Association between gastric intramucosal pH and splanchnic endotoxin, antibody to endotoxin, and tumor necrosis factor-alpha concentrations in patients undergoing cardiopulmonary bypass.

Abstract

To determine the association between gastric intramucosal pH, a minimally invasive marker reflecting the adequacy of oxygen delivery to the gastrointestinal tract, and splanchnic endotoxin, antibody to endotoxin, and tumor necrosis factor (TNF)-alpha concentrations in patients undergoing cardiopulmonary bypass. Single-arm, prospective study. University hospital. Adults (n = 10) free of hepatic, pulmonary, and renal disease undergoing nonemergent coronary artery bypass surgery. After induction of general anesthesia and endotracheal intubation, a tonometer nasogastric tube was positioned in the stomach, and triple-lumen fiberoptic catheters were inserted into the hepatic vein and pulmonary artery. Hepatic venous and mixed venous blood samples were analyzed for endotoxin, antibody to endotoxin, and TNF-alpha at six times: 30 mins after induction of anesthesia (time 1); during vena caval cannulation (time 2); after 15 mins of hypothermic cardiopulmonary bypass (time 3); during spontaneous left ventricular ejection after release of the aortic cross-clamp, but before termination of cardiopulmonary bypass (time 4); 15 mins after termination of cardiopulmonary bypass (time 5); and 1 hr after termination of cardiopulmonary bypass (time 6). Gastric intramucosal pH, systemic oxygen delivery (DO2), mixed venous oxygen saturation, hepatic venous oxygen saturation, and hepatic venous lactate concentrations were recorded at these same times. Data for each variable were compared with baseline values (time 1) for statistical significance. Cardiopulmonary bypass was associated with an increase (p < .05) in systemic endotoxin concentrations from ventricular ejection until the end of the study. Virtually identical changes in the splanchnic circulation at this time approached, but did not reach, statistical significance, because hepatic venous endotoxin concentrations were higher than the mixed venous endotoxin concentrations at baseline (41.6 +/- 11.2 vs. 16.9 +/- 4.9 pg/mL). Gastric intramucosal pH was abnormal (< 7.35) at 15 mins (p > .05) and at 1 hr after termination of cardiopulmonary bypass (p > .05). The relationship between endotoxin and gastric intramucosal pH was not statistically significant (p = .15). The decrease in endotoxin antibody was small and statistically insignificant. TNF-alpha was not detected in any patient. Systemic DO2 decreased (p < .05) after 15 mins of hypothermic cardiopulmonary bypass, but returned to baseline values thereafter. There were no significant changes in mixed venous and hepatic venous oxygen saturation values. Splanchnic lactate concentrations increased at cannulation (p < .05), after 15 mins of hypothermic cardiopulmonary bypass (p < .05), and 15 mins after termination of cardiopulmonary bypass (p < .05). These observations are consistent with the hypothesis that impaired gut-barrier function is responsible for endotoxemia occurring during cardiopulmonary bypass. It is unclear whether increased mucosal permeability and mucosal acidosis are causally related phenomena or simply independent markers of damage to gut epithelium.