无创正压通气治疗全麻拔管后呼吸衰竭

目的 评价无创正压通气(NIPPV)治疗全身麻醉手术拔管后呼吸衰竭的疗效及影响因素.方法 全麻手术拔管后48 h内发生呼吸衰竭的患者34例,应用BiPAP Vision呼吸机实施无创正压通气治疗,比较治疗后避免再插管(成功组)和需要再插管(失败组)患者的基础状态、通气疗效及临床结果,并分析可能的影响因素.结果 无创正压通气使70.6%的术后呼吸衰竭患者避免插管.与失败组相比,成功组心肺并发症所致呼吸衰竭的比例和需要人工辅助吸痰的比例明显低(P<0.05),麻醉药残留呼吸抑制的比例高(P<0.01).结论 无创正压通气治疗全身麻醉手术后呼吸衰竭能够减少再插管率,但可能不适用于存在心肺并发症和排痰障碍的患者.     

伴呼吸衰竭脊柱侧凸的围手术期处理及治疗策略

目的 探讨伴有呼吸衰竭的脊柱侧凸的术前肺功能评估及相应的临床治疗策略.方法 2000年9月至2008年6月,收治16例脊柱侧凸患者接受系统完整的术前呼吸功能训练并成功接受后路矫形内固定手术,动脉血气分析达到呼吸衰竭的诊断标准,肺活量(vital capacity,VC)为预计值的25%～34%.5例为特发性脊柱侧凸,男2例,女3例;年龄10～16岁,平均13.5岁.11例为先天性脊柱侧凸,男5例,女6例;年龄10～14岁,平均12.4岁;椎体形成不良2例,分节不良4例,混合型5例;其中8例存在并肋畸形,7例合并肋骨缺失.按照累及部位划分,胸段脊柱侧凸10例,胸腰段脊柱侧凸1例;胸腰双主弯3例,三弯2例.16例患者术前Cobb角平均126.6°±15.5°;身高120～160 cm,平均137.6cm;体重18～40 kg,平均32.5 kg.根据术前肺功能状况和畸形严重程度决定手术方法.术前呼吸功能治疗包括:清醒状态下无创呼吸机辅助呼吸,Halo牵引,呼吸训练.结果 16例患者经过规范的呼吸训练和呼吸机及牵引治疗后,呼吸状况均有明显改善,可以耐受脊柱侧凸矫形手术.10例患者术后1 h顺利拔除气管插管,能够自主呼吸;另6例患者术后须转ICU,呼吸机辅助呼吸,24 h内恢复自主呼吸而拔管.术后2例患者发生肺水肿(其中1例合并肺部感染),未出现肺不张及重要脏器功能衰竭等严重并发症.术后Cobb角72.0°±13.2°,平均矫正率43%,外观改善明显.结论 通过完备的术前肺功能评估和围手术期准备,伴有呼吸功能衰竭的脊柱侧凸患者可以接受脊柱矫形手术并获得良好的治疗效果.     

脊柱侧凸患者术前肺功能、手术方式与术终气管拔管时间的相关性分析

目的对脊柱侧凸患者术前肺功能指标、手术方式与术终拔管时间的相关性进行回顾性研究。方法选取我院脊柱外科于2000年9月至2005年6月收治的115例脊柱侧凸患者为研究对象,应用多元线性回归分析对患者术前肺功能及手术方式与拔管时间的关系进行相关性分析。结果术终气管拔管时间经胸组与未经胸组之间无显著差异,而行胸廓成形术组显著大于不行胸廓成形术组（P=0．009）。多元线性回归分析结果显示侧凸患者术终气管拔管时间与肺活量百分比、最大通气量百分比、第一秒最大呼气容积百分比、用力呼气中期流速百分比及是否行胸廓成形术之间呈显著负相关。结论肺活量百分比、最大通气量百分比、第一秒最大呼气容积百分比、用力呼气中期流速百分比及是否行胸廓成形术是影响术终气管拔管时间的主要因素。术前肺功能测定及术式的选择对术终气管拔管时间的判断有指导意义。     

马方和类马方综合征合并脊柱侧凸患者肺功能障碍的模式及影响因素

目的 探讨合并脊柱侧凸的马方和类马方综合征患者肺功能损害的模式及其影响因素.方法 回顾性分析1998年2月至2007年9月行脊柱侧凸矫形内固定手术且有术前肺功能资料的25例马方和类马方综合征患者(A组)的临床资料,其中男性11例,女性14例;年龄11～20岁,平均15岁.分析其肺功能指标(实测值与预计值的比值)与冠状面Cobb角、胸弯顶椎位置、受累节段数以及胸椎后凸角的关系.并与同期行脊柱侧凸矫形内固定术且弯型与此匹配的38例青少年特发性脊柱侧凸(MS)患者(B组)的肺功能指标进行比较分析.结果 A组患者肺活量(VC)、用力肺活量(FVC)、第1秒最大呼气容积(FEVI)等指标与冠状面Cobb角呈显著负相关(r=0.514、-0.503、-0.464,P<0.05);VC、FVC、FEV1以及最大呼气中期流量(MMEF)等指标明显小于B组(P<0.05);顶椎位置在T_(4～8)与在T_(9～12)的患者之间肺功能指标差异无统计学意义;受累节段≥8的患者,VC、FVC、FEV1和最大自主通气量(MVV)等指标小于受累节段<8者(P<0.05);胸椎后凸角与肺功能指标之间无明显相关性.结论 合并脊柱侧凸的马方和类马方综合征患者肺功能损害较MS患者严重,其肺功能主要受胸弯受累节段数和胸弯冠状面Cobb角共同影响.     

