Pancreatic exocrine secretion in acute experimental pancreatitis.
Pancreatic exocrine secretion in acute experimental pancreatitis.
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急性实验性胰腺炎的胰腺外分泌分泌。
DOI：
10.1016/0016-5085(90)90633-c
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发表时间：
1990
期刊：
影响因子：
29.4
通讯作者：
Grendell,JH
中科院分区：
文献类型：
--
作者：
Niederau,C;Niederau,M;Lüthen,R;Strohmeyer,G;Ferrell,LD;Grendell,JH
目前对急性胰腺炎患者胰腺外分泌功能知之甚少，特别是在疾病的早期阶段。因此，本研究在四种不同的急性胰腺炎模型中评价了体内和体外的基础和刺激胰腺分泌，这些模型反映了其严重程度的临床谱：（a）在大鼠中通过每小时间隔七次IP注射50 μg/kg雨蛙肽诱导的水肿性胰腺炎;（B）通过以每小时间隔七次IP注射50 μg/kg雨蛙肽在小鼠中诱导的水肿性胰腺炎伴细胞坏死;（c）通过喂食补充乙硫氨酸的胆碱缺乏饮食66小时在小鼠中诱导出血性胰腺炎;和（d）通过将0.6 mL 5%牛磺胆酸钠逆行输注到胰管中在大鼠中诱导出血性胰腺炎。在胰腺炎发作后的不同时间进行体内和体外分泌研究。结果表明，在所有四种动物模型中，在急性胰腺炎发作后，胰腺外分泌部逐渐变得对胆囊收缩素刺激具有抵抗性。胆缩素刺激的分泌几乎被废除在体内和体外在最大的组织学损伤的时候。体内基础分泌也减少。在体外有一个增加的基础释放淀粉酶从孤立的腺泡，这不是由管腔分泌的增加，但从受损细胞的酶释放。急性实验性胰腺炎后分泌功能改善的时间进程取决于胰腺炎的严重程度。重症坏死性胰腺炎比水肿性胰腺炎分泌能力的恢复需要更长的时间。然而，分泌功能的最终解决是显着的，特别是在严重出血性胰腺炎。在所有四种模型中，在形态学改变完全解决之前，分泌能力就与正常情况难以区分。目前的实验数据表明，胰腺分泌，特别是胰腺分泌胆囊收缩素的反应，也可能减少急性胰腺炎发病后的早期患者。
Little is known about exocrine pancreatic secretory function in patients with acute pancreatitis, in particular during the early phase of the disease. Therefore, this study evaluates basal and stimulated pancreatic secretion in vivo and in vitro in four different models of acute pancreatitis which reflect its clinical spectrum of severity: (a) edematous pancreatitis induced in the rat by seven IP injections of 50 μg/kg cerulein at hourly intervals; (b) edematous pancreatitis with cellular necrosis induced in the mouse by seven IP injections of 50 μg/kg cerulein at hourly intervals; (c) hemorrhagic pancreatitis induced in the mouse by feeding an ethionine-supplemented, choline-deficient diet for 66 hours; and (d) hemorrhagic pancreatitis induced in the rat by retrograde infusion of 0.6 mL 5% sodium taurocholate into the pancreatic duct. Secretory studies were performed in vivo and in vitro at various times after onset of pancreatitis. The results show that the exocrine pancreas gradually became resistant to cholecystokinin stimulation after the onset of acute pancreatitis in all four animal models. Cholecystokinin-stimulated secretion was almost abolished in vivo and in vitro at the time of maximal histological damage. In vivo basal secretion was also reduced. In vitro there was an increase in basal release of amylase from isolated acini that was not caused by an increase in luminal secretion but by enzyme release from damaged cells. The time course of improvement of secretory function after acute experimental pancreatitis depended on the severity of the pancreatitis. Recovery of secretory capacity took longer after severe necrotizing pancreatitis than after edematous pancreatitis. However, the ultimate resolution of secretory function was remarkable, in particular after severe hemorrhagic pancreatitis. In all four models, secretory capacity became indistinguishable from normal before the morphological alterations had completely resolved. The present experimental data suggest that pancreatic secretion, and particularly pancreatic secretory response to cholecystokinin, may also be reduced in patients early after the onset of acute pancreatitis.