罗格列酮保护大鼠重症急性胰腺炎肾损伤的机制

目的 探讨高选择性过氧化物酶体增殖物激活受体-γ( PPAR-γ)的激动剂罗格列酮(ROSI)保护大鼠重症急性胰腺炎(SAP)肾损伤的可能机制.方法 将雄性Wistar大鼠54只随机分为假手术组(SO组)、重症急性胰腺炎组(SAP组)和罗格列酮处理组(ROSI组),每组大鼠18只.胆胰管逆行注射5％牛磺胆酸钠制备重症急性胰腺炎模型.ROSI组造模前30 min经股静脉注射10％二甲基亚砜(DMSO)溶解的罗格列酮(6 mg/kg);SO组、SAP组则经股静脉注射等量10％DMSO(0.2 ml/100 g).术后3、12、24h分批剖杀大鼠,每个时间点6只.分别取肾组织检测一氧化氮(NO)及其合成酶(iNOS)的水平和核转录因子-κB( NF-κB)/p65蛋白表达水平,并观察不同时间点组大鼠肾脏肿瘤坏死因子-α( TNF-α)和细胞间黏附分子-1(ICAM-1)的mRNA及蛋白表达.结果 SAP组各时点NO含量分别为(2.34±0.31)、(7.73 ±0.48)、( 17.33±0.89) mg/g;SAP组各时点NF-κB/p65含量分别为30648.11 ±2655.13、53 654.63±3065.94、70 546.85±5046.55;SAP组各时点TNF-α表达水平为4.18±0.61、5.69 ±0.82、11.86±2.49;SAP组各时点ICAM-1表达水平为3.68±0.58、6.48 ±0.76、8.62±1.09,均与SO组各时间点比较显著升高,差异有统计学意义(P＜0.05);ROSI组12、24h时点NO含量分别为(4.10±0.62)、(6.09±0.79) mg/g;ROSI组24h时点NF-κB/p65含量为30468.48±2684.59; ROSI组24h时点TNF-α表达水平为6.60±1.34;ROSI组24h时点ICAM-1表达水平为2.92±0.88,均较SAP组下降,差异有统计学意义(P＜0.05).结论 罗格列酮通过抑制NF-κB的表达,从而减少TNF-和ICAM-1的产生,减轻炎症反应的发生发展,显示其参与了保护重症急性胰腺炎所诱发的肾损伤机制.     

急性出血坏死性胰腺炎大鼠胰腺组织结构改变与内毒素血症的关系及纳屈酮的治疗作用

为探讨大鼠急性出血坏死性胰腺炎（ＡＨＮＰ）胰腺组织结构改变与内毒素血症的关系及纳屈酮的治疗作用，用５％牛磺胆酸钠逆行胰胆管注射制成ＡＨＮＰ模型。取Ｗｉｓｔａｒ大鼠１１０只随机分为假手术组（ｎ＝２０）、ＡＨＮＰ组（ｎ＝４５）、纳屈酮治疗组（ｎ＝４５），分别于术后６、１２、２４小时称取胰腺重量，观察ＡＨＮＰ大鼠胰腺组织结构改变，同时测定其血浆淀粉酶和内毒素水平，并与假手术组比较。结果：与假手术组比较，ＡＨＮＰ组血浆淀粉酶、内毒素及胰腺系数升高，在光镜及电镜下可见胰腺损害随时间延长而加重。纳屈酮治疗组与ＡＨＮＰ组相比，其血浆淀粉酶、内毒素及胰腺系数下降，而且胰腺损害减轻。本实验结果提示：ＡＨＮＰ引发内毒素血症，纳屈酮可通过改善胰腺缺血性损害而降低血浆内毒素，延长大鼠生存时间及降低病死率     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

