Intramucosal pH and pCO(2) do not strictly correlate with intestinal energy metabolism in experimental peritonitis.

This study aimed to investigate tissue hypoxia on the cellular level in sepsis. Eighteen pigs weighing 18-27 kg were studied. Intramucosal-arterial PCO(2) gradient (PCO(2)-gap) and intramucosal pH (pH(i)) were calculated using tonometry. A blind loop of the small intestine was constructed for repeated tissue biopsies to measure intestinal energy-related metabolites and lactate concentration. Six animals served as controls. In 12 animals, faecal peritonitis was induced. Six of these animals were studied without further interventions, while the others were resuscitated with dextran to maintain cardiac index at baseline level. Untreated peritonitis caused an increase in PCO(2)-gap and a drop in pH(i). The intestinal energy metabolism was not disturbed until the end of the experimental period, with a decreased energy charge value and a moderately increased lactate concentration. In peritonitis-dextran animals, PCO(2)-gap and pH(i) remained at baseline level and the energy metabolism was not disturbed. We conclude that in peritonitis, PCO(2)-gap - like pH(i) - can be influenced by other factors than strictly anaerobic tissue metabolism.