Pathological Changes In Pancreas Research Articles

Identification of miR-126 knockdown mouse and the change of blood glucose

To detect the expression of miR-126 in different tissues and organs and the change of peripheral blood glucose in microRNA-126 knock down (miR-126 KD) mouse, and to explore the pathological significance. Total RNAs were isolated from twelve kinds of tissues and organs in wild-type mouse (WT) and miR-126 KD mouse respectively. Th en, the expression level of miR-126 was detected by real-time PCR assay. Th e levels of peripheral blood glucose and body weight of miR-126 KD mice were measured. Th e pathologic changes of pancreas and lung tissue were observed by HE staining. Compared with the WT mice, the relative expression of miR-126 in spleen, liver, muscle and lung from the miR-126 KD mice were dramatically decreased respectively (P<0.05). The level of peripheral blood glucose in the miR-126 KD mouse increased significantly at seven week and sixteen week after the birth (P<0.05). HE staining showed that the pathological structure of pancreas and liver were abnormal. The body weight of miR-126 KD mice was increased obviously from thirteen week after birth (P<0.05). Peripheral blood glucose levels in the miR-126 KD mouse were dramatically elevated, which might be related to the pathological changes in the structure of pancreas and liver. These results suggest that miR-126 may play an important role in the metabolism of blood glucose and the development of type 2 diabetes mellitus.

Simvastatin Potentiates the Antihyperglycemic, Antidyslipidimic and Antioxidative Effect of Glibenclamide on Alloxan-Induced Diabetic Rats

The aim of the current study is to investigate the effect of combination of glibenclamide; an antidiabetic drug and simvastatin; a HMG-CoA reductase inhibitor on long-term (four weeks) alloxan-induced diabetes rats (ADRs). Methods: Alloxan (120 mg/kg body weight, BW) was injected intra-peritonially (i.p.) in rats. At first alloxan (120 mg/kg BW) induced diabetic rats were treated with single dose of glibenclamide (1.2 mg/70kg BW) and simvastatin (10 mg/70kg BW) for two weeks. Then fixed dose combinations of glibenclamide (0.6 mg/70kg BW) and simvastatin (5 mg/70kg BW) were injected along with those of two drugs for four weeks. Results: At first it was found that glibenclamide reduced significant amount of glucose in blood, but it had no significant effect on lipid profile on short term (two weeks) ADRs. In contrast, simvastatin had no effect on blood glucose level, whereas it significantly reduced total cholesterol (TC), triglycerides (TG) and low density lipoprotein cholesterol (LDL-C) and increased significant amount of high density lipoprotein cholesterol (HDL-C). However, pathological changes of pancreas’s Islets of Langerhans were observed only after long-term (four weeks) induction of alloxan in rats. The inhibitory effect of combination therapy on blood glucose, TC, TG and LDL-C level was higher than those of monotherapy alone on long term ADRs. In addition, treatment with combination therapy on long term ADRs showed higher amount of HDL-C level and super oxide dismutase and catalase enzyme activity than those with monotherapy. They also decreased serum glutamic pyruvic transaminase (SGPT) and Serum glutamic oxaloacetic transaminase (SGOT) level. Administration of simvastatin recovered Langerhans cells from shrinkage whereas glibenclamide displayed slight recovery. But the combination therapy showed complete recovery of Langerhans cells as compared with diabetic rats. Conclusion: Our present findings suggest that treatment of glibenclamide in combination with simvastatin may be more effective than mono-therapy for preventing diabetes in rats. It may also suggest that this combination may have some beneficial effects on reducing cardiovascular risks from long term diabetes in rats.

Antidiabetic and antioxidative effect of jiang tang xiao ke granule in high-fat diet and low-dose streptozotocin induced diabetic rats.

