K_(ATP)通道与吸入麻醉药的心肌保护

K_(ATP)通道是内向整流K~+通道超家族成员之一,其开放导致动作电位持续时间迅速下降,这种下降通过电压调节的Ca~(2+)通道,抑制Ca~(2+)向细胞内流,降低细胞内Ca~(2+)蓄积,从而产生心肌保护作用。这种机制在缺血或吸入麻醉药预处理心肌保护的众多机制中,具有极其重要的信息传导的终末效应器作用。     

麻醉药心肌保护的线粒体K(ATP)通道机制

线粒体膜ATP敏感性钾通道(mitoKATP)在心肌缺血预处理及麻醉药预处理中起重要作用，mitoKATP通道的开放可能是预处理心肌保护作用的最终效应器。麻醉药通过活化或抑制mitoKATP通道活性而影响预处理的心肌保护作用。     

实验性糖尿病大鼠胰腺组织Kir6.2表达及药物干预

目的:观察实验性糖尿病大鼠胰腺组织KATP,通道的Kir 6.2亚基表达变化,以及那格列奈、丹参素对其干预.方法:Wistar大鼠建立糖尿病模型后,随机分为模型组、西药组、中药组,并设空白组,激光共聚焦显微镜观察免疫荧光染色的各组胰腺组织Kir6.2的表达变化.结果:模型组大鼠胰腺Kir6.2表达显著下降,两药物组Kir6.2的组织表达水平较模型组有不同程度上调(P<0.01).结论:糖尿病大鼠表现出胰腺组织Kir6.2表达降低,可能是β细胞适应高血糖和胰岛素抵抗的一种代偿机制;那格列奈、丹参素对其表达有一定的上调作用,可能是二者的一个重要降糖机制.     

MitoK_(ATP)通道对重症急性胰腺炎心肌的保护机制

<正>重症急性胰腺炎(severe acute pancreatitis,SAP)是一种病情凶险、并发症多的急腹症,常并发胰外脏器损害,包括心血管失代偿、急性呼吸窘迫综合征(acute respiratory distresssyndrome,ARDS)、消化道出血、急性肾功能衰竭、胰性脑病,     

ATP敏感钾通道在大鼠逼尿肌不稳定膀胱中的表达及变化

目的：探讨ATP敏感钾通道（KATP）与逼尿肌功能变化之间的关系。方法：根据膀胱压力容积测定结果将动物分为稳定组（29只）和不稳定组（9只）,其中稳定组分为BOO（11只）、SCI模型（9只）和对照组（9只）,通过RT-PCR技术测定逼尿肌中各型KATPmRNA表达及变化。结果：正常大鼠中逼尿肌不稳定发生率为24．3％。KATP在各组模型大鼠逼尿肌中均有表达。KATP的SUR2B亚型在BOO和SCI组逼尿肌中的表达高于正常对照组;IDI组中SUR2B的含量与正常对照组无明显差别。结论：KATP的表达异常可能是导致平滑肌细胞静息电位降低、兴奋性增高,引起逼尿肌不稳定的重要原因。     

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.     

Inhibition of ATP-sensitive K+ channels in pancreatic beta-cells by nonsulfonylurea drug linogliride

Linogliride is a nonsulfonylurea drug that lowers blood glucose levels in nondiabetic and diabetic humans and animals. Linogliride also stimulates insulin release in vitro. In the perfused pancreas, pretreatment with tolbutamide desensitizes beta-cells to the action of linogliride. We tested the hypothesis that linogliride, like tolbutamide, affects the activity of ATP-sensitive K+ channels, which are thought to control insulin release. We used the whole-cell voltage-clamping technique to measure the K+ current through ATP-sensitive K+ channels in the plasma membrane of single rat beta-cells, which were dialyzed with 30 microM ATP. Linogliride (10-300 microM) inhibited the K+ current; half-maximal inhibition was observed at 6-25 microM, depending on how much time was allowed for equilibration of the drug. Reversal of the inhibition was slow (t1/2 approximately 4 min). In summary, linogliride leads to a decrease in the activity of ATP-sensitive K+ channels.     

慢性胰腺炎伴胰管结石外科治疗体会

目的 探讨慢性胰腺炎伴胰管结石外科治疗的术式选择.方法 对1991年6月至2006年6月收治的17例慢性胰腺炎伴胰管结石手术治疗的患者进行回顾性分析,总结不同类型的胰管结石的手术方式及结果.结果 本组17例中胰头部胰管结石13例,胰体尾部胰管结石4例,合并胆石症6例,其中6例行胰管切开取石胰管空肠吻合术(Partington法);4例行胰管胃吻合术(Warren法);3例行保留十二指肠胰头次全切除术(Beger法);3例行胰尾切除胰腺空肠吻合术(Duval法);1例行胰尾、脾切除胰腺空肠吻合术.17例临床治愈,其中上腹部顽固性疼痛完全缓解15例,血糖控制2例,胰漏2例,1例术后11个月死于胰腺癌.结论 针对慢性胰腺炎合并胰管结石患者的不同状况采取的手术方式应高度个体化,有主胰管扩张者采取引流术,无胰管扩张及局部胰腺病变者采取胰腺部分切除联合内引流术,同时注意尽量保存胰腺组织功能,可明显改善患者生活质量.     

