风湿性二尖瓣病变患者血流动力学的改变对左心功能影响

对５２例风湿性二尖瓣病变血流动力学和左心室功能参数测定，ＭＲ＋ＭＳ组血流动力学参数比较无显著差异（Ｐ＞０．０５）；而左心室功能测定值两组间比较有显著差异。将血流动力学参数与左心功能测定值对比分析，血流动力学异常改变与ＤＳ、Ｄｄ、ＥＤＶＩ、ＥＳＶＩ呈正相关，而与ＦＳ、ＣＩ、ＬＶＳＷＩ呈负相关。研究提示血流动力学异常改变显著影响左心室功能     

146例严重肺动脉高压者二尖瓣替换术疗效分析

评价风湿性二尖瓣病变伴重度肺高压病人的手术效果。采用方差分析、卡方检验对肺动脉收缩压（ＳＰＡＰ）≥９．３３ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）并接受二尖瓣替换术（ＭＶＲ）的１４６病人的临床资料进行分析，将其分为４组。Ａ组：极重度肺高压（ＳＰＡＰ≥１３．３ｋＰａ）；Ｂ组：心功能严重低下组（心脏指数ＣＩ≤３３．３４）；Ｃ组：心功能减低或正常组（３３．３４≤ＣＩ≤６６．６８）；Ｄ组：高心排血量组（ＣＩ≥６６．６８）。其中每组按一次和二次手术再分为２个亚组。结果示一次手术组总死亡率为５．３％；Ａ１、Ｂ１、Ｃ１、Ｄ１４组术前临床情况、所用术式和心脏阻断时间等无差异，但Ｂ１组低心排（２４．２％）早期死亡率（１５．２％）明显高于其它３组（Ｐ＜０．０５），而Ｄ组无死亡。二次手术组总死亡率为２８．２％；各亚组低心排及死亡率均明显高于一次手术各组。由此认为，二尖瓣病变伴重度肺动脉高压病人，ＭＶＲ后低心排和早期死亡率与术前心脏指数有关。当心脏指数＞３３．３４时，即使肺动脉压和全肺阻力同时极度增高者，术后低心排和死亡率亦不因此增加。当ＣＩ＜３３．３４时，术后低心排及早期死亡率较高。重度肺动脉高压者施行二次ＭＶＲ手术时风险性较大     

心脏人工瓣膜替换术510例

１９８７年６月至１９９７年１２月,我们共为５１０例病人施行了心脏人工瓣膜替换术。现就术前准备、手术方法以及术后处理等进行讨论如下。临床资料　本组中男２４８例,女２６２例;年龄１４～６４岁。风湿性心脏病４５１例,其中单纯二尖瓣狭窄（ＭＳ）６６例,单纯二尖瓣关闭不全（ＭＩ）５例,ＭＳ＋ＭＩ１７４例,二尖瓣病变（ＭＶＤ）加三尖瓣病变（ＴＶＤ）６３例,主动脉病变（ＡＶＤ）３５例,ＭＶＤ＋ＡＶＤ１０２例,ＭＶＤ＋ＡＶＤ＋ＴＶＤ６例;先天性心脏病３０例,其中ＭＶＤ１０例,ＡＶＤ１０例,动脉导管未闭（ＰＤＡ）…     

风心病二尖瓣狭窄合并小左心室的瓣膜替换术

１９８７～１９９３年３８９例二尖瓣狭窄（ＭＳ）行二尖瓣替换术（ＭＶＲ）的病人中有小左室者１２６例，其中左室萎缩２８例。心功能ＩＩＩ级７６例、ＩＶ级３５例，重度肺动脉高压６４例。手术死亡率９５％，明显高于同期非小左室病人。主要死亡原因为右心衰、急性左心衰及瓣膜功能障碍。晚期死亡率为１６％／病人－年，１、５年生存率为９６５％和８８４％。术后心脏超声显示小左室及左室萎缩者均出现左室构形和功能的重建，后者重建过程较长。结果表明，小左室主要影响术后早期效果，重度ＭＳ合并小左室，尤其是伴有严重肺动脉高压及左室萎缩，是手术的高危指标。     