Diabetes mellitus (DM), a kind of metabolic disease, is increasing over the last four decades in the world. The purpose of this study was to investigate the effect of Jiang Tang Xiao Ke (JTXK) granule, a naturally occurring ingredient from Chinese herbal medicines, on serum glucose, lipids, and oxidative stress in DM rats induced by high-fat diet and streptozotocin. JTXK granule 9 g/kg (based on crude herb equivalent) and pioglitazone 1.5 mg/kg (as a positive control for comparison) were orally administrated to DM rats for 4 weeks. Results showed that administration of JTXK granule reduced serum glucose, total cholesterol, triglyceride, and low density lipoprotein levels (by 12%, 33%, 57%, and 44%, resp.) but increased high-density lipoprotein level by 69%, compared with the drug-untreated DM rats. Serum malondialdehyde and nitric oxide levels were lowered (by 34% and 52%, resp.) associated with the elevation in serum superoxide dismutase levels (by 60%) after JTXK granule treatment. In addition, JTXK granule suppressed serum alanine aminotransferase activity (up to 50%) and alleviated pathological changes of pancreas and liver tissues in DM rats. The beneficial changes of pioglitazone on biomarkers were also found in DM rats. These findings suggested that JTXK granule may be an alternative medicine for the management of DM.

Sa1863 Cd38/ADP Ribosyl Cyclase Mediates Bile Acid-Induced Ca2+ Signals and Acinar Cell Injury

G A A b st ra ct s staining and western blot respectively. Acute pancreatitis was induced by ten injections of cerulein (50 μg/kg, i.p.) at hourly intervals. Mice were monitored for up to 7 days after induction of pancreatitis. Pancreatic injury was determined by measuring serum levels of amylase and examining pathologic changes of pancreas. For quantifying severity of tissue inflammation, we measured mRNA levels of myeloperoxidase (MPO, a marker of neutrophil infiltration) with real-time RT-PCR. Results: We found that MFG-E8 was constitutively expressed in murine pancreas. The protein was revealed to localize in pancreatic ductal epithelial cells. As expected, administration of cerulein induced acute pancreatitis ranging from the acute phase (i.e. 1 h after the final injection of cerulein) to recovery phase (i.e. up to 7 days after cerulein treatment) in WT mice. Pancreatic MFG-E8 was markedly increased 24 hours after induction of pancreatitis. The protein expression was maintained at high levels during the recovery phase. Using MFG-E8 KO mice, we found that MFG-E8 deficiency did not affect the severity of acute phase of cerulein-induced pancreatitis. However, pancreatic recovery following cerulein-induced pancreatitis was markedly delayed in the KO mice comparing to WT controls. Conclusions: Together, the data suggested that MFGE8 is a critical protein that protects against progression of acute pancreatitis. MFG-E8 deficiency impairs pancreatic recovery and it is needed in pancreatic recovery from pancreatitis. This novel finding may benefits the development of a potential novel molecular agent for pancreatitis therapy.

Protective effect of low-molecular-weight heparin on pancreatic encephalopathy in severe acute pancreatic rats

Pancreatic encephalopathy (PE) is a severe complication and significant cause of death in patients with severe acute pancreatitis (SAP). We have reported previously that low-molecular-weight heparin (LMWH) treatment could reduce incidence of PE in SAP patients. Our objective here was to investigate the protective effect of LMWH and its mechanism on PE in SAP rats. SD rats were randomly divided into three groups: (1) Sham-operation (S) group, (2) SAP group, and (3) LMWH treatment (LMWH) group. LMWH was administrated 4 h after the SAP model conducted. The levels of serum amylase, myelin basic protein (MBP), tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), brain water content, occurrence of apoptosis, and pathological changes of pancreas and brain were measured at 1 day after models were set up in the SAP and S groups, and 1 day after LMWH treatment was administrated in the LMWH group. (1) The levels of serum amylase, TNF-α, and IL-6 in the SAP group were increased significantly more than those in the S and LMWH groups (all P < 0.001), as were the levels of serum MBP in the SAP group compared to those in the S and LMWH groups (P < 0.01, <0.05 respectively). However, while the level of serum amylase and IL-6 in the LMWH group were significantly increased compared to those in the S group (P < 0.05, <0.001 respectively), the levels of TNF-α and MBP showed no significant difference between the LMWH and S groups (all P > 0.05). (2) The brain water content in the SAP group was significantly increased compared to the S group and LMWH group (P < 0.01, <0.05 respectively). (3) Neuronal apoptosis, demyelination, and mitochondrial vacuolation in neuronal cells were observed in the SAP group; in contrast, in the LMWH group, significantly lower rates of neuronal apoptosis, demyelination and mitochondrial edema were observed in neuronal cells. The protective effect of LMWH on PE progression in SAP rats might result from inhibition of inflammatory activation and reduction of the occurrence of neuronal apoptosis.

