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J Appl Physiol 86: 1311-1318, 1999;
8750-7587/99 $5.00
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Vol. 86, Issue 4, 1311-1318, April 1999

Gas supersaturation in the cecal wall of mice due to bacterial CO2 production

Henrik Rasmussen1, Gunnvald Kvarstein2, Helge Johnsen1, Hubert Dirven1, Tore Midtvedt3, Peyman Mirtaheri4, and Tor Inge Tønnessen5

1 Research and Development, Nycomed Imaging AS, N-0401 Oslo; 2 Department of Anesthesiology, The National Hospital, N-0027 Oslo, Norway; 3 Department of Cell and Molecular Biology, Laboratory of Medical Microbiological Ecology, Karolinska Institute, S-17177 Stockholm, Sweden; and 4 Medinnova and 5 Department of Anesthesiology and The Interventional Center, The National Hospital, N-0027 Oslo, Norway

PCO2 in the lumen and serosa of cecum and jejunum was measured in mice. The anesthetic used was a fentanyl-fluanisone-midazolam mixture. PCO2 was recorded in vivo and postmortem. PCO2 was 409 ± 32 Torr (55 ± 4 kPa) in the cecal lumen and 199 ± 22 Torr (27 ± 3 kPa) on the serosa in normal mice. Irrigation of the cecum resulted in serosal and luminal PCO2 levels of 65-75 Torr. Cecal PCO2 was significantly lower in germ-free mice (65 ± 5 Torr). Cecal PCO2 increased significantly after introduction of normal bacterial flora into germ-free mice. Introduction of bacterial monocultures into germ-free mice had no effect. After the deaths of the mice, cecal PCO2 increased rapidly in normal mice. The intestinal bacteria produced the majority of the cecal PCO2, and the use of tonometry in intestinal segments with a high bacterial activity should be interpreted with caution. We propose that serosal PCO2 levels >150-190 Torr (20-25 kPa) in the cecum of mice with a normal circulation may represent a state of gas supersaturation in the cecal wall.

carbon dioxide; carbon dioxide pressure; serosa; germ free; gnotobiotic; inherent unsaturation


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