L-精氨酸诱导大鼠暴发型胰腺炎模型建立

The rat model of fulminate acute pancreatitis induced by L-arginine

目的建立L-精氨酸诱导大鼠暴发性胰腺炎动物模型。方法用20％L-精氨酸（450mg，120mg／100g大鼠体重）序贯腹腔和皮下给药建立大鼠暴发性胰腺炎模型。结果实验大鼠胰腺有广泛变性、坏死，48h达高峰，胰腺病理评分13．21±3．02；大鼠6—48h死亡率为56．67％；血清淀粉酶和脂肪酶显著升高，皆12h达到高峰，分别是（4120±759）、（1490±354）U／L；肺功、肝脏酶学和肾功能皆有显著性改变，48hPaO2（78．24±3．56）mmHg（1mmHg=0．133kPa），48h谷丙转氨酶（224．67±4．73）U／L，12h肌酐（94．53±13．49）μmol／L；肺、肝、肾分别有轻到重度病理改变。

Objective To establish the rat model of L-arginine-induced fulminate acute pancreatitis （FAP）. Methods FAP in Wistar male rats was induced by intraperitoneal injection of 20% L-Arg of 450 mg/100 g body weight and subcutaneous injections of 20% L-Arg of 120 mg/100 g body weight in an interval of 2 h. Results The extensive pancreatic necrosis and degeneration appeared in pancreatic exocrine tissue. Histological scores of pancreas were maximal to 13.21 ± 3.02 at 48 h in rats with FAP. The mortality of rats with FAP was 56.67% during 6-48 h. The levels of serum amylase and lipase were significantly increased and reached the peak [ （4120 ±759） and （1490 ±354） U/L respectively] at 12 h. The levels of serum PaO2, ALT and Cr were significantly changed. PaO2 was （78.24 ±3.56 ） mmHg at 48 h, ALT （ 224.67 ±4.73 ） U/L at 48 h, and Cr （94.53 ± 13.49 ） μmol/L at 12 h, respectively. Histological scores of lung and liver were Ⅱ -Ⅲ degrees, and those of kidney showed Ⅰ - Ⅱ degrees. Conclusion The model of FAP is induced by L-Arg in rats.