Ⅰ型神经纤维瘤病合并脊柱侧凸患者肺功能损害模式的研究

目的 分析I型神经纤维瘤病(NF1)合并脊柱侧凸患者肺功能损害的模式,以及影响其肺功能的影像学因素.方法 选取2003年1月至2009年6月间收治的NF1合并脊柱侧凸患者36例(NF1组),特发性脊柱侧凸(IS)患者64例(IS组),术前检测患者的肺活量(VC)、用力肺活量(FVC)、第1秒用力呼气容积(FEV1)、最大呼气中期流量(MMEF)、最大自主通气量(MVV).比较两组肺功能参数的差异.按照弯型部位及有无萎缩性改变将NF1组患者分类并分类比较肺功能损害的差异,分析影响肺功能的影像学指标.结果 两组肺功能参数VC、FVC、FEV1、MMEF、MVV差异均无统计学意义(P>0.05).NF1组胸弯患者肺功能显著低于非胸弯患者;营养不良型患者与非营养不良型患者肺功能损害差异无统计学意义(P>0.05);顶椎位置以及Cobb角与肺功能参数显著相关(P<0.05).结论 NF1合并脊柱侧凸患者的肺功能损害模式与IS患者类似,胸弯患者比非胸弯患者肺功能损害严重,侧凸位置以及Cobb角大小是影响患者肺功能的主要因素.     

单一后路矫形术对严重脊柱侧凸肺功能的影响

目的探讨单一后路矫形手术对严重脊柱侧凸患者肺功能恢复的影响。方法 2007～2009年间有完整肺功能资料的胸弯Cobb角〉70°伴有肺功能障碍的严重脊柱侧凸患者30例纳入本次研究。患者年龄为10～36岁,平均17.0岁;其中男11例,女19例。使用肺功能检查评估患者术前和术后3个月、2年时的肺功能状况。结果患者术前平均Cobb角为109.1°,脊柱侧凸矫形术后Cobb角平均下降至65.6°,侧凸矫正率平均为43.0%。术后3个月患者肺功能有轻微的改善,与术前相比差异无统计学意义（P〉0.05）。术后2年患者的肺活量（vital capacity,VC）升高了23.8%、VC与预计值的比升高了17.6%、用力肺活量（forced vital capacity,FVC）升高了23.6%、FVC与预计值的比升高了17.1%、1秒用力呼气量（forced expiratory volume in 1 s,FEV1）升高了25.6%,与术前相比差异有统计学意义（P〈0.05）;FEV1与预计值的比升高了21.9%,与术前相比差异无统计学意义（P〉0.05）。患者术前肺功能参数与术前Cobb角成负相关,术后肺功能参数的改善率均与术前Cobb角成正相关。结论单一后路矫形手术可以有效的改善脊柱侧凸患者的肺功能,并随着术后时间的延长肺功能的改善越发显著,术前脊柱侧凸越严重术后肺功能的恢复效果也越明显。     

生长棒技术治疗早发性脊柱侧凸术后的肺功能变化

 目的 分析生长棒技术治疗早发性脊柱侧凸术后的肺功能变化。方法 2002年9月至2011年7月,以生长棒技术治疗早发性脊柱侧凸患者10例,男3例,女7例;年龄6~9岁,平均(7.0±1.1)岁。9例为先天性脊柱侧凸,1例为神经肌肉型脊柱侧凸。4例已完成最终融合手术(已融合组),6例未完成最终融合手术(未融合组)。记录每次手术术前的用力肺活量(FVC)、一秒钟用力呼气容积(FEV1)、Cobb角、C7-S1距离,计算FVC、FVC/FVC预测值百分比、FEV1、FEV1/FEV1预测值百分比变化,分析FVC变化与Cobb角变化及C7-S1距离变化的相关性。结果 已融合组中FVC与FEV1均增高,其中最终融合术前与生长棒置入术前FVC的差异有统计学意义。未融合组中FVC与FEV1均增高,末次延长术前与生长棒置入术前FVC、FEV1的差异均具有统计学意义。两组病例生长棒置入术前与末次手术前FVC/FVC预测值百分比及FEV1/FEV1预测值百分比的变化均无统计学意义。FVC变化与Cobb角变化及C7-S1距离变化值无相关性。结论 生长棒技术治疗早发性脊柱侧凸术后肺功能得到改善,肺功能的改善与Cobb角变化及C7-S1距离变化无关。     

