Alcohol predisposes to acute pancreatitis by an unknown mechanism and is known to reduce regional pancreatic blood flow.
To investigate whether increased blood alcohol causes functional impairment of pancreatic microperfusion as indicated by reduced tissue oxygenation.
Prospective, randomized, controlled study.
University hospital laboratory.
Forty adult female Wistar rats.
Intravenous infusion of ethanol (2 g/kg) or saline over 60 minutes. Tissue hemoglobin oxygenation saturation and hemoglobin content were measured using reflectance spectroscopy in the pancreas, stomach, and kidney at baseline and at 10-minute intervals for 1 hour.
Blood ethanol levels (mean±SEM) peaked at 1810±94 mg/L. Compared with saline controls, pancreatic hemoglobin oxygen saturation in ethanol-treated rats had significantly decreased by 40 minutes and remained depressed, while pancreatic hemoglobin content was unchanged. The magnitude of the depression was at least as great as that previously observed in acute experimental pancreatitis of moderate severity. Neither hemoglobin oxygen saturation nor hemoglobin content was affected in the stomach or kidney by ethanol.
A raised blood ethanol level was associated with acutely decreased hemoglobin oxygen saturation in the pancreas but not in the stomach or kidney. This observation of provoked hypoxia provides a possible mechanism by which alcohol contributes to pancreatic injury.(Arch Surg. 1995;130:357-361)