Background: Alcohol predisposes to acute pancreatitis by an unknown me
chanism and is known to reduce regional pancreatic blood flow. Objecti
ve: To investigate whether increased blood alcohol causes functional i
mpairment of pancreatic microperfusion as indicated by reduced tissue
oxygenation. Design: Prospective, randomized, controlled study. Settin
g: University hospital laboratory. Subjects: Forty adult female Wistar
rats. Interventions: Intravenous infusion of ethanol (2 g/kg) or sali
ne over 60 minutes. Tissue hemoglobin oxygenation saturation and hemog
lobin content were measured using reflectance spectroscopy in the panc
reas, stomach, and kidney at baseline and at 10-minute intervals for 1
hour. Results: Blood ethanol levels (mean+/-SEM) peaked at 1810+/-94
mg/L. Compared with saline controls, pancreatic hemoglobin oxygen satu
ration in ethanol-treated rats had significantly decreased by 40 minut
es and remained depressed, while pancreatic hemoglobin content was unc
hanged. The magnitude of the depression was at least as great as that
previously observed in acute experimental pancreatitis of moderate sev
erity. Neither hemoglobin oxygen saturation nor hemoglobin content was
affected in the stomach or kidney by ethanol. Conclusion: A raised bl
ood ethanol level was associated with acutely decreased hemoglobin oxy
gen 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.