Acute Hemorrhagic-necrotizing Pancreatitis Research Articles

Therapeutic Management of Trauma-related Acute Pancreatitis in a Heart Transplant Recipient

Acute pancreatitis is a very mortal disease, mortality that increases even more in patients with cardiac transplantation. Medical-surgical management of acute pancreatitis in transplanted patients can make the difference between life and death. The aim of this paper was to highlight the severity of this pathology especially because the patient is immunosuppressed after cardiac transplant. A case of 36-year-old man, known with heart transplant, immunosuppressive treatment and chronic renal frailer, who arrived to Emergency Department, with severe abdominal pain and abdominal distention which started after a traumatic accident. Investigations revealed acute pancreatitis that needed three surgeries for acute necrotic hemorrhagic pancreatitis, acute bleeding, left subphrenic abscess and intensive care therapy. With favorable postoperative evolution, patient is discharged 60 days later He�s follow up reveled no gastrointestinal or cardiac complication with an improved quality of life.

RETRACTED: MiR-21-3p aggravates injury in rats with acute hemorrhagic necrotizing pancreatitis by activating TRP signaling pathway

To evaluate the expression and effect of miR-21-3p in pancreas and lung injury of acute hemorrhagic necrotizing pancreatitis (AHNP) rats. AHNP rat model was constructed via retrograde injection of 5% sodium taurocholate into biliary pancreatic duct. Then rats were divided into normal, sham, AHNP, mimics negative control (NC), miR-21-3p mimics, inhibitors NC, miR-21-3p inhibitors, miR-21-3p mimics + phosphate buffer saline and miR-21-3p mimics + Gd3+ groups (N = 10 in each group). The expression of miR-21-3p, TRP signaling pathway factor, apoptosis related protein and histology were studied in pancreatic and lung tissues. Apoptosis of pancreatic acinar cells was detected. Oxidative stress indexes were detected in lung tissues. The level of PaO2 and PaCO2 and the expression of amylase, lipase and inflammatory factors were detected in blood. Compared with normal and sham groups, the miR-21-3p expression was increased in pancreatic and lung tissues of AHNP rats. MiR-21-3p expression was successfully regulated. Down-regulated miR-21-3p promoted apoptosis of pancreatic acinar cells and restored its function in AHNP rats. Up-regulated miR-21-3p reduced the lung oxygenation function, promoted pathological damage, and aggravated oxidative stress injury in AHNP rats. Meanwhile, up-regulated miR-21-3p also promoted the expression of serum enzymes and inflammatory factors, and activated TRP signaling pathway in AHNP rats. And miR-21-3p aggravated pancreatitis and lung injury by activating transient receptor potential (TRP) signaling pathway in AHNP rats. miR-21-3p promoted the pancreatic injury, inhibited apoptosis of necrotic acinar cells and aggravated lung oxidative stress injury by activating TRP signaling pathway in AHNP rats.

Forensic Pathology Analysis of 363 Sudden Death Cases in Yunnan Province.

To study the epidemiological and pathological features of sudden death （SD） in Yunnan Province and to provide scientific evidence for prevention and forensic identification of sudden death. Totally 363 SD cases were collected from the autopsies between 2009 and 2017 in the Forensic Centre of Kunming Medical University. The related factors such as etiology, age, inducing factor, time interval between the onset of disease and death, morbidity season and pathological change were retrospectively analysed. The incidence of SD in males was significantly higher than that of females. The peak age was ≥35-55 years. The mortality rate was relatively high within 6 h after the onset of disease. The season order with descending number of deaths was spring, summer, winter and autumn. The top ten causes of SD were coronary heart disease, sudden unexplained death （SUD）, cerebral hemorrhage, acute hemorrhagic necrotic pancreatitis, aortic dissection rupture, cardiomyopathy, pneumonia, pulmonary thromboembolism, amniotic fluid embolism and allergy. Exercise, infusion, surgery, medication and minor injury were the most common predisposing factors of sudden coronary death. Consciousness disorder or coma, chest pain or chest tightness, and abdominal pain were the most common premortem symptoms of sudden coronary death. The SD is more common in middle-aged males, which is the key population for the prevention of SD. For the forensic identification and prevention of SD, the attention on SUD should be paid.

