Cigarette smoke enhances ethanol-induced pancreatic injury

摘要: Alcohol induces pancreatic ischemia, but the mechanisms promoting inflammation are unclear. We investigated whether cigarette smoke inhalation is a cofactor in development of ethanol-induced injury. Cigarette was administered to anesthetized rats alone or combination with intravenous ethanol infusion. Control animals received either saline alone. Pancreatic capillary blood flow and leukocyte-endothelium interaction postcapillary venules were evaluated by intravital microscopy. Leukocyte sequestration assessed measurement myeloperoxidase activity tissue, injury histology. Ethanol decreased progressively over 90 minutes (p < 0.001 vs. baseline), neither nor leukocyte altered. reduced temporarily 0.01 baseline) increased (roller p 0.001, sticker baseline). potentiated impairment perfusion caused ethanol, both number rolling leukocytes levels compared nicotine administration = 0.05 0.01, respectively). This study demonstrates that ischemia leads temporary minimal sequestration. potentiates amount generated Smoking therefore seems be contributing factor alcohol-induced pancreatitis rat model.