L-精氨酸对体外循环中红细胞保护作用的研究

目的：研究L－精氨酸（L-Arg)对体外循环（CPB）中红细胞的保护作用。方法：成年杂种犬12条，随机分为对照组（A组）和L－精氨酸组（B组），每组6条。两组动物均模拟临床开胸、建立体外循环、心肌缺血再灌注过程。B组于转机前静脉内注入L-Arg100mg/kg后，再持续静滴L-Arg10mg.kg^-1.min^-1至体外循环结束。分别于转前，并循5min，阻断15，45min，开放15，30min取静脉血测血浆一氧化氮（NO）代谢产物（NO^-2,NO^-3)、丙二醛（MDA）、游离血红蛋白（FHB）水平。结果：转机5min后的各时间段，B组的NO^-2、NO^-3水平显著高于A组，而血浆MDA及FHB水平显著低于C组。结论：L－精氨酸可使体外循环中血浆一氧化氮浓度明显增高，并使MDA、FHB浓度明显降低，因而能有效地保护CPB中红细胞。     

乌司他丁对体外循环中红细胞的保护作用探讨

目的研究体外循环对红细胞的损伤机制及乌司他丁对体外循环中红细胞的保护作用。方法外循环下行房室缺修补病人20例(CPB时间为30min左右),随机分为乌司他丁组(A组) 和对照组(B组),每组10人。观察两组病人不同时点的游离血红蛋白(FHb)、丙二醛(MDA),红细胞内钙、红细胞C3b受体花环率(RBC-C3bRR)、红细胞免疫复合物花环率(RBC-ICR)。结果(1) MDA、FHb、RBC-ICR、红细胞内钙:转机前,A、B组间无差异,两组转机30分钟后的各次标本含量均明显高于转机前,转机30分钟后A组含量又明显低于B组,组间差异有显著性。(2)RBC-3bRR:转机前两组RBC-C3bRR无明显差异,转机30分钟后两组RBC-C3bRR均明显低于转机前。但转机30 分钟后A组RBC-C3bRR又明显高于B组,组间差异有显著性。结论CPB可导致红细胞损伤及免疫功能下降。体外循环中加入乌司他丁可抑制体外循环中的炎症反应、减轻红细胞内钙离子超负荷,对体外循环中红细胞损伤有较好的保护作用。     

N-乙酰半胱氨酸对体外循环致大鼠脑损伤的保护作用

目的:探讨N-乙酰半胱氨酸(NAC)对体外循环(CPB)致大鼠脑损伤的保护作用.方法:将24只成年雄性SD大鼠随机分为假手术组(S组)、CPB组(C组)、CPB+NAC组(N组),每组8只.N组在CPB预充液中加入NAC 100mg/kg,然后以20 mg/(kg·h)速度输注直到停转流,C组输注等量生理盐水.停CPB后2h,测定血浆神经元特异性烯醇化酶(NSE)、S-100β蛋白、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平,检测脑组织丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-px)含量,透射电镜下观察海马区神经元细胞超微结构的变化.结果:与S组比较,C组血浆NSE,C组和N组血浆S-100β蛋白、TNF-α和IL-6水平及脑组织MDA、GSH-px含量均发生一定程度的改变;且N组血浆NSE、S-100β蛋白、TNF-α和IL-6水平,脑组织MDA和GSH-px含量均显著优于C组.与S组比较,C组和N组海马区神经元细胞超微结构均有一定程度的病理学改变,且N组的损伤程度较C组明显减轻.结论:NAC可减轻CPB致大鼠脑损伤,其机制可能与抗氧化、抗炎作用有关.     

N-乙酰半胱氨酸对体外循环期间大鼠肠屏障功能的影响

目的:观察N-乙酰半胱氨酸(MAC)对体外循环(CP8)期间大鼠肠黏膜屏障功能的影响.方法:雄性SD大鼠18只,体质量300～400 g,随机分为假手术组(S组)、体外循环(CPB)组(C组)和CPB+N-乙酰半胱氨酸(NAC)组(A组).建立大鼠CPB模型,S组仅在各部位插管,不转流,A组在预充液中加入100mg/kgNAC,然后以20mg·k-1·min-1速度输注直到停转流,C组输注等量生理盐水.采用分光光度计法和鲎试验偶氮显色法测定CPB后2 h大鼠血浆D-乳酸含量、二胺氧化酶(DAO)活性和内毒素(LPS)水平,透射电镜下观察各组大鼠小肠上皮病理改变.结果:与S组比较,C组和A组血浆D-乳酸含量、DAO活性和LPS水平升高(P<0.05);与C组比较,A组血浆D-乳酸含量、DAO活性和LPS水平降低(P<0.05);A组小肠上皮病理损伤程度较C组明显减轻.结论:CPB期间应用NAC能有效地降低大鼠血浆D-乳酸含量、DAO活性和LPS水平,提示NAC对CPB期间肠黏膜屏障功能具有一定的保护作用.     

