Influence of gastrointestinal hormones on the course of acute experimental pancreatitis

The influence of exogenous administration and endogenous release of certain g.i. hormones on the course of acute experimental pancreatitis was studied. Administration of 2 g of a pellet diet every eight hours decreased survival, as did repeated s.c. administration of the cholecystokinin-analogue caerulein. Also oral administration of a trypsin inhibitor--releasing intestinal factors or hormones stimulating pancreatic enzyme synthesis and secretion--decreased survival. On the other hand repeated s.c. administration of secretin or an anticholinergic drug (Pro-Banthine), or oral administration of 0.1 N HCl every eight hours did not influence survival. At blind macroscopic evaluation, caerulein was found to cause signs of more severe disease. All pancreatic rats had increased S-amylase levels, but there was no difference between any of the groups. In peritoneal fluid, however, caerulein caused an increase in the amylase activity. The results suggest that elevated S-levels of g.i. hormones, which primarily stimulate pancreatic enzyme synthesis and secretion, are harmful in acute experimental pancreatitis.     

Pulmonary complications in fatal acute hemorrhagic pancreatitis

Morphological changes of the lung occur frequently in fatal acute hemorrhagic pancreatitis. The pulmonary alterations are independent of mechanical ventilation and therefore not due to iatrogenic damage caused by high inspired oxygen concentrations. The histological findings are similar to those seen in the so-called shock lung syndrome. The pulmonary lesion develops progressively and three stages can be separated: early, late, and final phase. The pulmonary complications in acute hemorrhagic pancreatitis may be explained by the release of mediators such as pancreatic enzymes or free fatty acids into the blood stream. In acute hemorrhagic pancreatitis a close monitoring for shock parameters is necessary. A fall in arterial Po₂ is an early indication for mechanical ventilation, including positive end-expiratory pressure.     

纳屈酮治疗大鼠急性出血坏死性胰腺炎内毒素血 症的效果

目的探讨纳屈酮治疗大鼠急性出血坏死性胰腺炎内毒素血症的效果．方法应用５０ｇ／Ｌ牛磺胆酸钠逆行胰胆管注射诱发大鼠急性出血坏死性胰腺炎（ＡＨＮＰ）模型,观察对照组、ＡＨＮＰ组及纳屈酮（ＮＴＸ）治疗组６,１２,２４ｈ大鼠血浆淀粉酶、内毒素（ＥＴ）及胰腺组织光镜和电镜下病理改变,并统计３组大鼠４８ｈ存活率结果ＡＨＮＰ组较对照组：于６,１２,２４ｈ时点血浆淀粉酶（２４０７±５１２,２８７２±４１３,３４１５±５９４,ｎｍｏｌ／ｓ）、ＥＴ（４５±２３,９３±１２,１６０±３５,ＥＵ／Ｌ）升高;ＮＴＸ组较ＡＨＮＰ组：血浆淀粉酶（１５３２±５６７,１８９５±５９４,２４８３±８１８,ｎｍｏｌ／ｓ）、ＥＴ（２８±３,２１±８,６９±９,ＥＵ／Ｌ）下降;而且光镜及电镜下,ＮＴＸ组胰腺腺胞及间质病理损害减轻．结论ＮＴＸ可通过降低ＡＨＮＰ大鼠血浆ＥＴ,而改善胰腺病理损害,降低其死亡率     

Dengue hemorrhagic fever presenting with acute pancreatitis

Acute pancreatitis is an uncommon manifestation of dengue fever. Here we present a 47 year old male with dengue hemorrhagic fever who presented with acute pancreatitis and associated hyperglycemia. To our knowledge, this is the first reported case of dengue complicated with acute pancreatitis from South Asia.     

Pancreatic and bile duct obstruction exacerbates rat caerulein-induced pancreatitis: a new experimental model of acute hemorrhagic pancreatitis

Background Pancreatic duct obstruction induces edematous but not hemorrhagic pancreatitis even when combined with maximal secretory stimulation. The aim of the present study was to test the hypothesis that pancreatic and bile duct obstruction exacerbates edematous pancreatitis induced by supramaximal secretory stimulation by caerulein. Methods In in vivo studies using rats, biliopancreatic duct ligation was combined with supramaximal stimulation of caerulein, and pancreatic histology, serum amylase level, pancreatic edema, and intrapancreatic trypsin activation were evaluated. In in vitro studies, the pancreatic acini were isolated from the rats with biliopancreatic duct ligation, and amylase secretion, intracellular trypsin activation, and acinar cell fragility were evaluated. Results Biliopancreatic duct ligation exacerbated caerulein-induced pancreatitis from edematous to hemorrhagic only when the obstruction preceded caerulein administration. The amylase secretion from the acini was inhibited, and intracellular trypsin activation and the acinar cell fragility on the supramaximal stimulation with cholecystokinin in vitro were enhanced by the preceding in vivo biliopancreatic duct obstruction. Conclusions Preceding biliopancreatic duct obstruction exacerbates caerulein-induced pancreatitis. Enhancement of intracellular trypsin activation is possibly involved in this mechanism.     

