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由于细菌产生二氧化碳导致小鼠盲肠壁气体过饱和。

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

作者信息

Rasmussen H, Kvarstein G, Johnsen H, Dirven H, Midtvedt T, Mirtaheri P, Tønnessen T I

机构信息

Research and Development, Nycomed Imaging AS, N-0401 Oslo, Norway.

出版信息

J Appl Physiol (1985). 1999 Apr;86(4):1311-8. doi: 10.1152/jappl.1999.86.4.1311.

Abstract

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.

摘要

在小鼠中测量了盲肠和空肠肠腔及浆膜的二氧化碳分压(PCO2)。使用的麻醉剂是芬太尼 - 氟胺酮 - 咪达唑仑混合物。在活体和死后记录PCO2。正常小鼠盲肠肠腔内的PCO2为409±32托(55±4千帕),浆膜处为199±22托(27±3千帕)。冲洗盲肠导致浆膜和肠腔内的PCO2水平为65 - 75托。无菌小鼠的盲肠PCO2显著降低(65±5托)。将正常细菌菌群引入无菌小鼠后,盲肠PCO2显著升高。将单一细菌培养物引入无菌小鼠没有影响。小鼠死亡后,正常小鼠的盲肠PCO2迅速升高。肠道细菌产生了大部分盲肠PCO2,在细菌活性高的肠段使用张力测量法时应谨慎解释。我们提出,在循环正常的小鼠盲肠中,浆膜PCO2水平>150 - 190托(20 - 25千帕)可能代表盲肠壁中的气体过饱和状态。

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