Breviscapine attenuates acute pancreatitis by inhibiting expression of PKCα and NF-κB in pancreas

To study the effect of breviscapine (Bre) on activity of protein kinase Cα (PKCα) and nuclear factor (NF)-κB in pancreas, and the mechanism of Bre attenuating acute pancreatitis (AP). One hundred and eight rats were randomly divided into acute necrotizing pancreatitis (ANP) group, Bre group (ANP + Bre group) and sham operation (SO) group, 36 rats in each group. ANP model was induced by a retrograde injection of 4% sodium deoxycholate into the bilio-pancreatic duct. Fifteen minutes after the ANP model was induced, the rats in Bre group were intraperitoneally injected with Bre (0.4 mg/100 g body weight or 0.1 mL/100 g body weight). Survival time and mortality of rats were calculated. Serum amylase and malondialdehyde levels were measured, volume of ascites was recorded and morphology of pancreas and lung was evaluated at 1, 5 and 10 h, after the ANP model was induced, respectively. Expressions of PKCα and subunit p65 of NF-κB in pancreas were detected by immunohistochemistry and Western blotting. The life span of rats was longer and the mortality was lower in Bre group than in ANP group 13.51 ± 5.46 vs. 25.36 ± 8.11 (P < 0.05). The amylase and MDA levels as well as the volume of ascites were lower and the pathological changes in pancreas and lung were less in Bre group than ANP group (P < 0.05), indicating that the pancreatitis is less severe in Bre group than ANP group. The activation of PKCα and NF-κB p65 in pancreas was induced rapidly and reached their peak at 1 h or 5 h after ANP, but their activity in Bre group was significantly inhibited. Bre exerts its therapeutic effect on AP by inhibiting the activation of PKCα and NF-κB p65 in pancreas.

Pioglitazone: A Promising Therapeutic Tool in Sodium Taurocholate-Induced Severe Acute Pancreatitis

Studies suggest that peroxisome proliferator-activated receptor γ(PPARγ) ligands may represent a therapeutic option in acute pancreatitis, yet most of them have been prophylactic administrated. To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate. Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined. Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved. Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.

Death caused by severe acute pancreatitis:an anlaysis of 144 cases

Objective To explore the main causes for death due to severe acute pancreatitis (SAP) to improve the level of diagnosis and treatment. Methods The clinical data of 1162 SAP cases treated in our hospital from June 1997 to May 2005 were retrospectively analyzed. Among which, 144patients (12. 39%) died, 82(7.06%)abandoned treatment and 936(80.55%)were cured. Results the APACHE Ⅱ scores and pancreas Balthazar CT scores of the death group were higher than that of the survival group. The percentage of single one organ dysfunction and multiple organ dysfunction syndrome (MODS) was significantly higher in the death group than in the survival group. The mortality rate of SAP without obvious inducing factors was significantly higher than that of SAP with inducing factors. Conclusion Integrated traditional and western non-surgical treatment is effective for SAP.The treatment for SAP without obvious inducing factors is a challenge. The mortality rate of SAP is primarily related to the pathological changes of pancreas and the patient's general condition. Early diagnosis and treatment is important to decrease mortality rate and maintaining the function of important organs is basic to ensure curative effect. Key words: Pancreatitis; Death; Cause

The intervention effects of different drugs on dendritic cells in acute pancreatitis in mouse