Chloroquine relieves acute lung injury in rats with acute hemorrhagic necrotizing pancreatitis

SummaryThis study preliminarily investigated the mechanism by which chloroquine (CQ) relieves acute lung injury (ALI) complicated in acute hemorrhagic necrotizing pancreatitis (AHNP). Sixty male Wistar rats were randomized into sham-operated group (group A, n=10), AHNP group (group B, n=10), L-arginine-treated group (group C, n=10), L-N-nitro-L-arginine methyl ester (NAME)-treated group (group D, n=10), CQ-treated group (group E, n=10) and CQ+L-NAME-treated group (group F, n=10). TLR4 expression was measured by using real time-PCR and Western blotting respectively. The results showed that, in the group B, the expression of TLR4 and the levels of TNF-α and IL-6 in the lungs were significantly increased, and the nitric oxide (NO) concentration was reduced, as compared with those in the group A (P<0.05 or P<0.01). Lung injury was aggravated with the increased expression of TLR4. When the inhibitor and stimulator of TLR4, namely L-Arg and L-NAME, were added respectively, lung injury was correspondingly relieved or aggravated (P<0.05 or P<0.01). In the group E, TLR4 expression was substantially lower and NO concentration higher than those in the group B (P<0.05 or P<0.01). However, in the group F, NO concentration was markedly decreased, and the inhibitory effect of CQ on TLR4 expression and the relief of lung injury were weakened when compared with those in the group E (P<0.05 or P<0.01). It was concluded that TLR4 may play an important role in the pathogenesis and development of ALI complicated in AHNP. CQ could relieve ALI by decreasing the TLR4 expression and increasing the NO release.

Blocking abdominal lymphatic flow attenuates acute hemorrhagic necrotizing pancreatitis -associated lung injury in rats

BackgroundAcute hemorrhagic necrotizing pancreatitis (AHNP) is a severe acute inflammatory of pancreas that can lead to extrapancreatic organ disfunction. The lung and intestine is the most common involved organs, and abdominal lymphatic flow may contribute to AHNP- associated organ injury. In this study, we investigated the impact of thoracic duct ligation and drainage on lung and intestine injury in rats with AHNP.MethodsThirty-two male Wistar rats were randomly divided into 4 groups: sham operation group, AHNP group, AHNP + ligation group and AHNP + drainage group. Rat AHNP model was induced by retrograde injection of 3.5% sodium deoxycholate into the biliopancreatic duct, and the sham operation group was injected only with saline. In AHNP + ligation group and AHNP + drainage group, thoracic duct was ligated or drainaged before model induction. At 6 h after model induction, the bronchoalveolar lavage fluid (BALF) were collected for determination of tumor necrosis factor-alpha (TNF-alpha), and the tissues of lung, intestine and pancrease were harvested individually for pathohistological evaluation and the myeloperoxidase (MPO) activity determination. In addition, the activity of serum amylase and diamine oxidase (DAO) was determined in each group.ResultsThe pathohistological damage and MPO of lung, intestine and pancrease, TNF-alpha of BALF, serum amylase and DAO were all increased in AHNP group compared to those in sham operation group (P < 0.05). In AHNP + ligation group, the pathohistological damage and MPO of lung and TNF-alpha of BALF were reduced, but the pathohistological damage and MPO of intestine and pancrease were increased compared with AHNP group (P < 0.05), however the activity of serum amylase and DAO was no changed. In AHNP + drainage group, the pathohistological damage and MPO of lung, intestine and pancrease, TNF-alpha of BALF, serum amylase and DAO were all reduced compared to those in AHNP group (P < 0.05).ConclusionsOur finding suggest that thoracic duct ligation can reduce neutrophil infiltration and TNF-alpha release and then attenuates lung injury in rats with AHNP, but aggravates the injury of intestine and pancrease. While thoracic duct drainage attenuates the injury of lung, intestine and pancreaseat the same time in rats with AHNP.