Lipo-PGE1对体外循环患者围术期S100β蛋白的影响及机制

目的 观察前列腺素E1脂微球载体制剂(Lipo-PGE1)对心肺转流(CPB)患者围术期S100β蛋白的影响.方法 30例CPB患者随机均分成Lipo-PGE1(P)组和对照(C)组.P组CPB前持续静脉泵人Lipo-PGE1 3ng·kg-1·min-1至手术结束;C组给予相同容量的生理盐水.两组均于麻醉后手术前(T1)、CPB后30 min(T2)、开放升主动脉后1 h(T3)、CPB后6 h(T4)、CPB后24 h(T5)采颈静球血4 ml,分别测定血浆S100β、肿瘤坏死因子α(TNF-α)、丙二醛(MDA)、超氧化物歧化酶(SOD)浓度.结果 组内比较,T2～T4两组S100β、TNF-α浓度较T1升高(P<0.05或P<0.01).组问比较,P组T2～T4 S100β、TNF-α低于C组(P<0.05或P<0.01).T2～T4两组MDA浓度升高,SOD活性下降(P<0.05或P<0.01).组问比较,P组T2～T4 MDA浓度低于C组,SOD活性高于C组(P<0.05或P<0.01).结论 Lipo-PGE1可以减轻CPB患者围术期脑损伤的生化标志物S100β蛋白的表达水平,其可能机制主要是抑制炎性因子TNF-α的释放、减少MDA的产生和增加SOD活性.     

REM-PCL对体外循环犬心肌能量代谢的影响

目的观察犬体外循环(CPB)中REM-PCL对心肌能量代谢的影响。方法采用CPB心肌缺血再灌注模型,12只犬随机分为REM-PCL组(RP组,n=6)和对照组(C组,n=6)。RP组和C组分别于转机前静脉注射0.2mg/kg REM-PCL及等量生理盐水。分别于转机前、缺血60min和再灌注60min时,测定心肌线粒体肿胀度(MSD)、丙二醛(MDA)含量、腺苷酸(ATP、AMP、ADP、EC、TAN)、活性氧(ROS)和总抗氧化能力(T-AOC)。分别于转机前、再灌注30min和60min时测定平均动脉压(MAP)、心输出量(CO)和心率(HR)。结果两组与转机前比较,缺血后MDA、MSD和ROS均增加,TAN、EC、T-AOC及ATP含量均下降(P0.01);C组再灌注后MDA、MSD和ROS均增加(P0.01),TAN、EC、T-AOC及ATP含量均下降(P0.01);缺血60min和再灌注60min时RP组MDA、MSD和ROS均明显低于C组(P0.01),TAN、EC、T-AOC及ATP含量均明显高于C组(P0.01)。再灌注30min和60min时RP组MAP、CO和HR较C组恢复迅速(P0.01)。结论 REM-PCL通过保护心肌线粒体结构及改善缺血心肌能量代谢,减轻缺血心肌再灌注损伤。     

复方丹参注射液对大鼠体外循环后肺损伤的影响

目的:研究大鼠体外循环(CPB)后肺组织损伤以及复方丹参注射液对肺损伤的影响。方法:24只SD大鼠随机分为3组,对照组、CPB组和丹参组,每组8只。CPB组和丹参组建立体外循环,丹参组为停循环前5 min经体外循环的储血器给入复方丹参注射液1 ml.kg-1体重。对照组为假手术对照。CPB后60 min取部分肺组织,测定并计算丙二醛(MDA)、髓过氧化物酶(MPO)和组织含水量。取部分肺组织用多聚甲醛固定,制作石蜡切片,HE染色后观察形态学改变。结果:光学显微镜下观察可见,CPB组肺组织间质增厚、细胞浸润,丹参组的程度较CPB组有所减轻。CPB组和丹参组肺组织中MDA含量、MPO含量和含水量均明显高于对照组(P<0.05),丹参组升高程度小于CPB组(P<0.05)。结论:体外循环过程中应用复方丹参注射液能有效减轻肺损伤程度,可能与其清除氧自由基、减轻中性粒细胞浸润等作用有关。     

