Alcohol induces pancreatic ischemia, but the mechanisms promoting pancreati
c inflammation are unclear. We investigated whether cigarette smoke inhalat
ion is a cofactor in the development of ethanol-induced pancreatic injury.
Cigarette smoke was administered to anesthetized rats alone or in combinati
on with intravenous ethanol infusion. Control animals received either salin
e or ethanol alone. Pancreatic capillary blood flow and leukocyte-endotheli
um interaction in post-capillary venules were evaluated by intravital micro
scopy. Leukocyte sequestration was assessed by measurement of myeloperoxida
se activity in pancreatic tissue, and pancreatic injury evaluated by histol
ogy. Ethanol decreased pancreatic blood flow progressively over 90 minutes
(p < 0.001 vs. baseline), but neither leukocyte-endothelium interaction nor
leukocyte sequestration was altered. Cigarette smoke alone reduced pancrea
tic blood flow temporarily (p < 0.01 vs, baseline) and increased leukocyte-
endothelium interaction (roller p < 0.001, sticker p < 0.01 vs, baseline).
Cigarette smoke potentiated the impairment of pancreatic capillary perfusio
n caused by ethanol, and both the number of rolling leukocytes and myeloper
oxidase activity levels were increased compared to ethanol or nicotine admi
nistration alone (p less than or equal to 0.05 and p less than or equal to
0.01, respectively). This study demonstrates that ethanol induces pancreati
c ischemia and that cigarette smoke leads to both temporary pancreatic isch
emia and minimal leukocyte sequestration. Cigarette smoke potentiates the a
mount of pancreatic injury generated by ethanol alone. Smoking therefore se
ems to be a contributing factor in the development of alcohol-induced pancr
eatitis in the rat model.