Effects of alpha 1-acid glycoprotein on acute pancreatitis and acute lung injury in rats.

alpha 1-Acid glycoprotein (AAG), a highly negatively charged glycoprotein, well known for its capillary stabilizing effect, was tested in rat models of acute edematous pancreatitis, acute hemorrhagic-necrotizing pancreatitis, and acute respiratory distress syndrome (ARDS). In cerulein-elicited edematous pancreatitis AAG improved histological alterations at 200 mg/kg i.v. and plasma amylase activity at 1800 or 4200 mg/kg i.v. All other parameters (edema, plasma lipase) were not affected in a biologically relevant manner. In glycodeoxycholic acid-induced hemorrhagic-necrotizing pancreatitis AAG was without effect on parameters measured (plasma amylase, plasma lipase activity, histological scores) at 1800 or 4200 mg/kg i.v. At the extremely high dose of 1500 mg/kg i.v. plasma amylase and lipase levels were decreased. In lipopolysaccharide-mediated ARDS, AAG was tested at 50, 200 or 600 mg/kg i.v. AAG, but also the placebo formulation decreased the myeloperoxidase content in the bronchoalveolar lavage fluid. Histological alterations were improved by AAG, however, not by the placebo formulation. Lung water content was not significantly influenced by AAG, whereas Evans blue extravasation was significantly diminished by all three doses of AAG. It is concluded that the edematous pancreatitis is the first in vivo condition with increased extravascular fluid accumulation, in which AAG is not effective. Based on data presented here and literature data, there is evidence for a beneficial effect of AAG in acute lung injury.

Effect of bone mesenchymal stem cells on toll-like receptor 2/4 expression in lungs of rats with acute hemorrhagic necrotizing pancreatitis

Objective To investigate the effect of bone mesenchymal stem cells on Toll-like receptors (TLR) 2/4 expression in the lungs of rats with acute hemorrhagic necrotizing pancreatitis (AHNP). Methods Seventy SD male rats were randomly divided into sham-operation group (n=10), AHNP group(n=30) and MSCs-treated group(n=30). Masc rate of BMSCs with surface mark were measured by flow cytometer. TLR2/4mRNA expression in the the lung were measured by RT-PCR, and The ratio of Wet/dry and lung histological changs were observed. Results TLR2/4 mRNA could be detected in the lungs with low values in sham-operation group, markedly increased in 3 h, and peaked in 12 h in AHNP group (P＜0.05). Lung injuries were aggravated and the levels of TNF-α in the lung were increased (P＜0. 05) . Treatment with MSCs could effectively inhibit TLR2/4 mRNA expression and relieve lung injuries. The levels of TNF-α in the lung were decreased (P＜0.05). Conclusions The expression of TLR2/4 mRNA is increased in the lungs in AHNP and the lung injuries are aggravated. MSCs could markedly inhibit TLR2/4 mRNA expression in the lungs in AHNP, which would lead to relief of lung injury. Key words: Toll-like receptor; Acute hemorrhagic necrotizing pancreatitis; Lung; BMSCs

Clinical and pathologic characteristics of pancreatic necrosis in critically ill children.