冠状动脉旁路移植术中舒芬太尼、芬太尼对血浆细胞因子和乳酸的影响

目的:比较体外循环(CPB)冠状动脉旁路移植术中舒芬太尼和芬太尼麻醉对血浆细胞因子和乳酸的影响.方法:择期冠状动脉旁路移植术30例,随机分为舒芬太尼组(S组)和芬太尼组(F组),每组15例.S组诱导麻醉为舒芬太尼1.0 μg·kg-1,继以1.5～3.0 μg·kg-1·h-1维持.F组诱导麻醉为芬太尼10μg·kg-1,继以15～30 μg·kg-1·h-1维持.分别于麻醉后切皮前(T1)、体外循环30 min(T2)、开主动脉后30min(T3)、停CPB 1 h(T4)、术后4 h(T5)、术后24 h(T6)采患者静脉血测定血浆IL-1β,IL-6,IL-10及乳酸浓度,并记录术中舒芬太尼或芬太尼的用量.结果:与T1相比,两组IL-1β,IL-6,IL-10和乳酸在CPB后均升高(P＜0.05,P＜0.01);IL-1β于T2～T5时S组低于F组(P＜0.05,P＜0.01);IL-6于T2～T5时s组低于F组(P＜0.05,P＜0.01);IL-10于T3～T6时S组高于F组(P＜0.01);乳酸于T3和T4时S组低于F组(P＜0.01);术中芬太尼的用量约为舒芬术尼的8倍.结论:在同等效应下舒芬太尼调节机体炎性反应效能强于芬太尼,并可减少乳酸生成,用于冠状动脉旁路移植术要比芬太尼更为理想.     

西维来司钠对大鼠重症急性胰腺炎后急性肝损伤的保护作用

目的:探讨西维来司钠对大鼠重症急性胰腺炎(SAP)后急性肝损伤的治疗价值。方法:SD大鼠54只随机分为3组,A组为对照组,仅开腹,轻翻动胰腺,B组采用经十二指肠乳头逆行胆胰管注射3.5%牛磺胆酸钠的方法制备大鼠SAP模型,C组为西维来司钠药物治疗组,在制备SAP大鼠模型后微量泵持续静脉滴注西维来司钠;各组又分为3h、6h、12h3个亚组,每时间点6只。检测血浆白介素-6(IL-6)、中性粒细胞弹性蛋白酶(NE)、淀粉酶(AMY)及肝组织匀浆中超氧化物歧化酶(SOD)、丙二醛(MDA)的水平并观察肝、胰病理变化。结果(:1)B组IL-6、NE、AMY、MDA较A组明显升高(P<0.05),SOD明显降低(P<0.05),镜下可见胰腺水肿、炎细胞浸润、坏死,肝脏肝窦充血、细胞浊肿及坏死,且损伤程度随时限延长而加重。(2)C组较B组血浆IL-6、NE、AMY(12h)及肝组织匀浆中MDA水平下降(P<0.05),SOD升高(P<0.05),胰、肝病理损害程度减轻。结论:西维来司钠通过抑制NE的活性及在肝组织中的表达,抑制SAP急性期炎症反应及有效提高机体对氧自由基的清除能力,减轻SAP致肝损伤的程度。     

