulated duodenal bicarbonate secretion in mice.

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE(2)-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na(2)CO(3) solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE(2) was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15-7.21 and the base excess was about -8 mM at the end of experiments. The continuous infusion of Na(2)CO(3) solution completely compensated for the acidosis. The blood pH was 7.36-7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE(2)-stimulated DMBS were markedly greater in animals treated with Na(2)CO(3) solution than in those treated with Ringer solution. MAP was slightly higher after Na(2)CO(3) solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE(2)-stimulated DMBS as well as the responsiveness to PGE(2), effects prevented by a continuous infusion of Na(2)CO(3). When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na(2)CO(3) infusion to maintain a normal acid-base balance.