目的 探讨水通道蛋白1(AQP1)在急性坏死性胰腺炎(ANP)大鼠胰腺的表达及其意义.方法 将48只雄性SD大鼠随机分为对照组和ANP组,制模后3、6、12、18 h各时间点分别处死6只.记录腹水量,测定血清淀粉酶;采用酶联免疫吸附试验(ELISA)检测血清AQP1含量;苏木素-伊红(HE)染色观察胰腺组织病理改变;伊文思兰染料(EB)血管外渗法检测胰腺组织毛细血管通透性;免疫组织化学和Westem blot法检测胰腺组织AQP1蛋白表达;荧光定量聚合酶链反应(PCR)检测AQP1基因mRNA表达.结果 (1)对照组3、6、12、18 h血清淀粉酶水平分别为(1308±759)、(1077±508)、(1325±761)、(1328±762)U/L,ANP组分别为(9102±2199)、(8799±1634)、(9398±1473)、(9484±862)U/L;对照组胰腺组织EB含量分别为(205.61±32.99)、(141.46±27.18)、(96.94±26.79)、(61.43±24.82)mg/L;ANP组分别为(273.59±23.47)、(253.51±31.68)、(221.15±73.68)、(185.28±42.35)mg/L;血清AQP1含量对照组为(74.08±11.80)、(78.49±9.06)、(75.77±7.37)、(72.75±13.87)mg/L,ANP组为(73.29±9.61)、(62.85±7.28)、(62.07±4.39)、(46.33±11.91)mg/L,两组比较差异均有统计学意义(P<0.01).(2)对照组3、6、12、18 h免疫组织化学灰度值分别为114.13±7.92、122.39±7.99、145.98±6.48、113.98±6.48,ANP组分别为80.07±14.89、110.54±4.45、103.77±10.48、99.18±6.95;对照组Western blot蛋白含量分别为1.19±0.33、1.02±0.25、0.90±0.33、1.06±0.20,ANP组分别为0.83±0.11、0.96±0.21、0.58±0.28、0.72±0.14.结果 均显示ANP组胰腺AQP1蛋白表达低于对照组(P<0.05);(3)对照组3、6、12、18 h荧光定量PCR检测ANP组胰腺AQP1基因mR-NA表达分别为2.13±0.63、2.02±1.40、2.07±0.86、2.49±2.47,ANP组为0.91±0.22、1.01±0.83、0.48±0.23、0.61±0.51,ANP组较对照组减弱(P<0.01).结论 ANP大鼠胰腺组织AQP1表达明显减弱,这可能在毛细血管渗漏综合征的发生中起重要作用.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

重症急性胰腺炎早期合并胰腺感染的危险因素分析

目的探讨与重症急性胰腺炎（SAP）早期胰腺感染有关的危险因素。方法回顾性分析2002年1月-2007年3月间收治的86例重症急性胰腺炎患者的年龄、性别、病因、人院时APACHEⅡ评分、血淀粉酶、血钙、血糖、血细胞比容、平均动脉压、ALT、AST、总胆红素、血清白蛋白、血肌酐、尿素氮、胰腺坏死、低氧血症、机械通气、肠功能障碍及导管应用等因素和胰腺感染的相关性。结果禁食时间、胰腺坏死程度、胆源性致病因素、低氧血症、肠功能障碍、血肌酐、尿素氮和人院血细胞比容与SAP患者继发感染的发生率呈正相关（P〈0．05），血清白蛋白水平与SAP患者继发感染的发生率呈负相关（P〈0．01）；其余各影响因素与胰腺感染均无明显相关性（P〉0．05）。结论在SAP发病过程中，禁食时间较长、胰腺坏死程度增高、胆源性致病因素、低氧血症、肠功能障碍以及血肌酐、尿素氮和人院血细胞比容的升高可能是导致胰腺发生感染的重要因素。     

依达拉奉联合乌司他丁对重症急性胰腺炎大鼠脑损伤的保护作用

目的 研究依达拉奉联合乌司他丁对重症急性胰腺炎(SAP)大鼠脑损伤的保护作用.方法 100只雄性远交系大鼠随机分为10组:正常对照6h组、48 h组,SAP 6 h组、48 h组,依达拉奉处理6h组、48 h组,乌司他丁处理6h组、48 h组,依达拉奉联合乌司他丁处理6h组、48 h组;每组各10只.分别在术后第6h、48 h观察神经功能评分.采集血液、胰腺组织、脑组织标本,观察血清淀粉酶水平、脑组织伊文蓝含量、脑组织含水量、胰腺组织及脑组织镜下病理学变化.应用放射免疫法检测血清肿瘤坏死因子(TNF)-α含量,逆转录-聚合酶链反应(RT-PCR)法检测脑组织TNF-α信使核糖核酸(mRNA)含量,免疫组织化学法检测脑组织核因子(NF)-κB p65活性.结果 依达拉奉联合乌司他丁处理48 h组血清淀粉酶水平、脑组织EB含量、脑组织含水量、胰腺组织及脑组织镜下病理学评分、血清TNF-α含量、脑组织TNF-α mRNA含量及脑组织NF-κB p65活性均较依达拉奉48 h组、乌司他丁48 h组及SAP 48 h组显著降低,而神经功能评分则显著升高(P＜0.01).结论 依达拉奉联合乌司他丁对SAP大鼠脑损伤有较好的保护作用.     