不同剂量异丙酚对心内直视手术患者肌钙蛋白Ⅰ和血流动力学的影响

目的 观察异丙酚对体外循环下行冠脉搭桥术患者心肌缺血再灌注损伤保护作用的剂量相关性,以及不同剂量对血流动力学的影响,寻求产生最佳心肌保护作用和使患者心功能得到最佳恢复的剂量.方法 选择45例择期常规体外循环下行冠脉搭桥术患者,随机分成A、B、C三组.诱导后用微量注射泵持续输注异丙酚A组3 mg/(kg·h);B组5 mg/(kg·h);C组8 mg/(kg·h)直到手术结束.分别于体外循环前、主动脉开放后30min、6 h、24 h自桡动脉采血,测定血浆心肌肌钙蛋白Ⅰ(cTnI)浓度.分别测定开胸前、主动脉插管前、停体外循环、关胸前、关胸毕的平均动脉压(MAP)、外周血管阻力指数(SVRl)、心脏指数,同时观察主动脉开放后的心脏自动复跳情况.结果 三组从诱导至体外循环开始时间、体外循环时间、主动脉阻断时间、心肌保护方法以及心脏自动复跳情况无明显差异.三组患者cTnI水平于主动脉开放后迅速升高,主动脉开放后6小时处于高峰期.与A组比较,主动脉开放后B、C组患者cTnI值较低(P<0.01);B组与C组比较各时间点均无明显差异.三组患者停体外循环后心脏指数较开胸前升高明显(P<0.01),SVRI在停体外循环后均有下降(P<0.01),其中C组SVRI下降较其它两组显著,C组停体外循环后各时闻点心脏指数值较B组要低(P<0.05).结论 在冠脉搭桥术中,异丙酚以5 mg/(kg·h)持续输注至术毕,能减轻体外循环中心肌缺血再灌注损伤,血浆cTnI水平较低,有较高的心脏指数和满意的SVRI,能维持较为理想的血流动力学.     

Effects of breviscapine on pulmonary inflammatory response and lung injury in children undergoing open heart surgery

This study examined the effects of breviscapine (1) on pulmonary inflammatory response and lung function in pediatric patients undergoing open heart surgery. Forty-five children (ASA II or III, aged 2-72 months) were randomly assigned to control group (saline, Group C), low dose 1 group (0.5?mg/kg, Group Bre0.5), and high dose 1 group (1.0?mg/kg, Group Bre1.0), 15 cases each group. Plasma concentrations of procalcitonin (PCT) and neutrophil elastase (NE) were measured and compared at different time points. Plasma concentrations of PCT and NE were increased after cardiopulmonary bypass (CPB) induction, and the concentrations were lower in 1-treated groups. The present results indicated that continuous infusion of 1 before the CPB suppressed the production of PCT and NE attenuated systemic inflammatory response, which could result in lung protective effect in children undergoing open heart surgery.     

Protective effect of Sivelestat in a porcine hepatectomy model prepared using an intermittent Pringle method

The effect of Sivelestat, a neutrophil elastase inhibitor, on hepatic ischemia-reperfusion injury was examined in a pig hepatectomy model. An internal jugular vein-splenic vein bypass was prepared in male pigs and about 40% hepatic resection (left lobe) was performed under 15-min liver ischemia and 5-min intermittent reperfusion. Six animals received Sivelestat (10 mg/kg/h) intravenously and six control animals received physiological saline (10 mg/kg/h) from commencement of laparotomy. Hemodynamics, blood chemistry, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), lactic acid, hyaluronic acid, nitrite/nitrate (NOS), and tumor necrosis factor-alpha (TNF-alpha) were compared between the groups. The effects of Sivelestat on NOS generation and expression of iNOS mRNA and TNF-alpha mRNA were also assessed in J774 cells. Expression of TNF-alpha mRNA in hepatic tissues was examined using RT-PCR. The blood pressure of control animals was significantly lower immediately and 3 h after ischemia-reperfusion, compared with that at commencement of laparotomy, whereas there was no decrease of blood pressure in animals administered Sivelestat. Serum AST (P=0.0045), NOS (P=0.0098), and TNF-alpha (P=0.041) levels were significantly lower 3 h after hepatectomy in animals receiving Sivelestat. Sivelestat inhibited NOS production in J774 cells, but did not inhibit expression of iNOS mRNA or TNF-alpha mRNA. In hepatic tissues, Sivelestat showed a greater tendency to inhibit expression of TNF-alpha mRNA and fewer TUNEL-positive cells were present in the hepatic sinusoidal endothelium after Sivelestat treatment, although these differences were not statistically significant. We conclude that Sivelestat inhibits production of TNF-alpha and NO by inhibiting neutrophil elastase, and thus reduces hepatic injury and stabilizes hemodynamics after ischemia-reperfusion.     

