天普洛安在ERCP中的应用

自 1999年 6月至 2 0 0 0年 12月共行内窥镜逆行胰胆管造影 (ｅｎｄｏｓｃｏｐｉｃｒｅｔｒｏｇｒｄｅｃｈｏｌａｎｇｉｏ ｐａｎｃｒｅａｌｏｇ ｒａｐｈｙ ,ＥＲＣＰ) 15 0例 ,我们将病人随机分为天普洛安(乌司他丁 )实验组与对照组 ,实验组术前、术后常规使用天普洛安 ,与对照组比较天普洛安对ＥＲＣＰ病人的影响。临床资料乌司他丁实验组 75例中ＥＲＣＰ失败 2例 ,入选73例 ,其中男性 4 6例 ,女性 2 9例 ,年龄 2 1～ 77岁。对照组 75例ＥＲＣＰ全部成功 ,其中男 4 5例 ,女 30例 ,年龄 19～ 71岁。两组ＥＲＣＰ分类见表 1。表 1　乌司他…     

间置胆囊肝管空肠吻合治疗低位恶性阻塞性黄疸的探讨

目的　探讨间置胆囊肝管空肠吻合姑息治疗低位恶性阻塞性黄疸的价值。方法　对2 4例低位恶性阻塞性黄疸采用间置胆囊肝管空肠吻合姑息治疗。结果　 2 4例中术后未发生吻合口瘘 ,无胆道逆行感染 ,无手术死亡。血清胆红素下降 14例 (5 8.3 % ) ,术后 15d血清胆红素≤ 171μmol/L ,10例 (4 1.7% )术后 3 0d血清胆红素≤ 171μmol/L ;术后黄疸消退时间 18～ 3 5d ;术后 6个月、12个月、18个月生存率分别为 91.7%、62 .5 %、12 .5 %。结论　间置胆囊肝管空肠吻合是姑息治疗低位恶性阻塞性黄疸的有效措施。     

肝癌术后黄疸原因分析

目的　研究围手术期影响肝癌术后胆红素水平的相关因素以及相应的处理办法。方法　回顾分析 2 94例肝癌手术病例 (排除术前存在梗阻性黄疸者 ) ,找出影响术后胆红素的因素。对比术后胆红素≥ 5 1.3m mol/ L 与术后胆红素 <5 1.3mm ol/ L 两组病人在危险因素与近期疗效的差别。结果　术后胆红素与术前胆红素水平、肝硬化程度、手术持续时间和术中出血量明显相关。 4 8例观察组病人术前胆红素水平更高 (P<0 .0 0 1)、肝硬化较重 (P<0 .0 0 1)、手术持续时间长 (P<0 .0 0 1)、术中出血多 (P<0 .0 1)、住院时间长 (P<0 .0 1)、并发症和死亡率增高 (P<0 .0 0 1)。结论　 1围手术期胆红素水平在判断肝癌病人近期疗效中具有价值。 2手术应选择肝硬化程度轻或 /无 ,肝储备功能良好的病人、控制手术时间、减少术中出血量、及时处理术后胆道梗阻、加强围手术期治疗     

保留肛垫分瓣式缝吊内注术治疗环状混合痔的临床研究

目的 :探讨用新的手术方式治疗环状混合痔价值。方法 :以保留肛垫分瓣缝吊内注术治疗的病例为试验组 ,外剥内扎术治疗的病例为对照组。观察两个组的术后肛门解剖生理变化、术后并发症、术后恢复情况等指标。结果 :肛门解剖生理变化 :肛门周长试验组术前 (8.3± 0 .3) cm,术后 (8.1± 0 .4 ) cm,对照组术前 (8.4± 0 .3) cm,术后 (7.5± 0 .3) cm。术后肛管狭窄试验组0 ,对照组 14 .2 9% (4 / 2 8)。肛管弹性试验组手术前后无明显改变 ,对照组手术后明显变差。术后并发症 :术后疼痛、肛门水肿、大便失禁、肛门坠胀等发生率试验组明显低于对照组。创面愈合时间 :试验组 (13.6 1± 3.2 5 ) d,对照组 (2 0 .91± 3.82 ) d。结论 :保留肛垫分瓣缝吊内注术治疗环状混合痔能够保持肛门解剖生理结构 ,明显减少术后并发症 ,缩短创面愈合时间。     

胆肠搭桥内引流术治疗恶性梗阻性黄疸

总结胆肠搭桥内引流术治疗恶性梗阻性黄疸的疗效 ,分析、总结 1 991～ 1 999年间应用胆肠搭桥内引流术治疗晚期无法切除的恶性肿瘤所致肝外胆道阻塞性黄疸 39例的临床资料。结果显示 :血清总胆红素在术后 3d内以每日 (58.70± 46 .33 ) μmol/L的速度下降 ,术后 7～ 1 0d内以每日 (2 2 .3 6±1 1 .32 ) μmol/L的速度下降 ,ALP及GGT迅速下降。多在术后 2～ 4周黄疸消退 ,食欲及全身情况明显改善 ,无并发症发生 ,随访 30例平均生存 1 0个月。提示 :胆肠搭桥内引流术能迅速有效地解除胆道梗阻性黄疸 ,对晚期恶性肿瘤所致肝外胆道阻塞系一有效可行的姑息性治疗方法     

