Noc M, Weil M H, Sun S, Gazmuri R J, Tang W, Pakula J L
Institute of Critical Care Medicine, University of Health Sciences/ The Chicago Medical School, Illinois.
Circ Shock. 1993 Jul;40(3):194-9.
Measurement of gastric wall PCO2 has emerged as a promising monitor of perfusion deficits during low-flow states of circulatory shock. In the present study, gastric luminal PCO2 measured with the gastric tonometer was compared with the PCO2, measured directly in the wall of the stomach during hemorrhagic shock in two groups of five Sprague-Dawley rats. One group was pretreated with the H2 blocker, ranitidine. During a 120-min interval of hemorrhage, tonometer PCO2 increased from 60 +/- 7 mmHg to 90 +/- 10 mmHg, and time-coincident gastric wall PCO2 from 52 +/- 5 mmHg to 131 +/- 14 mmHg. Following reinfusion of shed blood, tonometer PCO2 remained elevated for an interval exceeding 60 min, but gastric wall PCO2 returned to control levels within approximately 10 min. Ranitidine pretreatment did not alter the relationships between gastric wall PCO2 and tonometer PCO2. These observations indicate that gastric luminal PCO2 underestimates relatively rapid increases in gastric wall PCO2 during profound hemorrhagic shock in rats.
胃壁二氧化碳分压（PCO2）的测量已成为循环性休克低流量状态下灌注不足的一种有前景的监测指标。在本研究中，将用胃张力计测量的胃腔内PCO2与两组各五只Sprague-Dawley大鼠失血性休克期间直接在胃壁测量的PCO2进行了比较。一组用H2阻滞剂雷尼替丁进行预处理。在120分钟的出血间隔期间，张力计测量的PCO2从60±7 mmHg增加到90±10 mmHg，同时胃壁PCO2从52±5 mmHg增加到131±14 mmHg。回输 shed blood后，张力计测量的PCO2在超过60分钟的时间段内仍保持升高，但胃壁PCO2在约10分钟内恢复到对照水平。雷尼替丁预处理并未改变胃壁PCO2与张力计测量的PCO2之间的关系。这些观察结果表明，在大鼠严重失血性休克期间，胃腔内PCO2相对低估了胃壁PCO2的快速升高。 （注：原文中shed blood表述有误，可能是shed blood（失血），但这里无法准确修正后翻译）