Elastase inhibition reduced death associated with acid aspiration-induced lung injury in hamsters

This study examined whether the specific inhibition of neutrophil elastase by sivelestat sodium hydrate (sivelestat) reduced deaths associated with severe acute lung injury after hydrochloric acid (HCl) aspiration in hamsters. Animals that received a single intratracheal instillation of HCl (0.2 N, 200 microL) time-dependently died by occlusion of their trachea with inflammatory exudate. In a time course study, these animals developed severe lung injury, peaking 12 to 24 h after HCl instillation, as indicated by hemorrhage and a massive increase in the protein concentration of bronchoalveolar lavage fluid. These changes were closely correlated with neutrophil elastase activity in bronchoalveolar lavage fluid. Sivelestat (0.01, 0.1 and 1 mg/kg/h), when intravenously infused during the first 48 h post-HCl instillation, dose-dependently reduced death in HCl-instilled hamsters. In a separate experiment, analysis of bronchoalveolar lavage fluid parameters and partial pressure of arterial oxygen (PaO(2)) 8 h post-HCl instillation showed that sivelestat at 1 mg/kg/h, i.v. significantly improved both bronchoalveolar lavage fluid parameters and PaO(2) levels with evidence of the inhibition of neutrophil elastase activity in bronchoalveolar lavage fluid. These results suggest that neutrophil elastase plays a significant role in this type of severe acute lung injury that leads to death by respiratory failure.     

Pharmacological profile of a specific neutrophil elastase inhibitor,Sivelestat sodium hydrate

Imbalance between neutrophil elastase (NE) and its endogenous protease inhibitors has been considered to be one of possible mechanisms by which NE causes lung tissue destruction. It has been shown that the amount and/or activity of NE is increased in blood and bronchoalveolar lavage fluid in patients with acute lung injury. Accordingly, animals undergoing acute lung injury have increased NE activity such as in blood and bronchoalveolar lavage fluid. Sivelestat sodium hydrate (Sivelestat) is a synthetic inhibitor of NE with highly specificity to NE. Many studies have indicated that Sivelestat treatment improves inflammatory and edematous changes of lungs and survival as well as increased NE activity in several animal models of acute lung injury. Clinical studies have demonstrated that Sivelestat improves this injury that is associated with systemic inflammatory response syndrome. As compared with endogenous protease inhibitors that have high molecular mass, Sivelestat, a synthetic and low molecular weight elastase inhibitor, may be delivered to the inflammatory sites more easily and effectively and is considred to improve typical symptoms of acute lung injury. Clinical use of Sivelestat would further clarify the usefulness of this compound in clinical acute lung injury.     

Antioxidative effect of propofol during cardiopulmonary bypass in adults

INTRODUCTION Cardiopulmonary bypass (CPB) can lead to theproduction of damaging oxygen-derived free radicals[1].Some oxygen derivatives such as H2O2 and ·OH areconsidered to have potent oxidative activity to injurehost tissue[2]. These reactive oxygen species cause lipidperoxidation of the cell membrane and intracellular Ca2 overload, which are responsible for mechanical andmetabolic damage . Oxidant injury may be attenuated [3]byendogenous antioxidantdefenses. Antioxidantswithincell …     

体外循环手术中应用硝酸甘油减轻中性粒细胞对肺的损伤分析

目的探讨体外循环手术中应用硝酸甘油对肺的保护作用。方法11例行体外循环手术的患者随机分为空白对照组(6例)和试验组(5例)。试验组在手术切皮后即予硝酸甘油5mg/(kg?min),直到体外循环结束后2h,比较肝素化后体外循环前(T1)、鱼精蛋白中和肝素后(T2)、体外循环结束后2h(T3)和体外循环结束后24h(T4)4个时间点中性粒细胞计数、弹性蛋白酶浓度、肺泡-动脉血氧分压差(PA-aO2)和术后监护室内机械辅助通气时间的差别。结果体外循环后,两组中性粒细胞计数、弹性蛋白酶浓度及PA-aO2均明显上升(P值均<0.05)。两组PA-aO2及试验组弹性蛋白酶浓度在T4时间点恢复至术前水平。同组内动、静脉血之间中性粒细胞计数的差异无显著性(P值均>0.05)。在T2时间点,空白对照组桡动脉血弹性蛋白酶浓度为(1189.82±381.51)ng/mL,明显高于颈内静脉血的(674.01±359.40)ng/mL(P<0.05);试验组桡动脉血中性粒细胞计数为(11.06±6.38)×109/L,明显高于空白对照组的(4.51±2.61)×109/L(P<0.05);而试验组PA-aO2为(124.20±43.45)mmHg(1mmHg=0.133kPa),明显低于空白对照组的(209.61±66.35)mmHg(P>0.05)。两组术后在监护室机械通气时间的差异无显著性(P<0.05)。结论体外循环手术中应用硝酸甘油可能抑制中性粒细胞在肺内聚集和激活,减少弹性蛋白酶的释放,产生肺保护作用。     