Pancreatic damage in critically ill patients is associated with the progressive failure of multiple organs, but little is known about its clinical characteristics. At present, no guidelines are available for the diagnosis and management of pancreatic damage. This study was undertaken to analyze the clinical and pathologic characteristics of pancreatic necrosis in critically ill children, and to find some biological markers of pancreatic damage or pancreatic necrosis. We retrospectively reviewed the clinical data, laboratory results, and autopsy findings of 25 children, who were admitted to Hunan Children's Hospital, China from 2003 to 2009, and died of multiple organ failure. The autopsy revealed pancreatic necrosis in 5 children, in whom sectional or gross autopsy was performed. The 5 children had acute onset and a fever. Two children had abdominal pain and 2 had abdominal bulging, flatulence and gastrointestinal bleeding. Four children had abnormal liver function, characterized by decreased albumin and 3 children had elevated level of C-reactive protein (CRP). B-ultrasonography revealed abnormal acoustic image of the pancreas in all children, and autopsy confirmed pancreatic necrosis, which may be associated with the damage of the adrenal gland, liver, lung, heart, spleen, kidney, intestine, thymus, mediastinal and mesenteric lymph nodes and other organs. Children 1 and 2 died of acute hemorrhagic necrotizing pancreatitis (AHNP); children 3-5 died of multiple organ dysfunction syndrome (MODS) due to pancreatic necrosis. Pancreatic damage or pancreatic necrosis in critically ill children is characterized by acute onset, severity, short course, multiple organ damage or failure. It may be asymptomatic in early stage, and easy to be ignored.

Research on the pancreatic injury after autologous liver transplantation in rats.

Objective To investigate the causes of pancreatic injury after autologous liver transplantation in rats. Methods Forty-two SD rats were randomly divided into post autologons liver transplantation 1-hour group, 6-hour group, 12-hour group, 24-hour group, 48-hour group, 72-hour group and sham group (6 rats per group). The plasma concentrations of amylase and lipase were measured to assess pancreatic exocrine function. The histomorphological changes of pancreatic tissue were studied under optical and electron microscopes. All data were analyzed via one-way ANOVA. Results The plasma concentrations of amylase and lipnse in post autologous liver transplantation 1-hour group were significantly higher than those in sham group, and they gradually increased as time passed by. The plasma concentrations of amylase and lipase reached peak at hour 48, after which they decreased gradually. There was a significant difference in the plasma concentration of amylase and lipase among the 7 groups (F = 538.622,489.417, P < 0.05). Acute edematous pancreatitis was observed 1 hour after autolognus liver transplantation, and acute hemorrhagic necrotic pancreatitis was observed 6 hours after transplantation. The degree of injury reached a peak 48 hours after transplantation. The number of mitochondria was increased, and endoplasmic reticulum and Golgi apparatus were swollen 1 hour after transplantation, and the area, perimeter, specific surface area and mean gray value of mitochondria were (312±40) mm2, (80.3±3.8)mm, 0.332±0.039 and 113±11, respectively. As time passed by, the injury of the pancreatic cells was aggravated and autophagosomes were observed. The injury was most severe 48 hours after transplantation, and the area, perimeter, specific surface area and mean gray value of mitochondria were (466±7) mm2, (108.8±3.7) mm, 0.298±0.009 and 195±12, respectively. There were significant differences in the specific surface area and mean gray value among all the groups (F = 9.322, 76.560, P < 0.05). Conclusion The pancreatic injury after autologous liver transplantation is related to the energy metabolism of the pancreatic cells induced by hypoxia. Key words: Liver transplantation; Pancreas; Injury. Morphology; Rats

Establishment of animal model of acute lung injury induced by pancreatitis associated ascetic fluid in rats

Objective To explore the animal model of acute lung injury induced by pancreatitis associated ascetic fluid in SD rats and its significance.Methods Rats were induced with acute hemorrhagic necrotic pancreatitis(AHNP)to create PAAF.The animal model of acute lung injury in rats was established by injection of PAAF into their abdominal cavity.Respiratory frequency,Artery blood gas analysis,peripheral blood white blood cell count,serum amylase,and the change of structure of pancreas and lungs were observed.Results After injection,the respiratory frequency and peripheral white blood cell count in rats was higher,and the level of PaO2 decreased obviously and that of the PaCO2 increased significantly.The typical pathological changes of lung injury were found.Morphological examination demonstrated that a great deal of inflammatory cell infiltrated in the alveoli and interstitial tissue,and interstitial edema occurred in the lungs.The changes of structure of pancreas were not obvious,only tissue edema and inflammatory cell occurred.Conclusion The animal model of acute lung injury induced by PAAF was established successfully.The pathological changes of pancreas of rats induced by PAAF are slight,which suggests that this animal model can mask the affect of pancreatic pathological changes to lung,so as to provide a simple studying background for the study of pathogenesis of acute lung injury. Key words: Pancreatitis; Ascetic fluid; Lung injury; Animal model; Pathology

