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Because ethanol abusers are susceptible to pancreatitis in animal models, and interruption of the pancreatic circulatory supply may also cause pancreatitis, we studied the effect of ethanol infusion on pancreatic blood flow. We administered ethanol 0.5 g/kg and 1.5 g/kg iv, to 35 conscious dogs (ethanol blood levels, 117 ± 10 (SD) and 297 ± 67 mg/100 ml, respectively). Measurements were made of aortic pressure and regional blood flow by the radioactive microsphere method in the pancreas, stomach, spleen, intestines, adrenal glands, and kidneys. Pancreatic flows were 172 ml/min per 100 g control, 156 ml/min per 100 g after 0.5 g/kg ethanol and 108 ml/min per 100 g after 1.5 g/kg ethanol. After the higher dose, the decrease in pancreatic flow of 64 ml/min per 100 g or 37% was statistically significant (P< 0.01); pancreatic vascular resistance rose by 113% (P< 0.001). There were no significant changes in flow or resistance in the other organs studied. Similar changes in pancreatic flow and resistance occurred after 1.5 g/kg ethanol in groups of dogs pretreated with phenoxybenzamine, an α-adrenergic antagonist; propranolol. a β-adrenergic antagonist; cimetidine, a histamine H2 receptor antagonist; and meclofenamate, a prostaglandin synthetase inhibitor. The changes in pancreatic blood flow and resistance were substantially reversed by 25% mannitol, 3 ml/kg, iv, after infusion of ethanol. We conclude that ethanol, in high doses relevant clinically, selectively elevates pancreatic vascular resistance, probably by inducing perivascular cellular swelling.

Ethanol-induced alterations in pancreatic blood flow in conscious dogs.