晚期胰腺癌围手术期免疫调节治疗的疗效评价

目的　探讨晚期胰腺癌围手术期免疫调节治疗效果。方法　 43例晚期胰腺癌随机分为香菇多糖综合治疗组和对照组 ,动态观察术后T细胞亚群、NK细胞活性的变化 ,比较两组病人的生存期。结果　香菇多糖综合治疗组术后NK活性 ,CD3,CD4细胞数和CD4/CD8比值较对照组明显升高 (P <0 .0 5 ) ;术后平均生存期 (14.9± 8.5 )月 ,明显高于对照组 (7.7± 3.5 )月 (P <0 .0 0 1)。结论　晚期胰腺癌病人围手术期免疫调节综合治疗 ,有助于提高机体细胞免疫功能和改善病人生存期     

黄芪对梗阻性黄疸围手术期肝肾功能的保护作用

目的:研究黄芪注射液对梗阻性黄疸围手术期肝肾功能的保护作用.方法:以经手术证实的64例梗阻性黄疸为研究对象,34例为实验组(黄芪组),术后给予黄芪注射液30 mL加入生理盐水中静脉滴注7～10 d.对照组30例给予常规治疗.结果:术后3 d病人肌酐(Cr)、谷草转氨酶(AST)较术前明显增高,总胆红素(TBIL)、肌酐清除率(Ccr)明显降低;术后7 d,TBIL较术前明显降低,Cr及AST与术前比较差异无显著性,但对照组Ccr较术前仍明显降低,黄芪组内皮素(ET-1)较术前明显降低.两组同时段比较,黄芪组Cr、AST较对照组明显降低,Ccr较对照组明显增高.结论:黄芪注射液对梗阻性黄疸围手术期病人的肝肾功能起保护作用,可能与降低ET-1有关.     

天普洛安在消化道恶性肿瘤术前支持治疗体会

目的 观察天普洛安改善消化道恶性肿瘤患者术前蛋白质代谢异常的作用。方法 以30例伴有中度营养不良消化道恶性肿瘤患者为研究对象，随机分为治疗组和对照组，对治疗组患者术前给予天普洛安支持治疗，并检测，比较支持治疗前，后以及手术后的血浆白蛋白，血浆前白蛋白，血红蛋白以及体重的变化。结果 治疗组血浆白蛋白，血浆前白蛋白的水平以及体重均有较明显的改变，而对照组15例血浆白蛋白，血浆前白蛋白以体重无明显改变。结论 天普洛安具有改善消化道恶性肿瘤患者的手术前蛋白质代谢异常的作用。     

梗阻性黄疸患者的围手术期处理及死亡原因的探讨

目的　探讨梗阻性黄疸围手术期处理和死亡原因。方法　对 1991年 12月～ 2 0 0 0年 12月间的 12 0例梗阻性黄疸患者进行回顾性分析 ,将 1995年以前的 5 8例患者作为 A组 ,1995年之后的 6 2例做为 B组进行比较研究。并对围手术期处理和死亡原因的探讨进行总结。结果　 (1)梗阻性黄疸患者的内毒素血症 ,高胆红素血症及肝功、肾功受损和术后死亡有密切关系。(2 ) B组并发症和术后死亡率分别为 4 0 .3% (2 5 /6 2 ) ;6 5 % (4/6 2 ) ,较 A组并发症 81% (47/5 8)和术后死亡率 2 0 .7% (12 /5 8)有显著降低 (P<0 .0 0 1)。(3)血清胆红素 >342 μmol/L 患者的病死率 (45 .8% )明显高于血清胆红素≤ 342 μm ol/l(8.6 % )患者 (P<0 .0 0 5 )。恶性病例的病死率 (38.1% )也显著高于良性病例 (4.8% ) (P<0 .0 0 5 )。结论　加强围手术期处理 ,选择适当的手术方式可减少梗阻性黄疸患者的手术、术后病死率     

恶性梗阻性黄疸介入治疗

目的 回顾性分析恶性梗阻性黄疸患者的介入治疗方法及近期疗效。方法62例患者,其中肝癌7例,胆囊癌10例,胆管癌15例,胰腺癌17例,肝门部转移癌13例。43例行内外引流,19例放置了胆道支架。结果 黄疸消退明显55例,不明显7例。内外引流者血清总胆红素由（450.12±113.51）μmol/L降至（240.25±107.81）L（1周）-（90.91±101.72）μmol/L（2周）。胆道内支架置入者由（410.53±98.13）μmol/L降至（270.23±115.64）μmol/L（1周）-（105.43±97.85）μmol/L（2周）。内外引流与内支架置入疗效无明显差别,早期并发症29例,死亡7例。结论 介入治疗恶性梗阻性黄疸方法简单、安全、疗效肯定。     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.