Toxic products in hemorrhagic ascitic fluid generated during experimental acute hemorrhagic pancreatitis in dogs and a treatment which reduces their effect

Toxic substances produced in hemorrhagic ascitic fluid during experimental hemorrhagic pancreatitis in dogs were investigated. An average of 394 ml of ascitic fluid was produced within 5 h after the induction of acute pancreatitis by intraductal injection of a mixture of autologous bile and trypsin. Hemorrhagic ascitic fluid was collected under sterile conditions, which was confirmed by aerobic and anaerobic culture and a Limulus test. The sterile fluid was injected intraperitoneally into mice in doses of 2 and 3 ml, and the mortality rate 72 h after injection was 66.0 and 88.4%, respectively. It contained high concentrations of pancreatic enzymes, including trypsin and esterase activity, as well as bradykinin, histamine and prostaglandin. Autopsy and histological examination of mice revealed shock with lung damage. The results suggest that hemorrhagic ascitic fluid produced in pancreatitis may be an important factor for early deaths in acute pancreatitis. When a new synthetic antiprotease (nafamstat mesilate) in a dosage of 0.2 mg was mixed with 1 ml of ascitic fluid, trypsin was not detectable, and bradykinin was reduced 1.0 ng/ml from 8.0 ng/ml, while esterase activity decreased to one tenth of its previous activity. The mortality following injection of the solution decreased to 26.7 and 80.6%, respectively. These results indicate that peritoneal lavage with a solution containing antiprotease may be an effective treatment for hemorrhagic acute pancreatitis.     

Pancreatogastrostomy in experimental acute necrotizing pancreatitis

Experimental acute necrotizing pancreatitis was induced retrogradely in dogs with sunflower oil injected intraductally. Then, a zipper was sutured into the abdominal wound. From the first postoperative day, three different treatments were started: first group: only conservative therapy was used; second group: removal of necrotized tissue and single peritoneal lavage were aplied; and third group: the necrotic part of the pancreas was marsupialized into the stomach. Through the systematic opening of the zipper, the abdominal cavity could easily be explored and the temporal course of disease could be observed in all animals. During this regular procedure, the amylase concentration and the amount of peritoneal exudate were determined. The blood amylase and glucose levels were also measured. On the first postoperative day, the amylase level and the amount of peritoneal exudate were high in all groups. The dogs of the pancreatogastrostomized group showed a dramatic decrease of the exudate and the most advantageous temporal course of the blood amylase level. The survival rate similarly was advantageous in the pancreatogastrostomized group.     

大黄对大鼠急性出血性胰腺炎的影响

目的 观察中药大黄对大鼠急性出血性胰腺炎的作用以及对胰腺外分泌功能的影响。方法 采用铃蟾肽加水浸束缚应激的方法诱导大鼠急性出血性胰腺炎，经口灌服大黄醇抽提物75～150mg／kg2次。观察血清淀粉酶、胰腺湿重、胰腺血流量及胰腺组织病理改变；并观察大黄与奥曲肽对胰液外分泌功能的影响。结果 大黄治疗组的胰腺坏死和中性粒细胞浸润明显减轻；胰腺湿重、血清淀粉酶活性和胰腺血流量均有剂量依赖性改善。胰腺炎组大鼠胰液流量、胰液蛋白含量均明显下降，胰液碳酸氢根含量没有明显改变，大黄治疗组胰液淀粉酶活性明显降低，与奥曲肽治疗组比较无统计学差异，其胰液碳酸氢根含量明显升高，奥曲肽则无此作用。结论 大黄可有效改善大鼠急性出血性胰腺炎的严重程度，与抑制胰腺炎性反应、改善胰腺血流量和抑制胰酶分泌、促进胰液引流等多靶位作用有关。     

Effect of phenylbutazone on acute hemorrhagic pancreatitis in dogs

Experiments were conducted on 24 mongrel dogs to study the effect of phenylbutazone on acute experimental pancreatitis. Necrotico-hemorrhagic pancreatitis was produced by local infiltration of autologous bile. The severity of pancreatitis was assessed by biochemical estimation and histopathological examination. Pretreatment with phenylbutazone reduced the severity of pancreatitis, both biochemically and histologically (total score 6.0 +/- 1.52 in the test group vs 8.33 +/- 1.80 in the control group; p less than 0.01).     

急性出血坏死性胰腺炎肺损伤的发病机制

0 引言急性胰腺炎(AP)的研究进展较大,然而急性出血坏死性胰腺炎(AHNP)早期容易并发多器官功能衰竭(MODS),尤其是呼吸功能障碍在75%的急性胰腺炎(AP)患者中发生,临床症状从较轻的低氧血症到成人呼吸窘迫综合征(ARDS)均可出现.AHNP 相关的 ARDS 在临床表现和病理特征上均与其他原因如败血症、严重创伤所引起的 ARDS 相似,但是其发病机制还不清楚.最新的研究表明,AP 是一种全身炎症反应综合征,其发病机制复杂,与多种因素有关.近年来经大量研究,许多学者对 AP 相关肺损伤的发病机制有了较多的认识,其中包括胰酶、补体系统和激肽的作用,循