垂体腺苷酸环化酶激活肽在急性胰腺炎发病机制中的作用

【作者】 陈友岱；

【导师】 周总光；

【作者基本信息】 四川大学 ， 外科学， 2004， 博士

【摘要】 摘要:脑肠肽垂体腺苷酸环化酶激活多肽(Pituitary adenylate cyclase activating polypeptide,PACAP)在急性胰腺炎(acute pancreatitis,AP)发病机理和治疗中的作用尚不清楚,为此,本实验观察外源性PACAP对正常大鼠胰腺、实验性AP病程的影响。5～30μg/kg的PACAP可促使血清淀粉酶轻微增高、胰腺水肿形成(胰腺干湿比:实验组23.88±2.532%～25.86±1.974%vs正常组29.21±5.657%)、炎性细胞浸润、腺泡细胞空泡化、部分病例可见脂肪坏死和实质坏死灶。15μg/kg和30μg/kg PACAP可加重蛙皮缩胆囊肽诱发的AP,胰腺组织水肿更明显(胰腺干湿比:实验组13.45±2.045%～17.66±4.652%vs蛙皮缩胆囊肽组21.83±3.013%,P<0.05),血清淀粉酶增高,出现腹水、胰腺出血、脂肪坏死和实质坏死,腺泡细胞明显空泡化。5μg/kg和10μg/kg PACAP对牛磺胆酸钠诱发的急性出血坏死性胰腺炎病程的影响有所不同,可稍减轻胰腺水肿(胰腺干湿比:实验组19.18±2.102%～20.87±5.597%vs牛磺胆酸钠组17.52±1.505%;下同)、降低血清淀粉酶(1986.91±710.97～2944.33±1182.47 IU/L vs3690.87±2277.99IU/L,P<0.05),而胰腺出血和坏死加剧。除蛙皮缩胆囊肽诱发的AP外,其余各组机能毛细血管密度(Functional capillary density,FCD)均减少。实验结果表明,在大鼠AP发病中,PACAP有促炎性反应作用;合并使用PACAP和蛙皮缩胆囊肽可作为研究急性出血坏死性胰腺炎的新模型;蛙皮缩胆囊肽诱发的AP与牛磺胆酸钠诱发的AP对PACAP的反应可能有所不同。更多还原

【Abstract】 Pituitary Adenylate Cyclase Activating Polypeptide Aggravated Experimental Acute PancreatitisPACAP(pituitary adenylate cyclase activating polypeptide) is one kind of peptidergic transmitter, its role in the pathogenesis of acute pancreatitis remains to be elucidated. This experiment was conducted to examine the action of exogenous PACAP on rat pancreas and on the course of experimental acute pancreatitis. 5 ~ 30μg/kg of PACAP slightly increased serum amylase, induced pancreatic edema(pancreatic wet/dry weight ratio: 23.88±2.532% ~ 25.86±1.974% vs 29.21±5.657%), inflammatory cell infiltration, vacuolization of acinar cells, occasionally fatty and parenchymal necroses. 15~30μg/kg of PACAP aggravated cerulein-induced acute pancreatitis: pancreatic edema became more marked(pancreatic wet/dry weight ratio: 13.45±2. 045%~17.66±4. 652% vs 21.83 ±3. 013%, P<0.05), serum amylase higher, and ascites, pancreatic bleeding, fatty and parenchymal necroses and extensive vacuolization of acinar cells occurred. For sodium taurocholate-induced pancreatitis, 5~ 10μg/kg of PACAP mildly attenuated pancreatic edema, reduced serum amylase(1986. 91 + 710. 97~ 2944.33 + 1182.47 IU/L vs 3690. 87+2277. 99IU/L, P<0.05), while caused multifocal hemorrhage and prominent necrosis in pancreas. Except cerulein-induced pancreatitis, other groups were found to have reduced pancreatic functional capillary density(FCD). In conclusion, PACAP is proinflammatory in the pathogenesis of acute pancreatitis, PACAP plus cerulein can induce acutehemorrhagic/necrotizing pancreatitis, and the action of PACAP on cerulein-induced panceatitis possibly varied from that on sodium taurocholate-induced one.更多还原