To study the immunologic mechanism in pathogenesis of the acute pancreatitis (AP) and the intervention effects of sandostatin and magnolol. Ninety BALB/c mice were divided into negative control group, caerulein-induced model group, sandostatin-treatment group, magnolol-treatment group, combined sandostatin- and magnolol-treatment group by means of random number table, with 18 mice in each group. AP model was reproduced by seven intraperitoneal injections of caerulein at an interval of 1 hour. Every 30 minutes before the caerulein challenge, sandostatin was injected sub- cutaneously. Magnolol was injected intravenously immediately after the AP model was reproduced. Then at 9, 12, 24 hours after modelling, blood was drawn from orbital vein and serum was separated. Serum amylase (SA), interleukin-10 (IL-10) and gamma-interferon (IFN-gamma) were determined after the mice were sacrificed, and pancreas and spleen were harvested . The pathological changes of pancreas were observed, and the number and the ratio of myeloid- dendritic cells (MDCs) to lymphoid dendritic cells (LDCs) were measured with flow cytometry. Compared with control group [SA (1.12 + or - 0.05) kU/L, pancreatic score (PS) 0.09 + or - 0.10], both indexes increased progressively in the model group [SA (26.11 + or - 1.96) kU/L, PS 5.32 + or - 0.19, both P<0.01]. The ratio of MDCs/LDCs showed downward tendency at every time-point especially at 9th hour (0.421 + or - 0.049 vs. 1.712 + or - 0.372, P<0.05), while the ratio of IL-10 to IFN-gamma did not show significant differences. Compared with model group, both SA and PS significantly decreased in all the three drug intervention groups [SA (kU/L): 18.25 + or - 1.09, 17.32 + or - 1.26, 17.62 + or - 0.56, PS: 4.55 + or - 0.15, 4.16 + or - 0.18, 4.10 + or - 0.13, all P<0.01]. There was no significant difference in the two ratios of MDCs/LDCs and IL-10/IFN-gamma between sandostatin-treatment group and model group. However, the ratio of MDCs/LDCs of the magnolol-treatment group was higher than that in sandostatin-treatment group 9, 12, 24 hours after modelling (9 hours: 4.694 + or - 0.527 vs. 0.819 + or - 0.182, 12 hours: 2.566 + or - 0.463 vs. 1.421 + or - 0.163, 24 hours : 2.343 + or - 0.359 vs. 1.421 + or - 0.113, P<0.05 or P<0.01). At every time-point, the ratio of IL-10/IFN-gamma in the magnolol-treatment group was significantly higher compared with the model group, and at the 12-hour point, it was higher than that of sandostatin-treatment group (8.000 + or - 1.738 vs. 3.558 + or - 0.362, P<0.05 ). The combined treatment group showed similar changes as the magnolol-treatment group. When AP occurs, the differentiation from T helper (Th0) to Th1 is augmented, while differentiation of Th0 to Th2 decreases, thus inducing an imbalance in the relationship of pro- and anti-inflammatory response. Magnolol can induce the differentiation from Th0 to Th2 by modulating the different subtype dendritic cells, thus improving the anti-inflammatory response, resulting in attenuating local and systemic inflammatory response in AP. However, sandostatin did not show such effect.

Effect of MG-132 upon the expression of intercellular adhesion molecule-1 in cerulein-induced acute pancreatitis in mice

To investigate the effects of the proteasome inhibitor MG-132 upnon NF-kappaB and the expression of intercellular adhesion molecule-1 (ICAM-1) in cerulein-induced acute pancreatitis (AP) in mice. Forty-five BalB/c mice were randomly allocated into nine groups: control 3, 6, 12 h group (n = 5); AP 3, 6, 12 h group (n = 5) and MG-132 3, 6, 12 h group (n = 5). AP group was induced by an ip injection of 100 microg/kg cerulein six times with a 1 h interval. Control group received physiological saline likewise. MG-132 group was injected ip with 10 mg/kg MG-132 at 30 min before induction of AP. The levels of serum amylase and soluble ICAM-1 (sICAM-1) were tested. The pathological changes of pancreas were observed. The expression of NF-kappaB proteins was examined by immunohistochemistry and the expression of ICAM-1 mRNA analyzed by reverse transcription-polymerase chain reaction (RT-PCR). In MG-132 group, the levels of serum amylase (U/L) and sICAM-1 (pg/ml) markedly decreased in comparison with AP group (1629 +/- 59, 1794 +/- 123, 2910 +/- 152 vs 1282 +/- 61, 1525 +/- 103, 1809 +/- 117, 133 +/- 10, 157 +/- 10, 217 +/- 43 vs 106 +/- 6, 135 +/- 4, 163 +/- 19, P < 0.05 or P < 0.01); the scores of pathological changes decreased in pancreas (5.7 +/- 1.0, 7.1 +/- 1.2, 9.6 +/- 2.1 vs 3.2 +/- 1.0, 5.3 +/- 1.0, 6.9 +/- 0.8, P < 0.05 or P < 0.01);the expression of NF-kappaB protein (3.8 +/- 1.1, 4.6 +/- 1.2, 6.7 +/- 0.4 vs 1.9 +/- 0.6, 3.1 +/- 1.0, 4.7 +/- 1.0, P < 0.05 or P < 0.01) were significantly lowered than those in AP group. ICAM-1 mRNA also decreased more than those in AP group (0.3 +/- 0.1, 1.0 +/- 0.2, 1.2 +/- 1.0 vs 0.3 +/- 0.2, 1.8 +/- 0.2, 2.1 +/- 0.2, P < 0.05 or P < 0.01). The proteasome inhibitor MG-132 can obviously improve the outcome of acute pancreatitis. And the mechanism may be related to the down-regulated expression of cytokines, including adhesion molecules, through the suppression of NF-kappaB activation.

