Cigarette smoke enhances ethanol-induced pancreatic injury

Citation
W. Hartwig et al., Cigarette smoke enhances ethanol-induced pancreatic injury, PANCREAS, 21(3), 2000, pp. 272-278
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
PANCREAS
ISSN journal
0885-3177 → ACNP
Volume
21
Issue
3
Year of publication
2000
Pages
272 - 278
Database
ISI
SICI code
0885-3177(200010)21:3<272:CSEEPI>2.0.ZU;2-7
Abstract
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.