Liddle Rodger A, Nathan Jaimie D
Department of Medicine, Duke University, and Durham VA Medical Centers, Durham, NC 27710, USA.
Pancreatology. 2004;4(6):551-9; discussion 559-60. doi: 10.1159/000082180. Epub 2004 Nov 15.
Stimulation of primary sensory neurons produces local vasodilation, plasma extravasation, and pain and is due largely to the release of the tachykinins substance P and calcitonin-gene-related peptide. Pathological activation of sensory neurons and the inflammatory sequelae are known as neurogenic inflammation and appear to be important in many organ systems, including the pancreas. Factors that stimulate primary sensory neurons include hydrogen ions, heat, leukotrienes, arachidonic acid metabolites, bradykinin, and proteases such as trypsin, all of which may participate in the generation of acute pancreatitis. The current review examines the cellular and molecular mechanisms involved in sensory nerve activation within the pancreas and the potential contribution of neurogenic inflammation to the pathogenesis of pancreatitis.
初级感觉神经元的刺激会产生局部血管舒张、血浆外渗和疼痛,这主要是由于速激肽P物质和降钙素基因相关肽的释放所致。感觉神经元的病理性激活和炎症后遗症被称为神经源性炎症,在包括胰腺在内的许多器官系统中似乎都很重要。刺激初级感觉神经元的因素包括氢离子、热、白三烯、花生四烯酸代谢产物、缓激肽和蛋白酶(如胰蛋白酶),所有这些因素都可能参与急性胰腺炎的发生。本综述探讨了胰腺内感觉神经激活所涉及的细胞和分子机制,以及神经源性炎症对胰腺炎发病机制的潜在影响。