Protective Effect of HMGB1 A Box on Organ Injury of Acute Pancreatitis in Mice

To investigate the effects of high-mobility group box 1 (HMGB1) A box in experimental severe acute pancreatitis (SAP). Severe acute pancreatitis was induced by 20% L-arginine abdominal cavity injection in Institute of Cancer Research mice, and the treatment group received 2 abdominal cavity injections of A box 12 and 24 hours after the modeling injection. The serum levels of HMGB1, amylase, lipase, and biochemical indicators were measured 24 and 48 hours after induction of SAP. The pathological changes of the pancreas, lung, kidney, and liver for both SAP group and treatment group were observed and compared, as well as survival rate and surviving time. A box significantly improved the elevation of the serum levels of HMGB1, amylase, lipase, and biochemical indicators in SAP. The pathological changes of pancreas and organ injury in treatment group were more alleviated than that in SAP group. The mice survival rate of the treatment group (66.7%) was significantly higher than that of the SAP group (26.7%). A box has remarkable protective effect against pancreatitis and associated organ injury; HMGB1 probably participates in the inflammatory reaction and organ injury of SAP as a late-acting mediator of inflammation.

Experimental study of therapeutic efficacy of Baicalin in rats with severe acute pancreatitis

To observe the therapeutic efficacy of Baicalin in rats with severe acute pancreatitis (SAP) and explore its therapeutic mechanisms. The SAP rat models were randomly divided into the model control group, Baicalin treatment group, octreotide treatment group and sham operation group. All groups were randomly subdivided into 3 h, 6 h and 12 h groups with 15 rats in each group. The survival, ascites volume and pathological changes of pancreas in all rats were observed at different time points after operation. The plasma amylase content and serum TNF-alpha, IL-6, malonaldehyde (MDA) and PLA(2) contents were also determined. The survival was not obviously different between the treated groups, and was significantly higher in treated groups at 12 h compared to the model control group (P < 0.05, 15 vs 10). The ascites/body weight ratio at 3 h and 6 h was significantly lower in Baicalin treatment group compared to the model control group and octreotide treatment group (P < 0.05, 1.00 vs 2.02 and 1.43 and P < 0.001, 2.29 (1.21) vs 2.70 (0.80) and 2.08 (2.21), respectively). The contents of amylase, TNF-alpha, IL-6, MDA and PLA(2) were significantly lower in the treated groups than in the model control group (P < 0.05, 4342 vs 5303, 5058 vs 6272 in amylase, P < 0.01, 21.90 vs 36.30, 23.80 vs 39.70, 36 vs 54.35 in MDA and 56.25 vs 76.10 in PlA(2), or P < 0.001, 65.10 and 47.60 vs 92.15 in TNF-alpha, 3.03 vs 5.44, 2.88 vs 6.82, 2.83 vs 5.36 in IL-6, respectively). The pathological scores of pancreas in the treated groups were significantly lower than that in the model control group (P < 0.05, 9.00 vs 10.05, 6.00 vs 9.00, 8.00 vs 10.05), but no marked difference was found between the treated groups. The Baicalin injection has significant therapeutic effects on SAP rats, its effects are similar to those of octreotide. The Baicalin injection is also cheap and has a big application range, quite hopefully to be used in clinical treatment of SAP.