特发性与先天性脊柱侧凸患者肺功能障碍的差异性比较

目的：比较特发性脊柱侧凸（idiopathic scoliosis，IS）与先天性脊柱侧凸（congenital scoliosis．CS）患者肺功能参数的差异性。方法：术前检测214例脊柱侧凸患者的肺活量（vital capacity，VC）、用力肺活量（forced vital capacity，FVC）、第1秒用力呼气容积（forced expiratory volume in one second，FEV1）、最大呼气中期流量（maximal mid-expiratory flow，MMEF）、最大自主通气量（maximal voluntary ventilation，MVV），计算实测值占预计值百分比（实／预％），其中IS 141洌（IS组），CS73例（CS组），将肺功能指标与Cobb角进行相关分析。依据主弯顶椎所在位置分为胸段及非胸段侧凸两组，胸段侧凸依据Cobb角大小分为：Cobb角〈600（A组）、60&#176;≤Cobb角〈90&#176;（B组）、Cobb角≥90&#176;（C组）3组。分析胸段及非胸段IS、CS患者术前肺功能参数的差异．同时比较年龄≤10岁的IS、CS患者各参数的差异。结果：脊柱侧凸患者VC、FVC、FEV1、MMEF及MVV的实／预％与Cobb角呈显著性负相关（r=-0．40--0.55）。在胸段侧凸患者中，CS组的FEV1实／预％为64．2％，明显低于IS组患者的80．0％（P〈0．05）；不同Cobb角CS组患者的VC、FVC、FEV1、MVV实／预％值都较相应Cobb角的IS组患者低（P〈0．05）。非胸段侧凸患者中，CS组的VC、FVC、MVV的实／预％较IS组患者低（P〈0．05）。年龄≤10岁的CS与IS患者肺功能指标比较也具有显著性差异（P〈0．05）。结论：IS和CS患者均存在肺功能损害，但损害模式不同，IS以限制性通气功能障碍为特征，CS表现为混合性通气功能障碍；年龄和Cobb角相匹配时．无论在胸段还是非胸段，CS患者的肺功能损害均较IS患者严重；且两者肺功能损害的差异性在青春期前就存在。     

支具治疗对青少年特发性脊柱侧凸近期肺功能的影响

[目的]比较青少年特发性脊柱侧凸患者支具治疗前与末次随访肺功能的变化,探讨支具治疗对患者近期肺功能的影响。[方法]对2009年2月～2010年10月在本院接受规范支具治疗的40例青少年特发性脊柱侧凸患者;其中男性4人,女性36人;初诊时年龄10～14岁,平均12.2岁,骨骼发育Risser征0～Ⅱ度,平均1.1度;观察支具治疗前、末次随访时主侧凸冠状Cobb角以及肺功能等指标的变化。[结果]随访时间为6～17个月,平均8个月;支具治疗前主侧凸冠状Cobb角(28.41±6.45)°,末次随访时主侧凸冠状Cobb角(16.21±10.22)°,平均矫正率为43.56%,两者差异有显著性意义(P<0.05);支具治疗前、末次随访时肺功能指标VC(肺活量)、FEV1(第1 s时间肺活量)、MVV(最大通气量)实测值及占预计值百分率进行比较,结果有显著性差异(P<0.05)。随访期间患者脊柱侧凸的进展均得到有效控制,患者无明显呼吸困难及活动功能障碍等并发症。[结论]支具治疗对青少年特发性脊柱侧凸有矫正效果;但是对患者近期肺功能可能有消极影响,患者在佩戴支具期间需要加强对肺功能的锻炼。     

肥胖患者围手术期通气策略Meta分析

目的 系统评价围手术期不同通气策略对肥胖患者通气和肺功能的影响,选择最佳通气策略. 方法 网上检索EBSCO、PubMed、Spring、Ovid、Wiley、中国知网、维普网、万方数据等数据库,选择全身麻醉诱导期和拔管后的给氧模式以及术中不同潮气量对肥胖患者通气和肺功能影响的随机对照试验(randomized controlled trial,RCT),应用RevMan 5.3软件对纳入文献进行Meta分析. 结果 共纳入24篇RCT,946例患者.①麻醉诱导期头高位吸氧较平卧位吸氧无通气安全时限更长(P＜0.001),而自主呼吸时加用持续正压通气(continues positive airway pressure,CPAP)PaO2水平更高(P=0.005),转为机械通气后间歇正压通气(intermittent positive pressure ventilation,IPPV)+呼气末正压通气(positive end expiratory pressure,PEEP)较单用IPPV无通气安全时限更长(P＜0.001),PaO2更高(P＜0.001).②术中大潮气量比小潮气量通气联合PEEP获得更高的氧合指数(oxygenation index,OI)(P=0.02),但同时大潮气量通气可引起更高的气道压(P＜0.001).③拔管后采用无创正压通气(non-invasive positive pressure ventilation,NIPPV)较鼻导管吸氧PaO2更高(P=0.004). 结论 肥胖患者诱导期宜采用头高位CPAP以及IPPV+PEEP通气,术中采用大潮气量+高PEEP,术后拔管后采用NIPPV.     

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.