七氟醚预处理对心脏瓣膜置换术患者心肌酶的影响

目的 观察体外循环下七氟醚预处理对心脏瓣膜置换术患者心肌酶的影响.方法 择期全麻下行心脏瓣膜置换患者40例,美国麻醉医师协会(ASA)分级Ⅰ～Ⅲ级,随机分为七氟醚预处理组(S组)和对照组(C组),每组20例.S组于手术开始后持续吸入1.0MAC七氟醚,至体外循环开姑时结束;C组不用任何吸入性麻醉药.分别于麻醉前(T0),主动脉阻断即刻(T1),主动脉开放后0.5 h(T2)和1 h(T3),术后8 h(T4)和24 h(T5)采集桡动脉血,检测血浆心肌肌钙蛋白1(cTnl)的浓度、肌酸磷酸激酶(CK)和肌酸磷酸激酶同工酶(CK-MB)的活性.结果 两组患者麻醉前cTnl水平、CK和CK-MB活性均在正常范围,在主动脉开放后各时间点明显升高(P＜0.05);S组血清中cTnl水平、CK和CK-MB活性在各时间点均明显低于C组.结论 七氟醚预处理对心肌缺血/再灌注损伤有一定保护作用.     

Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice

Mechanical ventilation can paradoxically cause acute lung injury, which is termed ventilator-induced lung injury. Neutrophil recruitment and neutrophil elastase release play a central role in the pathogenesis of ventilator-induced lung injury including cell damage, extracellular matrix degradation and alveolar-capillary hyperpermeability. We therefore speculated that neutrophil elastase inhibition ameliorates ventilator-induced lung injury. Anesthetized C57/BL6 mice received mechanical ventilation with a high tidal volume (V(T); 20 ml/kg) for 4 h. The neutrophil elastase inhibitor (sivelestat, 100 mg/kg) or saline was given intraperitoneally (i.p.) 30 min before ventilation. Sivelestat completely inhibited both neutrophil elastase and myeloperoxidase activities that were increased by ventilation, and attenuated the histopathological degree of lung damage, neutrophil accumulation and lung water content, as well as the concentration of macrophage inflammatory protein (MIP)-2, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in bronchoalveolar lavage fluid and serum. Moreover, mechanical ventilation increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the expression of early growth response gene-1 (Egr-1) mRNA, and these increases were also recovered by sivelestat. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed apoptotic cells mainly in alveolar epithelial cells and their numbers corresponded to histological damage. These data suggested that sivelestat could protect against ventilator-induced lung injury by suppressing apoptotic responses through mechanical stress-induced cell signaling in addition to inhibiting neutrophil chemotaxis.     

七氟烷预处理对小儿体外循环后肠黏膜屏障功能的影响

目的：评价围体外循环期七氟烷预处理对肠道黏膜屏障功能的影响。方法选取择期在体外循环下行心内直视房间隔缺损和室间隔缺损修补术的患儿30例,随机分为七氟烷预处理组（ S组）和对照组（ C组）,每组15例。 S组在中心静脉成功置管后开始吸入浓度2％的七氟烷至CPB开始,C组不给任何吸入麻醉药。在CPB前（ T1）、停止CPB后即刻（ T2）、CPB结束后2h（T3）、CPB结束后6 h（T4）和CPB结束后24 h（T5）五个时间点分别抽取中心静脉血标本,测量血清中肠脂肪酸结合蛋白（I-FABP）、二胺氧化酶（DAO）、白介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的浓度。结果两组患儿CPB前（T1）的I-FABP、DAO、IL-6和TNF-α的血清浓度无显著性差异（P＞0．05）,与CPB前（T1）相比较,两组患儿CPB停止后各时间点的I-FABP、DAO、IL-6和TNF-α的血清浓度均显著升高,有统计学差异（P＜0．05）,S组的I-FABP、DAO、IL-6和TNF-α的血清浓度在CPB停止后各时间点均较C组降低,差异有统计学意义（P＜0．05）。结论（1）小儿体外循环心脏外科手术中有肠黏膜屏障功能的受损。（2）2％七氟烷预处理对围体循期炎症反应可能有抑制作用,对肠黏膜膜屏障可能有保护作用。