Effect of resveratrol on activation of nuclear factor kappa-B and inflammatory factors in rat model of acute pancreatitis

To observe the effect of resveratrol on nuclear factor Kappa-B (NF-kappaB) activation and the inflammatory response in sodium taurocholate-induced pancreatitis in rats. Seventy-two male SD rats were randomly divided into three groups: sham operation group (control), severe acute pancreatitis (SAP) group, and severe acute pancreatitis group treated with resveratrol (RES). A SAP model was established by injecting 4% sodium taurocholate 1 mL/kg through puncturing the pancreatic duct. In Res group, Res was given at 30 mg/kg b.m. intraperitoneally after the SAP model was successfully established. Eight animals from each group were sacrificed at 3, 6 and 12 h after modeling. The expression of NF-kappaB activation of pancreas was detected by immunohistochemical staining, whereas the levels of TNF-alpha and IL-8 in pancreatic tissues were estimated by radioimmunoassay. The pathological changes of pancreas and lungs were examined microscopically. Much less hyperemia, edema, dust-colored necrotic focus and soaps were noticed in pancreas in RES group than in SAP group. In RES group, hemorrhage, exudates and infiltration of inflammatory cells in pancreas and interstitial edema, destruction of alveolar wall in lung were significantly less than in SAP group. In the SAP group, the activation of NF-kappaB in pancreatic tissues was enhanced significantly at any measure point compared with control group (64.23+/-10.72% vs 2.56+/-0.65%, 55.86+/-11.34% vs 2.32+/-0.42%, 36.23+/-2.30% vs 2.40+/-0.36%,P<0.01), TNF-alpha,IL-8 were also increased and reached their peak at 6 h and then declined. The activation of NF-kappaB and the levels of TNF-alpha and IL-8 in RES group were significantly lower than those in SAP group (P<0.01): activation (52.63+/-9.45% vs 64.23+/-10.72%, 40.52+/-8.40% vs 55.86+/-11.34%, 29.83+/-5.37% vs 36.23+/-2.30%), TNF-alpha (132.76+/-15.68 pg/mL vs 158.36+/-12.58 pg/mL, 220.32+/-23.57 pg/mL vs 247.67+/- 11.62 pg/mL, 175.68+/-18.43 pg/mL vs 197.35+/-12.57 pg/mL) and IL-8 (0.62+/-0.21 microg/L vs 0.83+/-0.10 microg/L, 1.10+/-0.124 microg/L vs 1.32+/-0.18 microg/L, 0.98+/-0.16 microg/L vs 1.27+/-0.23 microg/L). The activation of NF-kappaB is involved in the inflammatory response of rats with SAP. Resveratrol could effectively inhibit the expression of NF-kappaB activation, alleviate the severity of SAP through its anti-inflammatory effects and regulate the inflammatory mediators.

Clinical characteristics and management of patients with early acute severe pancreatitis: experience from a medical center in China.

To study clinical characteristics and management of patients with early severe acute pancreatitis (ESAP). Data of 297 patients with severe acute pancreatitis (SAP) admitted to our hospital within 72 h after onset of symptoms from January 1991 to June 2003 were reviewed for the occurrence and development of early severe acute pancreatitis (ESAP). ESAP was defined as presence of organ dysfunction within 72 h after onset of symptoms. Sixty-nine patients had ESAP, 228 patients without organ dysfunction within 72 h after onset of symptoms had SAP. The clinical characteristics, incidence of organ dysfunction during hospitalization and prognosis between ESAP and SAP were compared. Impairment degree of pancreas (Balthazar CT class) in ESAP was more serious than that in SAP (5.31+/-0.68 vs 3.68+/-0.29, P<0.01). ESAP had a higher mortality than SAP (43.4% vs 2.6%, P<0.01), and a higher incidence of hypoxemia (85.5% vs 25%, P<0.01), pancreas infection (15.9% vs 7.5%, P<0.05), abdominal compartment syndrome (ACS) (78.3% vs 23.2%, P<0.01) and multiple organ dysfunction syndrome (MODS)(78.3% vs 10.1%, P<0.01). In multiple logistic regression analysis, the main predisposing factors to ESAP were higher APACHE II score, Balthazar CT class, MODS and hypoxemia. ESAP is characterised by MODS, severe pathological changes of pancreas, early hypoxemia and abdominal compartment syndrome. Given the poor prognosis of ESAP, these patients should be treated in specialized intensive care units with special measures such as close supervision, fluid resuscitation, improvement of hypoxemia, reduction of pancreatic secretion, elimination of inflammatory mediators, prevention and treatment of pancreatic infections.

