Hegyi Péter, Rakonczay Zoltán, Sári Réka, Góg Csaba, Lonovics János, Takács Tamás, Czakó László
University of Szeged, Faculty of Medicine, First Department of Medicine, PO Box 469, H-6701, Szeged, Hungary.
World J Gastroenterol. 2004 Jul 15;10(14):2003-9. doi: 10.3748/wjg.v10.i14.2003.
Despite medical treatment, the lethality of severe acute pancreatitis is still high (20-30%). Therefore, it is very important to find good animal models to characterise the events of this severe disease. In 1984, Mizunuma et al. developed a new type of experimental necrotizing pancreatitis by intraperitoneal administration of a high dose of L-arginine in rats. This non-invasive model is highly reproducible and produces selective, dose-dependent acinar cell necrosis. Not only is this a good model to study the pathomechanisms of acute necrotizing pancreatitis, but it is also excellent to observe and influence the time course changes of the disease. By writing this review we illuminate some new aspects of cell physiology and pathology of acute necrotizing pancreatitis. Unfortunately, the reviews about acute experimental pancreatitis usually did not discuss this model. Therefore, the aim of this manuscript was to summarise the observations and address some challenges for the future in L-arginine-induced pancreatitis.
尽管进行了医学治疗,重症急性胰腺炎的致死率仍然很高(20%-30%)。因此,找到合适的动物模型来描述这种严重疾病的发病过程非常重要。1984年,水沼等人通过向大鼠腹腔注射高剂量L-精氨酸,开发出一种新型实验性坏死性胰腺炎。这种非侵入性模型具有高度可重复性,并能产生选择性、剂量依赖性的腺泡细胞坏死。这不仅是研究急性坏死性胰腺炎发病机制的良好模型,也是观察和影响疾病病程变化的理想模型。通过撰写本综述,我们阐明了急性坏死性胰腺炎细胞生理学和病理学的一些新方面。遗憾的是,关于急性实验性胰腺炎的综述通常未讨论该模型。因此,本手稿的目的是总结相关观察结果,并探讨L-精氨酸诱导的胰腺炎未来面临的一些挑战。