Merkord J, Weber H, Sparmann G, Jonas L, Hennighausen G
Institute of Experimental and Clinical Pharmacology and Toxicology, University of Rostock, Germany.
Ann N Y Acad Sci. 1999 Jun 30;880:231-7. doi: 10.1111/j.1749-6632.1999.tb09527.x.
In summary, in addition to an acute interstitial pancreatitis the organotin compound DBTC induced a pancreatic fibrosis in rats. The course of the pancreatic fibrosis was studied 2-36 weeks after single i.v. treatment of rats with 6 or 8 mg/kg DBTC. The pancreatic fibrosis induced by DBTC differs from other experimental models of acute pancreatitis. Extensive infiltration by mononuclear cells is present in fibrotic areas without pancreatic atrophy or lipomatosis. The presence of chronic inflammatory lesions characterized by the destruction of exocrine parenchyma and fibrosis and in the later stages the endocrine parenchyma, indicate a chronic pancreatitis. In completion of the experimental model of the DBTC-induced acute interstitial pancreatitis in rats, the described late fibrotic effects on rat pancreas may be used as an experimental model of chronic pancreatitis.
总之，除了急性间质性胰腺炎外，有机锡化合物二丁基锡（DBTC）还可诱导大鼠胰腺纤维化。在用6或8mg/kg DBTC对大鼠进行单次静脉注射治疗后2至36周，对胰腺纤维化的病程进行了研究。DBTC诱导的胰腺纤维化与其他急性胰腺炎实验模型不同。纤维化区域存在大量单核细胞浸润，无胰腺萎缩或脂肪沉积。以腺泡实质破坏、纤维化以及后期内分泌实质破坏为特征的慢性炎症病变的存在，提示为慢性胰腺炎。作为大鼠DBTC诱导的急性间质性胰腺炎实验模型的补充，所描述的DBTC对大鼠胰腺的晚期纤维化作用可作为慢性胰腺炎的实验模型。