Effect of hydrogen peroxide on permeability of the main pancreatic duct and morphology of the pancreas

Background: The direct effect of free oxygen radicals, if any, on the morphology of the pancreas has never been studied in vivo. This study was designed to evaluate the effects of hydrogen peroxide (H 2O 2) on permeability of the main pancreatic duct (MPD) and morphology of pancreas in cats when administered intraductally or intraarterially. Methods: Thirty-six mongrel cats were randomly allocated into three groups, and all groups were divided into two subgroups. In group I and III, MPD was perfused with either standard perfusate (group IA and IIIA) or H 2O 2 at a concentration of 150 μM (group IB and IIIB) for 3 hours. In group II, the splenic artery was infused either with 0.9% sodium chloride (group IIA) or H 2O 2 (group IIB) for 3 hours. After 3 hours, in group I and II, MPD was perfused with 99mTc labelled dextran, and the percentage of the dextran permeated from the MPD into the portal vein was calculated for the evaluation of the pancreatic duct permeability. Then, tissue samples were obtained for the examination of early histopathological changes in pancreas. In group III, following ductal perfusion studies, the cats were allowed to recover. After 24 hours animals were killed, and samples were taken for the examination of late histological changes in pancreas. In all groups, an inflammatory score was created for each animal based on the pathological changes in pancreas: edema, leukocyte infiltration, parenchymal necrosis, and hemorrhage. Results: Group I: All cats developed acute edematous pancreatitis with significantly higher inflammatory scores than controls ( P <0.01). Desquamation of the single layer of columnar epithelium that normally lined the duct and leukocyte infiltration around the MPD duct were found. Pancreatic duct permeability was found to be increased significantly ( P <0.01). Group II: There were no statistical differences in inflammatory scores and pancreatic duct permeability between experimental and control groups ( P >0.05). Group III: All animals developed gross acute edematous pancreatitis after 3 hours of intraductal H 2O 2 perfusion. Histopathological changes at 24 hours were much more pronounced in group IIIB than in group IIIA including focal necrosis and hydropic degeneration of acinar cells. Conclusion: This study has shown that intraductal H 2O 2 perfusion induced acute edematous pancreatitis with marked histopathological changes and increased pancreatic duct permeability in cats. Intraarterial H 2O 2 infusion, however, has no effect on the permeability of the MPD and morphology of pancreas in our model.

Traditional Chinese medicine Qing Yi Tang alleviates oxygen free radical injury in acute necrotizing pancreatits.

AIM:To observe the changes in oxygen free radical (OFR) and the curative effect of traditional Chinese medicine Qing Yi Tang in acute necrotizing pancreatitis (ANP).METHODS:After induction of ANP by injection of sodium taurocholate into pancreatic duct, 16 dogs were randomly divided into control group and Chinese medicine group.Serum amylase, SOD and MDA were determined on postoperative day 1, 2, 4 and 7. The animals were sacrificed on day 7. SOD and MDA in organs were determined, and pathological changes in pancreas were observed.RESULTS: As compared with control group, the serum level of amylase (734U/L vs 2783U/L) and MDA (7.8nmol/ml vs 14.8nmol/ml) in Chinese medicine group were decreased on day 7 (P < 0.05), while SOD increased significantly (281nU/ml vs 55nU/ml, P < 0.01), and similar changes occurred in MDA and SOD in organs, especially in the pancreas; the pathological changes in the pancreas were alleviated as well.CONCLUSION: Qing Yi Tang is effective in clearing OFRs and alleviating pathological changes in ANP.

Isolation of a toga-like virus from farmed Atlantic salmon Salmo salar with pancreas disease

Pancreas disease (PD) of farmed Atlantic salmon Salmo salar has been recognised in Scotland, Ireland, Norway, the USA, France and Spaln and can cause severe economlc loss Thls paper reports the ~solatlon, flom PD-affected f ~ s h , of a virus with physicochemlcal characteristics and moiphology resembling members of the Togavirldae When Inoculated into Atlantic salmon post-smolts it causes pathological changes in pancreas h e a ~ t and muscle tlssues which are ind~stinguishable from those piesent in fleld outbreaks of PD I t is proposed that the virus be named salmon pancreas disease vlrus (SPDV)

On the interrelationship between virus concentration and pathological changes of pancreas in mice induced by EMC-virus.

On the interrelationship between virus concentration and pathological changes of pancreas in mice induced by EMC-virus.