Grönroos J M, Kaila T, Aho H J, Nevalainen T J
Department of Pathology, University of Turku, Finland.
Pharmacol Toxicol. 1989 Apr;64(4):356-9. doi: 10.1111/j.1600-0773.1989.tb00664.x.
The effect of eight months of alcohol intake on the number and affinity of muscarinic receptor sites in the rat pancreatic tissue were measured by using N-3H-methylscopolamine (NMS) as a radioligand. There were no differences in the receptor affinities for NMS between the alcohol-exposed and age-matched control animals, but the number of muscarinic receptor sites was 60 percent lower in the alcoholic animals. The present experimental model is consistent with altered food and water intake as consequences of chronic alcoholism and thus changes in food and water consumption may participate in mediating the effects of chronic alcohol intake on NMS binding sites. We suggest that the previously reported marked alcohol-induced increase in pancreatic acetylcholine levels, which has been proposed to play a crucial role in the pathogenesis of acute alcoholic pancreatitis, may be a secondary phenomenon induced by increased resistance at the muscarinic receptor level.
以N - 3H - 甲基东莨菪碱（NMS）作为放射性配体，测定了8个月酒精摄入对大鼠胰腺组织毒蕈碱受体位点数量和亲和力的影响。酒精暴露组动物和年龄匹配的对照组动物对NMS的受体亲和力没有差异，但酒精摄入组动物的毒蕈碱受体位点数量减少了60%。本实验模型与慢性酒精中毒导致的食物和水摄入量改变一致，因此食物和水消耗量的变化可能参与介导慢性酒精摄入对NMS结合位点的影响。我们认为，先前报道的酒精引起的胰腺乙酰胆碱水平显著升高，这被认为在急性酒精性胰腺炎的发病机制中起关键作用，可能是毒蕈碱受体水平抗性增加所诱导的继发性现象。