Phlegmasia cerulea dolens as a complication of a severe form of acute hemorrhagic-necrotizing pancreatitis

Phlegmasia cerulea dolens is an extreme form of deep venous thrombosis with a proximal localization of the blockage, most frequently in the ileofemoral area. Symptoms are graded as follows: swelling of the entire extremity, pain, and cyanosis. This form of the disease is rare, occurring most frequently in the terminal stage of malignancies. Diagnosis of phlegmasia usually causes no problems because the proper diagnosis is usually revealed during clinical examination and confirmed by imaging techniques. The authors present a case report of phlegmasia cerulean dolens and discuss the options for treatment.

Role of nitric oxide in Toll-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats

To investigate the role of nitric oxide (NO) in Toll-like receptor 2 (TLR2)/4mRNA expression in livers of acute hemorrhagic necrotizing pancreatitis (AHNP) rats. One hundred and ten SD male rats were randomly divided into sham-operated group (n=10), AHNP group (n=30), chloroquine (CQ)-treated group (n=30) and L-Arg-treated group (n=40). TLR2/4mRNA expression in the liver of AHNP rats was measured by RT-PCR. Expression of TLR2/4mRNA could be detected in the liver of AHNP rats in sham-operated group (0.155E-5+/-0.230E-6 and 0.115E-2+/-0.545E-4), but was markedly increased at 3 h in AHNP group (0.197E-2+/-0.114E-3 and 0.175+/-0.349E-2) peaking at 12 h (0.294E-2+/-0.998E-4 and 2.673+/-2.795E-2, P<0.01). Hepatic injuries were aggravated, TNF-alpha concentration in the liver was increased and NO concentration was decreased (P<0.05 or P<0.01). When TLR2/4mRNA expression was inhibited by CQ (3 h: 1.037E-4+/-3.299E-6 and 0.026+/-3.462E-3; 6 h: 1.884E-4+/-4.679E-6 and 0.108+/-6.115E-3; 12 h: 2.443E-4+/-7.714E-6 and 0.348+/-6.807E-3; P<0.01), hepatic injuries were relieved, NO concentration in the liver was increased and TNF-alpha concentration was decreased (P<0.05 or P<0.01). When rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the liver could be effectively inhibited (50 mg-T: 0.232E-2+/-0.532E-4 and 0.230+/-6.883E-3; 100 mg-T: 0.210E-2+/-1.691E-4 and 0.187+/-0.849E-2; 200 mg-T: 0.163E-2+/-0.404E-4 and 0.107+/-0.195E-2; 400 mg-T: 0.100E-2+/-0.317E-4 and 0.084+/-0.552E-2; P<0.01) and hepatic injuries were relieved. At the same time, NO concentration in the liver was markedly increased and TNF-alpha concentration was decreased (P<0.05 or P<0.01). The expression of TLR2/4mRNA is increased and hepatic injuries are aggravated in the liver of AHNP rats. TLR2/4mRNA gene expression in the liver of AHNP rats can be markedly inhibited by NO, leading to the relief of hepatic injuries.

Effects of IL-10 on intrahepatic expression of Bcl-2 and Bax and hepatocyte apoptosis in rats with acute hemorrhagic necrotizing pancreatitis

目的 探讨IL-10对急性坏死性胰腺炎(ANP)肝损害大鼠肝细胞凋亡、Bcl-2、Bax表达的影响.方法采用5%牛磺胆酸钠逆行胆胰管注射建立大鼠ANP肝损害模型,随机分成3组:30只大鼠作为正常对照组,IL-10静脉注射治疗组30只,急性坏死性胰腺炎组30只,观察肝细胞凋亡、Bcl-2、Bax表达变化,肝、胰腺组织病理改变.结果建立ANP模型后6 h、12 h、24 h,Bcl-2表达下降,Bax表达增高,伴有肝细胞凋亡数增高,IL-10治疗后,IL-10组Bcl-2表达增强,Bax表达降低,伴有肝细胞凋亡减少,肝、胰腺组织损害也相应减轻.结论肝细胞凋亡、Bcl-2、Bax表达参与ANP发病机制,在急性坏死性胰腺炎早期给予IL-10对减轻肝脏、胰腺病变程度,改善预后可能是有益的。

