Gut Dysoxia

Abstract

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 l%–2% Isoflurane/50% nitrous oxide/balanced O₂ and the tail artery and right atrium were cannulated. Severinghaustype 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.