Hartwig W, Werner J, Ryschich E, Mayer H, Schmidt J, Gebhard M M, Herfarth C, Klar E
Department of Surgery, University of Heidelberg, Germany.
Pancreas. 2000 Oct;21(3):272-8. doi: 10.1097/00006676-200010000-00009.
Alcohol induces pancreatic ischemia, but the mechanisms promoting pancreatic inflammation are unclear. We investigated whether cigarette smoke inhalation is a cofactor in the development of ethanol-induced pancreatic injury. Cigarette smoke was administered to anesthetized rats alone or in combination with intravenous ethanol infusion. Control animals received either saline or ethanol alone. Pancreatic capillary blood flow and leukocyte-endothelium interaction in postcapillary venules were evaluated by intravital microscopy. Leukocyte sequestration was assessed by measurement of myeloperoxidase activity in pancreatic tissue, and pancreatic injury evaluated by histology. 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 pancreatic 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 perfusion caused by ethanol, and both the number of rolling leukocytes and myeloperoxidase activity levels were increased compared to ethanol or nicotine administration alone (p < or = 0.05 and p < or = 0.01, respectively). This study demonstrates that ethanol induces pancreatic ischemia and that cigarette smoke leads to both temporary pancreatic ischemia and minimal leukocyte sequestration. Cigarette smoke potentiates the amount of pancreatic injury generated by ethanol alone. Smoking therefore seems to be a contributing factor in the development of alcohol-induced pancreatitis in the rat model.
酒精可诱发胰腺缺血，但促进胰腺炎症的机制尚不清楚。我们研究了吸入香烟烟雾是否是乙醇诱导胰腺损伤发生过程中的一个辅助因素。对麻醉大鼠单独给予香烟烟雾或与静脉输注乙醇联合给予。对照动物单独接受生理盐水或乙醇。通过活体显微镜评估胰腺毛细血管血流以及毛细血管后微静脉中的白细胞与内皮细胞相互作用。通过测量胰腺组织中的髓过氧化物酶活性评估白细胞滞留情况，并通过组织学评估胰腺损伤。乙醇在90分钟内逐渐降低胰腺血流（与基线相比，p < 0.001），但白细胞与内皮细胞相互作用及白细胞滞留均未改变。单独的香烟烟雾暂时降低胰腺血流（与基线相比，p < 0.01）并增加白细胞与内皮细胞相互作用（滚动白细胞，p < 0.001；黏附白细胞，与基线相比，p < 0.01）。香烟烟雾增强了乙醇所致的胰腺毛细血管灌注损伤，与单独给予乙醇或尼古丁相比，滚动白细胞数量和髓过氧化物酶活性水平均增加（分别为p ≤ 0.05和p ≤ 0.01）。本研究表明，乙醇可诱发胰腺缺血，香烟烟雾可导致暂时性胰腺缺血和轻微的白细胞滞留。香烟烟雾增强了单独乙醇所致的胰腺损伤量。因此，在大鼠模型中，吸烟似乎是酒精性胰腺炎发生的一个促成因素。