Effects of Octreotide on Lipid Peroxidation in Pancreas and Plasma in Acute Hemorrhagic Necrotizing Pancreatitis in Rats

Background: The therapeutic effects of octreotide in acute hemorrhagic necrotizing pancreatitis (ANP) have always been considered to be due to the inhibition of the exocrine pancreatic secretion in order to reduce pancreatic autodigestion. In this experimental study we analyzed whether octreotide has also antioxidative effects on acute pancreatitis. Methods: 40 male Wistar rats were randomized into four groups (n = 10). Group 1 underwent a laparotomy. Groups 2–4 received an injection of natrium taurocholate into the pancreatic duct to induce acute pancreatitis. One hour later group 2 was injected 1 ml NaCl solution intraperitoneally, while groups 3 and 4 received 0.1 or 0.2 mg octreotide, respectively. The severity of ANP was examined histologically. The lipid peroxide level as well as the activity of glutathione peroxidase and superoxide dismutase were measured in plasma and pancreatic tissue samples. Results: High-dose octreotide decreased the lipid peroxide level in plasma (2.1 ± 0.53 vs. 4.69 ± 1.35 nmol/l; p < 0.05) and pancreatic tissue samples 4.67 ± 1.37 vs. 13.20 ± 2.93 nmol/ml; p < 0.05) compared to the pancreatitis control group. Low-dose octreotide, however, did not reduce lipid peroxidation. Conclusion: Octreotide seems to have a dose-dependent antioxidative effect in natrium taurocholate-induced pancreatitis in rats.

The potential of HBOC in acute pancreatitis.

Acute pancreatitis is still an important problem when it progresses from the self limiting mild edematous to the more severe hemorrhagic necrotizing form. Mortality can reach 40% in severe necrotizing pancreatitis [1]. Disturbed microcirculation is a crucial effect in the cascade from self-limiting disease with preserved microcirculation to the often fatal form of acute hemorrhagic-necrotizing pancreatitis. After onset of acute pancreatitis, preservation or improvement of pancreatic microcirculation could possibly prevent further progression, tissue necrosis and infectious complications. This, in turn, may lead to a lower morbidity and mortality.

Experimental research on production and uptake sites of TNFalpha in rats with acute hemorrhagic necrotic pancreatitis.

AIM:To determine the site of production and uptake of tumor necrotic factor alpha (TNFalpha),and evaluate the relationship between serum TNFalphaand pla-sma endotoxin (ET) in rats with acute hemorrhagic necrotic pancreatitis (AHNP).METHODS:Sprague Dawley rats were divided into AHNP group and control group (n = 12). AHNP model was induced by retrograde injection of 5% sodium taurocholate via pancreatic bile duct. The blood samples were obtained through portal vein 2 and 6 hours after the operation.RESULTS:The contents of TNFalphain portal vein were increased rapidly in the development of AHNP. They were lower in hepatic vein (280.59 plus minus 20.02) and femoral artery (310.82 plus minus 7.97) than in portal vein (354.91 plus minus 25.50) (P < 0.05), and higher in femoral artery than in hepatic vein 6 hours after the operation (P <0.05). TNFalphalevel in plasma was increased significantly when ET level in portal vein showed no increase. CONCLUSION: Pancreas, spleen, liver, intestinal tract and lung are the main organs to produce TNFalpha, and liver is also an important site for TNFalphauptake in the development of AHNP. Plasma endotoxin is not a trigger for TNFalpharelease in rats with AHNP.

A histopathological study of pancreatic lesions after chronic administration of methamphetamine to rats.