重症急性胰腺炎患者QT间期离散度的临床意义

目的 探讨QT间期离散度(QT interval dispersion,QTd)对重症急性胰腺炎(severe acute pancreatitis,SAP)患者早期心脏损害的诊断价值及其预后判断意义.方法 对收治具有完整心电图资料的58例SAP(SAP组)及189例轻型急性胰腺炎(MAP组)患者资料进行回顾性分析,另选60例门诊健康体检者的心电图作为健康对照组.分别测定12导联心电图QT间期,并计算QTd、心率校正QTd(heart rate corrected QTd,QTcd).结果 SAP组较MAP组及健康对照组QTd、QTcd显著延长(P＜0.01),MAP组较健康对照组QTd、QTcd无明显延长(P＞0.05).结论 QTd、QTcd对SAP患者的早期心脏损害有较大诊断价值,对SAP患者的预后也有较大帮助,可作为评价SAP患者心功能状态的一项辅助指标.     

重症急性胰腺炎并发假性动脉瘤大出血的处理

目的探讨重症急性胰腺炎（severe acute pancreatitis,SAP）并发假性动脉瘤大出血的诊断和处理。方法回顾性分析1990年10月至2006年10月收治的12例SAP合并假性动脉瘤出血患者的临床资料。病因：胆源性胰腺炎6例,高脂血症3例,甲状旁腺功能亢进危象1例,原因不明2例。结果CT诊断假性动脉瘤出血6例（6／9）,血管造影均诊断正确（12／12）。受累血管主要为胰腺周围血管。8例“一点法”（出血血管近端）栓塞后成功止血,2例“两点法”（动脉瘤出血血管的近端和远端）血管栓塞后成功止血。2例急诊手术缝扎止血。“一点法”栓塞止血患者中有4例4～7d后再出血,2例急诊手术止血,2例改用“两点法”成功栓塞。3例死于感染和多器官功能不全综合征,总病死率为25％。结论血管造影是SAP并发假性动脉瘤大出血的主要诊断方法,“两点法”血管栓塞止血和急诊手术是有效的治疗手段。     

重症急性胰腺炎临床特征及治疗方案的选择

目的探讨重症急性胰腺炎的临床特征及治疗方案的选择与预后的关系。方法2001年1月至2005年12月共收治重症急性胰腺炎患者783例,治疗方案根据中华医学会外科学分会胰腺外科学组制定的《重症急性胰腺炎诊治原则草案》进行选择。其中胆源性胰腺炎375例,手术治疗182例,非手术治疗193例。非胆源性胰腺炎408例,手术治疗147例,非手术治疗261例。结果共治愈患者698例,治愈率89．1％。胆源性胰腺炎患者治愈357例,治愈率95．0％,其中手术治疗治愈171例,治愈率94．0％,非手术治疗治愈186例,治愈率96．4％;非胆源性胰腺炎患者治愈341例,治愈率84．0％,其中手术治疗治愈110例,治愈率74．8％,非手术治疗治愈231例,治愈率88．5％。存活患者中有48．3％发生了脏器功能障碍,其中18．3％为多脏器功能障碍综合征（MODS）;而死亡患者中100％有脏器功能障碍,其中97．6％为MODS。呼吸功能障碍、神经系统障碍与休克的发生率最高,分别为26．3％、11．7％和10．3％,死亡患者中呼吸、肾和心功能障碍的发生率最高分别为94．1％、60．0％和60．0％。存活与死亡患者真菌感染的发生率分别为8．9％与37．6％;消化道瘘发生率分别为0．9％和14．1％。结论针对胆源性胰腺炎的病因治疗和针对胰腺坏死感染的手术治疗是提高疗效的关键因素;MODS是造成胰腺炎患者死亡的主要原因,其中呼吸、肾和心功能障碍危险性较高。     

高渗盐水对重症急性胰腺炎大鼠全身性炎症反应的影响

目的研究高渗盐水治疗重症急性胰腺炎(severeacutepancreatitis,SAP)时大鼠炎性细胞因子、胰腺、肺组织病理损害的变化及其机制。方法Wistar大鼠48只,均分成对照组、SAP模型组、等渗盐水组、高渗盐水组,采用过量L精氨酸诱导大鼠SAP模型,等渗盐水组、高渗盐水组于24h、48h分别经静脉输入2mlkg的09%NaCl、75%NaCl,在48h、72h取血测肿瘤坏死因子α(TNFα)、白细胞介素6(IL6)、IL10水平,于72h检查大鼠胰腺、肺组织病理变化。结果高渗盐水组胰腺和肺组织病理学改变明显轻于等渗盐水组;等渗盐水组血清TNFα、IL6、IL10水平在48h和72h分别为[(311±22)、(43±5)、(22±4)]pgml和[(403±29)、(66±7)、(28±6)]pgml。高渗盐水组分别为[(278±20)、(38±6)、(26±7)]pgml和[(329±28)、(42±6)、(44±5)]pgml;高渗盐水组血清TNFα、IL6值明显低于等渗盐水组,IL10值明显高于等渗盐水组,尤其在72h两组之间差异有显著意义。结论高渗盐水治疗大鼠SAP能使血清TNFα、IL6水平显著降低和IL10水平显著增高,减轻胰腺、肺等组织损伤。     