急性胰腺炎时胰腺缺血与细胞因子相关性的实验研究

目的探讨大鼠急性胰腺炎(AP)时胰腺缺血和细胞因子过度释放的关系.方法以牛磺胆酸钠诱导大鼠AP,20只为急性水肿性胰腺炎(AEP)模型、20只为急性坏死性胰腺炎(ANP)模型,另取10只正常大鼠作为对照.术后12 h处死各组10只大鼠,取血和胰腺组织,检测肿瘤坏死因子α(TNF-α)和白细胞介素10(IL-10)水平,观察胰腺病理变化,并以多普勒超声仪检测大鼠胰腺血流(PBF).结果AEP大鼠血清和胰腺中TNF-α和IL-10水平均升高,分别为(186±13)、(210±30) pg/ml和(660±29)、(669±62) pg/ml;ANP大鼠两者分别为(337±56)、(443±60) pg/ml和(124±12)、(202±38)     

Impaired glucose sensitivity of ATP-sensitive K+ channels in pancreatic beta-cells in streptozotocin-induced NIDDM rats.

ATP-sensitive K+ channels (KATP channels) are known to play a key role in the cellular mechanism of insulin secretion from pancreatic beta cells. In order to examine the possible impairment of KATP channel function in non-insulin-dependent diabetes mellitus (NIDDM), we have studied the properties of the KATP channels in single beta cells of neonatally streptozotocin-induced diabetic rats (NSZ rats) using the patch-clamp technique. The unitary conductance of the channel in diabetic beta-cells was virtually identical to that in control beta cells and there was no difference in the sensitivity to ATP and glibenclamide of KATP channels between the NIDDM and control groups. In response to glucose, the activity of the KATP channels was diminished in a dose-dependent manner in both control and diabetic cells. However, the inhibition of the KATP channels in beta-cells of NSZ rats was significantly less than that in control cells. Even in the presence of 11.1 mM glucose, the openings of a few single KATP channels were consistently observed in cell-attached patch membranes of diabetic, but not control, beta-cells. Thus, it appears that the impaired insulinotropic action of glucose in beta-cells in NSZ rats is associated with a reduced sensitivity of the KATP channel to glucose, but not to ATP, presumably due to a deficiency in glucose metabolism.     

首发症状为急慢性胰腺炎的胰腺癌诊断与治疗

目的 总结首发症状为急慢性胰腺炎的胰腺癌的诊断与治疗经验.方法 回顾性分析2003年1月至2014年6月大连医科大学附属第一医院和大连医科大学附属中心医院收治的13例以急慢性胰腺炎为首发症状的胰腺癌患者的临床资料.患者术前行实验室和影像学检查,术前根据肿瘤部位、进展程度和患者意愿决定治疗方案.治疗方法包括手术、放疗、化疗或其他对症支持治疗.手术患者术中及术后行病理学检查.通过电话随访患者出院后生存情况,随访时间截至2014年7月.结果 13例患者表现为腹痛,7例表现为腰背痛.7例患者体质量下降.13例患者均无胰腺癌家族史.13例患者中1例拒绝采血化验,12例患者血清CA19-9值升高(其中11例＞1×105 U/L),5例患者血清CEA升高.13例患者均行腹部CT平扫或增强扫描,3例患者行MRI检查,3例患者行超声检查.肿瘤位于胰头部9例、胰颈部2例、胰尾部2例.肿瘤大小为1.7 cm×1.7 cm～4.9 cm ×4.8 cm.7例患者见胆总管、肝内胆管、胰管扩张.3例患者肿瘤侵犯肠系膜上静脉.腹腔内淋巴结明显肿大者4例,腹腔积液者3例.CT检查证实胆囊结石2例,MRCP检查证实胆总管结石1例.超声检查均提示胰腺体积增大,其中2例提示主胰管扩张.10例患者经影像学检查排除腹腔其他部位恶性肿瘤证实为胰腺癌晚期.依据影像学进行分期,临床分期为Ⅱ期5例、Ⅳ期8例.2例患者行胰十二指肠切除术,其中1例术后行放化疗.1例患者行姑息性胆肠吻合+胃空肠吻合术.10例非手术患者中1例施行放疗,2例施行化疗,其余7例患者采取对症支持治疗.2例行胰十二指肠切除患者的病理学检查结果均为中、低分化腺癌,瘤体大小分别为4.0 cm ×3.0 cm×2.5 cm和2.5 cm×2.0cm×1.0cm.13例患者中3例失访.慢性胰腺炎为首发症状的患者生存时间为0.5 ～10.0个月,中位生存时间为3.0个月.急性胰腺炎为首发症状的患者生存时间为2.0 ～6.0个月,中位生存时间为4.5个月.4例CEA升高的患者,出院后平均生存时间为3.5个月,5例CEA未升高的患者出院后平均生存时间为5.4个月.10例随访患者在随访期内均因胰腺肿瘤转移或复发死亡.结论 首发症状为急慢性胰腺炎的胰腺癌临床症状不典型,早期诊断较为困难,确诊时多为晚期,预后较差.联合实验室和影像学检查,并依据病情变化动态追踪可提高诊断的准确性.治疗采用以外科手术为主的综合治疗.     

