Gut dysoxia: comparison of sites to detect regional gut dysoxia

Dysoxia, a state in which O2 supply is inadequate to meet tissue metabolic needs, is often first detected in regional organs such as the gut. An increase in PCO2 is believed to reflect the development of gut dysoxia. The stomach is a well-documented clinical site for detecting gut PCO2; however, measurement issues make this a less than ideal monitoring site. Other sites along the GI tract may be equally sensitive to detect changes in PCO2. Rectal CO2 measurement may have the advantage of being less invasive, low risk, and continuous without the limitations associated with gastric monitoring. In this study, we compared PCO2 at two sites (gastric, rectum) at baseline and during a dysoxic challenge, cardiac arrest. We obtained similar values of PCO2 at both sites. Ten male Wistar rats were anesthetized with 1%-2% Isoflurane/50% nitrous oxide/balanced O2 and the tail artery and right atrium were cannulated. Severinghaus-type active tip PCO2 electrodes (Microelectrode Inc, Bedford, NH) were calibrated and one electrode was surgically inserted into the stomach (G-PCO2) and a second electrode was placed in the rectum (R-PCO2). Animals were stabilized following surgery. Cardiac arrest was induced by administering a rapid injection of norcuron (0.1-0.2 mg/kg) and potassium chloride solution (0.5 M/L; 0.12 mL/100 gm of body weight). Animals were monitored for 15 minutes post-arrest. Data were collected at one minute intervals using the software Data Collect. All data are reported as mean +/- SD. Baseline G-PCO2 was 64 +/- 17 torr, not significantly different from R-PCO2, 58 +/- 7 torr. After 15 minutes of cardiac arrest, G-PCO2 rose to 114 +/- 42 torr, again not significantly different from R-PCO2, which reached 112 +/- 35 torr. Monitoring PCO2 in the rectum is less invasive and might provide similar information when compared with gastric monitoring at baseline and during a dysoxic challenge.