80例双瓣替换术的体会

自１９８６年９月至１９９３年７月，为风湿性心脏瓣膜病人施行主动脉瓣，二尖瓣双瓣替换术８０例，手术死亡率３．７５％（３／８０）。８０例中男３８例，女４２例，年龄平均３５．４３岁，心功能Ⅱ级２例，Ⅲ级４５例，ＩＶ级３３例。围术期行血流动力学监测７２例。本组术后发生多脏器功能不全６例。作者对双瓣替换术中常遇到的难点及处理，术后多脏器功能不全（ＭＯＤ）的防治以及如何降低手术死亡率等问题进行了讨论。     

异氟醚和氧化亚氮吸入麻醉对不 同心功能心脏瓣膜手术病人血液动力学的

观察异氟醚和氧化亚氮麻醉对不同心功能损害病人血液动力学影响。方法：３９例心脏瓣膜病人按术前心功能分为两组，采用Ｓｗａｎ－Ｇａｎｚ导管监测血液动力学变化。结果：诱导后两组ＣＩ、ＬＶＷＩ、ＲＶＷＩ、ＨＲ及ＭＰＡ均有降低，但ＳＩ无变化。     

心脏粘液瘤外科治疗近远期疗效

198 6年 9月至 2 0 0 0年 2月 ,我们共手术治疗心脏粘液瘤71例 ,取得了满意的近、远期疗效。现报道如下。临床资料　 71例中男 30例 ,女 41例 ;年龄 17～ 6 6岁 ,平均 43岁。术前有活动后心悸、气急 5 3例 ,腹胀、纳差 14例 ,阵发性呼吸困难、不能平卧 2例 ,发作性晕厥 3例 ,脑栓塞 1例 ,下肢动脉栓塞 2例。ＮＹＨＡ心功能ＩＩ级 14例、ＩＩＩ级 49例、ＩＶ级 8例。所有病人均经心脏彩色超声心动图明确诊断 ,其中左心房粘液瘤 6 3例、右心房粘液瘤 5例、双心房粘液瘤 3例 ;合并房间隔缺损 2例 ,器质性二尖瓣病变 4例 (其中风湿性二尖瓣病变 …     

转子泵左心辅助41小时抢救严重低心排成功1例

转子泵左心辅助４１小时抢救严重低心排成功１例刘中民，朱洪生，周嘉，叶清，梁保罗，郑家豪病人女，４４岁。风湿性心脏病，二尖瓣狭窄闭式扩张术后再狭窄，重度三尖瓣关闭不全和肺动脉高压９．０６ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ），心功能ＩＶ级，明显心脏恶液质。...     

小切口胸骨下段劈开心脏跳动下心脏手术100例

20 0 0年我们完成各类心脏手术 30 0例 ,其中 10 0例在正中小切口胸骨不完全劈开心脏跳动下心脏手术 ,效果满意。临床资料　本组病人男 5 2例 ,女 4 8例。年龄 3～ 4 9岁 ;先天性心脏病平均 9 5岁 ,风湿性心脏病平均 35 5岁。病种包括室间隔缺损 (ＶＳＤ) 4 1例 ,房间隔缺损 (ＡＳＤ) 2 6例 ,部分型心内膜垫缺损 4例 ,二尖瓣病变 2 8例 (二尖瓣置换 2 6例 ,二尖瓣成形 2例 ) ,左心房粘液瘤 1例 (摘除术 )。心功能Ｉ～ＩＩ级者 71例 ,ＩＩ～ＩＩＩ级者 14例 ,ＩＩＩ～ＩＶ级者 15例。心胸比率0 4 8～ 0 5 7者 71例 ,0 5 8～ 0 70 2 0例 …     

重症心脏瓣膜置换手术的麻醉处理

重症心脏瓣膜病变患者由于术前病程长 ,心肌受累重 ,合并症多 ,尤其是心肌严重损害引起的血液动力学障碍 ,继发肺动脉高压及其他重要脏器功能障碍等使手术死亡率明显增高 ,施行瓣膜置换手术时麻醉危险性也明显增加。本文总结 31例重症心脏瓣膜置换术的麻醉处理经验。资料与方法一般资料　 31例重症心脏瓣膜病变患者 ,男性 13例 ,女性 18例 ;年龄 16～ 5 4岁 ,体重 39～ 6 9ｋｇ。疾病种类为风湿性二尖瓣病变 13例 ,主动脉瓣病变 6例 ,二尖瓣及主动脉瓣联合瓣膜病变 12例。心功能分级Ⅲ级者 14例 ,Ⅳ级者 17例 ,心胸比例 (Ｃ/Ｔ) 0 70～ 0 …     

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.