胰头肿块型胰腺炎诊断和外科治疗进展

随着慢性胰腺炎发病率的逐年升高,胰头肿块型胰腺炎发病率也逐年升高。在临床工作中,胰头肿块型胰腺炎与胰腺癌较难鉴别。但是两者的治疗方案决然不同,且预后差别大。因此胰头肿块型胰腺炎越来越多的受到临床工作者关注。笔者就胰头肿块型胰腺炎的诊断和外科治疗做一综述,以期望为临床提供一些参考。     

内源性一氧化氮对急性胰腺炎大鼠胰腺微血管通透性的影响

目的 探讨内源性一氧化氮（NO）对急性坏死性胰腺炎大鼠胰腺炎大鼠胰腺微血管通透性的影响。方法 以5%牛磺胆酸钠溶液胰胆管注射（1ml/kg）制成大鼠急性坏死性胰腺炎模型,以工具药L-硝基精氧酸（L-NNA）和内源性NO的阻断Evans Blue的漏出代表微血管的通透性,观察内源性NO对胰腺组织损伤程度、胰腺内Evans Blue漏出等的影响。结果 牛磺胆酸钠胆管注射造成大鼠胰腺组织明显坏死和炎性细胞浸润,以及血清淀粉酶浓度升高、胰腺湿/干重比率产加和明显的胰腺组织内Evans Blue积聚。以L-NNA（12.5mg/kg）阻断内源性NO后,胰腺组织坏死和炎性细胞浸润进一步加重,并使血清淀粉酶浓度升高,胰腺湿/干重比率增加,Evans Blue的漏出率也较之单纯胰腺炎组大鼠明显增加。结论 内源性NO具有胰腺保护作用,其保护机制可能与维持胰腺微血管的完整性有关。     

胰管结石伴发慢性胰腺炎急性发作临床诊治探讨

目的 探讨胰管结石伴发慢性胰腺炎急性发作的临床治疗方案.方法 回顾性分析南华大学附属南华医院1998年1月至2006年9月收治的11例胰管结石伴发慢性胰腺炎急性发作病人的临床资料,11例均接受手术治疗,其中胰头部胰管切开加十二指肠乳头成形及胆总管切开T管引流术2例,胰管切开取石并胰管空肠Roux-en-Y吻合术5例,胰体尾切除加胰断端面胰管空肠Roux-en-Y吻合2例.单纯胰尾切除2例.结果 术后疼痛治愈率54.54%(6/11),好转率45.45%(5/11),胰漏(瘘)或出血27.27%(3/11).9例平均随访时间(39.2±36.2)个月,均无并发症出现.结论 胰管结石伴发慢性胰腺炎急性发作者早期宜非手术治疗,3个月后接受适宜的外科手术治疗,效果肯定.并发症发生率较低,术式根据结石部位、主胰管是否通畅决定.     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.     

胰管开口炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗

目的 探讨胰管开口部位炎性病变导致的慢性阻塞性胰腺炎的诊断和外科治疗方式.方法 对我院自2002年1月至2010年11月收治的28例慢性阻塞性胰腺炎患者的临床资料进行回顾性总结.其中13例患者血清淀粉酶和脂肪酶升高伴有反复急性腹痛,经影像学检查显示胰管全程扩张改变,外科探查明确诊断为胰管开口部位炎性病变导致的慢性阻塞性胰腺炎.对此13例患者的临床表现、诊断方法、手术探查发现和治疗方法进行分析,并对术后的状况包括疼痛复发、生活质量、胰腺的影像学变化和血清胰腺酶学进行随访观察.结果 13例患者均具有典型的慢性阻塞性胰腺炎的临床表现,但12例患者的影像学表现有别于十二指肠乳突、壶腹或胰腺导管内肿瘤导致的慢性阻塞性胰腺炎的图像特征,手术探查和影像学揭示多数患者的胆胰共同通道过短或存在胰腺分裂畸形,对12例患者实施十二指肠乳突、壶腹及胰管开口切开成形术或副乳突切开成形术,术后随访结果显示均未再伴有胰腺酶学升高的急性腹痛发作.结论 以胰管扩张为主而不伴有胆管慢性梗阻是胰管开口炎性病变导致的慢性阻塞性胰腺炎的影像学特征,十二指肠乳突炎症或副乳突炎症时容易在过短的胆胰共同通道或胰腺分裂畸形的患者中引发胰管开口的狭窄而发生慢性阻塞性胰腺炎,纠正胰管开口狭窄、改善胰管引流的局部成形术是简单、有效的治疗方法.