摘要:目的: 探討益活清下法治療重癥急性胰腺炎(severe acute pancreatitis, SAP)對血清單核趨化蛋白1及對器官功能不全的影響。 方法 : 依據納入和排除標準,選取SAP患者24例,按1︰1隨機分為治療組和對照組,在接受相同西醫治療的基礎上,治療組使用中藥“益活清下”法治療,對照組同時接受中藥安慰劑治療。測定患者第0、1、3、5、7天血清MCP1的濃度水平,比較各器官功能不全的發生率與持續時間。 結果 :兩組入院時Rason評分、CT評分、急性生理和慢性健康評價指標Ⅱ評分無統計學差異(〖WTBX〗P gt;005)。對照組第3天MCP1濃度水平明顯高于治療組,差異有統計學意義(〖WTBX〗P lt;005),對照組腸、肝功能不全的發生率高于治療組,持續時間長于治療組,但無統計學差異(〖WTBX〗P gt;005)。 結論 :益活清下法治療重癥急性胰腺炎,可降低患者血清MCP1的水平。Abstract: Objective: To investigated the impact of Yihuo Qingxia method on the serum monocyte chemoattractant protein1 of severe acute pancreatitis (SAP)and on the organs disfunction. Methods : Twentyfour SAP patients who admitted to hospital within 72h after onset were randomized into treatment group (n=12) and control group (n=12). The patients in the treatment group were treated by Yihuo Qingxia method, and the control group were administrated with placebo.The level of the serum mcp1 of the patients on the first,3rd,5th,7thday were measured, as well as the incidence and the duration of disfunction of the organs were compared.〖WTHZ〗Results :There were no statistical significance in admission Rason scores, CT scores, Acute physiology and chronic health evaltionⅡscores(APACHEⅡscores)(Pgt;005). The level of the serum Monocyte chemoattractant protein1 of the treatment group was lower than that of the placebo group generally(Plt;005).At the 3rd day after onset,the serum mcp1 level of the control group was significantly higher than that of the treament group(Plt;005).The incidence of the control group of the intestin disfunction and hepatic inadequacy was obviously higher than those of the treatment group,and the duration of the former was longer than that of the latter,but with no satistical significance. Conclusion :Yihuo Qingxia method can effectively cut down the level of the serum mcp1 of severe pancreatitis patients.
To evaluate the effects of different pressure and duration of autologous bile perfusion into dog’s pancreatic duct on the severity of induced acute pancreatitis. Thirty mongrel dogs were divided into five groups, with each group consisting of six dogs. Histological changes of pancreas were observed. Results: Histological changes of pancreas were correlated with the pressure and duration of autologous bile perfusion into pancreatic duct. It was easier to produce acute hemorrhagic necrotizing pancreatitis in the groups with a higher pressure and a longer duration of perfusion than in the groups with a lower pressure and a shorter duration. The results indicated that there was a significant effect of higher pressure and longer duration bile perfusion into pancreatic duct on the severity of induced acute pancreatitis.
Objective To evaluate the activity of the pancreatic tissue phospholipase A2 (PLA2) in acute pancreatitis (AP) and the therapeutic effects of verapamil in rats. MethodsThe model of rat AP induced by a closed duodenal loop technique was established to observe the changes of PLA2 activity in AP group and treated group. The pancreatic histology was examined by light and electron microscopy. Results At 16 and 24 hours after induction of AP in rats, significant inhibition of the pancreatic tissue PLA2 activity was shown in the treated group as compared with AP group, with 32.34±3.87u, 35.26±4.52u and 44.83±5.31u, 47.77±5.86u respectively. The treated animals also showed a decrease in the severity of pancreatic hemorrhage, necrosis and damage to the cellular ultrastructures. Conclusion There exists high activity of PLA2 in rats AP. Calcium channel blocker, verapamil might take therapeutic effects on AP by inhibiting activity of PLA2.
Objective To summarize the role of inflammatory cytokines in the pathogenesis of acute pancreatitis (AP) and gut barrier dysfunction in recent years. Methods Literatures on cytokines and experimental pancreatitis as well as clinical pancreatitis were collected and reviewed. Results Tumor necrosis factor-α and other inflammatory cytokines were elevated significantly during pancreatitis in many tissues, especially in pancreas and alimentary tract, in a fashion independent of the animal model used. Anti-cytokine therapy could decrease the concentration of the cytokines in experimental animal. Conclusion Inflammatory cytokines are believed to be primarily responsible for the pathogenesis of acute pancreatitis and its associated distant organ dysfunction. Further study of the nature of these cytokines may provide a new approach to treating this disease.
【Abstract】Objective To investigate the role of interleukin-10（IL-10） and interleukin-18 （IL-18） in the pathogenesis of acute lung injury in experimental severe acute pancreatitis.Methods Forty-eight SD rats were divided into control group and SAP group by the random data table. The model of experimental severe acute pancreatitis was established by injection of 3.5% sodium taurocholate into the bili-pancreatic duct. Lung wet weight index, ascities and level of serum amylase, IL-10 and IL-18 were quantitatively measured in different time. Intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were detected by semiquantitative RTPCR. The histopathology of pancreas and lung were observed under the light microscope.Results Lung wet weight index, ascities, level of serum amylase, IL-10 and IL-18, intrapulmonary expressions of IL-10 mRNA and IL-18 mRNA were significantly increased in SAP group (P＜0.01). The level of serum IL-18 and intrapulmonary expression of IL-18mRNA are positively correlated with lung wet weight index （r=0.68,P＜0.01; r=0.72,P＜0.01） and lung injury score （r=0.74,P＜0.01; r=0.79,P＜0.01) respectively, whereas the level of serum IL-10 and intrapulmonary expression of IL-10 mRNA are negatively correlated with lung wet weight index（r=-0.62,P＜0.01; r=-0.69,P＜0.01） and lung injury score（r=-0.66,P＜0.01; r=-0.60,P＜0.01）. Conclusion IL-18 may play a key role in the pathogenesis of acute lung injury in experimental severe acute pancreatitis, and IL-10 exerts the protection role in this process.