The effects of chronic administration of methamphetamine on pancreatic tissues were histopathologically studied in experimental models. Methamphetamine (1 ml/kg body weight/day) was subcutaneously injected into 14 five-week-old male Wistar Kyoto rats (WKY) for 12 weeks. Age and sex matched 5 WKY rats served as controls. With light microscopy, some scattered edematous lesions and moderate vacuolization were demonstrated in the pancreas of 8 of the methamphetamine treated rats. However, in 4 of the rats, severe regional hemorrhage, partial acinal cell necrosis, destruction of the acinal cells, neutrophile infiltration, interstitial vessel dilatation, interstitial edema and fatty cell invasion were observed after the injections of methamphetamine. In 2 other animals, fibrosis and cirrhosis-like lesions with destruction and degeneration of the acinal cells were observed the small vessels had a slight degeneration of the endothelial cells. In the control animals, no lesions, except for some edematous lesions were found. In all cases, there were no nesidioblastosis-like lesions or necrosis of the Langerhans's islets. In the immunohistochemical study using anti- alpha 1-chymotrypsin antibody, more positive reactive cells were demonstrated among the interstitial and inter acinal cells, both in number and degree, in the methamphetamine treated rats. In addition to the animal model, there were 4 autopsy cases of sudden death in chronic methamphetamine abusers. The autopsies demonstrated a severe acute necrotic hemorrhagic pancreatitis, with only scattered slight hemorrhaging in the brain and lungs. These findings indicate that chronic administration of methamphetamine to rats evoked significant changes in pancreatic tissues including some degeneration of the endothelial cells of the small vessels in this hypoxia-vulnerable organ.

The effect of blood-purifikation in the initial treatment of severe acute hemorrhagic-necrotizing pancreatitis of the rat

The effect of blood-purifikation in the initial treatment of severe acute hemorrhagic-necrotizing pancreatitis of the rat

Acute experimental hemorrhagic-necrotizing pancreatitis induced by feeding a choline-deficient, ethionine-supplemented diet. Methodology and standards.

The present work evaluates the methodology and standards of acute hemorrhagic-necrotizing pancreatitis induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet to mice. The diet model appears to be a good approximation of severe necrotizing human pancreatitis. Both the gross and histological appearance of the pancreatic and peripancreatic inflammation as well as the clinical and biochemical course of diet-induced pancreatitis resemble human disease. By limiting the period of feeding the diet, one can control the mortality at any desired level between 0 and 100%. Ascites, acidosis, hypoxia and hypovolemia occur in this model as well as in human pancreatitis. The time course of the morphological and biochemical alterations have extensively been studied and are, thus, well defined in this model. Despite the differences in pathogenesis of pancreatitis induced in this model versus human disease, the experimental pancreatitis and clinical pancreatitis share several pathophysiologic features. Therefore, the model is suitable to study pathophysiologic aspects of this disease. The diet model is particularly well suitable to study the potential for new therapeutic substances. The small size of the animals used, however, is a limitation for the evaluation of surgical procedures and of new diagnostic tools. Several pitfalls and problems have to be considered in order to obtain valuable data. The amount of injury produced by the CDE diet depends critically on sex, age and weight of the mice. Special care has to be taken to guarantee that the intake of the CDE diet is identical between different experimental groups. Therefore, each set of experiments needs to include a separate control group of mice which receive the CDE diet without any other special treatment. The potential benefit of an experimental therapy can be assessed by measuring survival, various biochemical and histological features, and alterations in hematocrit, pH and blood gases.

Surgical indications in acute pancreatitis

The indication for surgery in acute hemorrhagic necrotizing pancreatitis (AHNP) depends on the severity of the disease and the clinical course. Both factors must be determined daily, based on clinical and laboratory data. CAT-scan does not contribute much to indication. An early operation is necessary if despite an optimal intensive care septic symptoms and signs persist and renal and respiratory failure occur. Surgery is indicated 2-3 weeks after onset of AHNP if septic complications (re)-occur. A close follow up is mandatory.