粘附分子基因表达在大鼠急性坏死性胰腺炎肺损伤中的作用

目的　研究急性坏死性胰腺炎 (ANP)大鼠肺组织细胞间粘附分子 1(ICAM 1)mRNA的表达情况及其与肺损伤的关系。方法　将 33只Wistar大鼠随机分为正常对照组和胰腺炎不同时间点 (1、4、12和 2 4h)各组 ,用逆行胰胆管注射方法制备ANP模型。采用逆转录聚合酶链反应法检测ANP大鼠肺组织中ICAM 1mRNA表达 ,同时观察肺组织髓过氧化物酶 (MPO)及病理改变。结果造模ANP 1h后大鼠肺组织中ICAM 1mRNA(0 82± 0 0 3)比正常对照组 (0 41± 0 0 4)的表达水平高 (P <0 0 5 ) ,并持续升高至 12h及 2 4h(分别为 1 17± 0 0 5及 1 11± 0 0 4) ,同时伴有肺组织病理损害 ,其严重程度与ICAM 1mRNA表达、MPO及肺MPO与ICAM 1mRNA表达均呈正相关 ,相关系数分别为0 85、0 85及 0 96 (P <0 0 5 )。结论　ANP大鼠早期肺组织中ICAM 1mRNA呈过度表达 ,肺损伤严重程度与ICAM 1mRNA表达的高低有关。肺组织中ICAM 1过度表达及中性粒细胞浸润是ANP肺损害发生的原因之一。     

重症急性胰腺炎治疗模式的转变与胰性脑病

目的探讨重症急性胰腺炎（severe acute pancreatitis,SAP）合并胰性脑病的临床预防和治疗措施。方法按不同时间段回顾性研究1987年1月至2006年12月收治的22例SAP合并胰性脑病患者的临床资料。研究分为2组,A组（1987年1月至1996年12月）13例;B组（1997年1月至2006年12月）9例,结合SAP治疗措施的差异分析胰性脑病的发生情况、临床表现、治疗过程等。结果A组中早期胰性脑病（EPE）8例,迟发性胰性脑病（DPE）5例,此期仅1例EPE存活,病死率为92．3％。B组均为EPE病例,无一例死亡。死亡病例集中在前10年,均合并多器官功能衰竭。B组胰性脑病病例集中在前5年（1997年1月至2001年12月）,近5年没有发现胰性脑病病例。结论积极消除各种诱因、治疗原发病和营养支持等有助于降低胰性脑病的发生率及病死率。     

重症急性胰腺炎68例治疗结果分析

目的探讨重症急性胰腺炎(severeacutepancreatitis,SAP)手术时机与预后的关系。方法对我院1988年1月~2004年12月收治的68例SAP病人的手术时机选择与并发症发生率、病死率和再手术率进行回顾性分析。结果早期手术组、延期手术组和非手术组的并发症发生率分别为73.3%、33.3%、26.0%,早期手术组较后两组差异有显著意义(P<0.05);病死率分别为33.3%、13.3%、13.0%,早期手术组明显高于后两组(P<0.05);早期手术组再手术率为46.6%,而延期手术组为16.6%(P<0.01)。结论SAP应避免在急性期手术,而尽量采用非手术或延期手术治疗。     

腹腔镜联合动脉区域灌注治疗重症急性胰腺炎

目的探讨腹腔镜联合动脉区域灌注治疗重症急性胰腺炎（severe acute pancreatitis,SAP）的效果。方法将75例SAP患者随机分为常规治疗组（35例）和联合治疗组（40例）。常规组进行常规的内科治疗,联合组在常规内科治疗的基础上附加动脉区域灌注及腹腔镜胆囊造瘘和引流。对比两组的有关临床指标和治疗效果。结果联合治疗组慢性健康状况评分Ⅱ评分明显降低（P〈0．05）,肝、肾功能明显改善（P〈0．05）,胰腺损害的CT评分显著降低（P〈0．05）,炎性因子、肿瘤坏死因子α及IL-1β明显减少,IL-10明显增多（P〈0．05）,器官衰竭发生率明显下降（P〈0．05）,器官衰竭治疗成功率明显升高（P〈0．05）,病死率明显降低（P〈0．05）。结论在常规治疗基础上附加动脉区域灌注及腹腔镜胆囊造瘘和引流,能有效提高SAP的治疗效果,降低病死率。