异丙酚对体外循环中致炎细胞因子TNF-α、IL-8及呼吸指数影响的临床研究
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摘要
背景和目的：体外循环(CPB)相关的急性肺损伤所导致的术后肺功能障碍一直是心脏外科工作中常见的临床问题。由于CPB是一种非生理性的循环方式，由此诱发的全身性炎症反应综合症(SIRS)是导致体外循环相关急性肺损伤的重要原因。近年来的研究表明致炎细胞因子在体外循环相关急性肺损伤(ALI)中起重要的作用。异丙酚(Propofol)具有麻醉、抗氧化、清除氧自由基和抑制中性粒细胞的功能及致炎细胞因子的释放等作用。本实验将异丙酚用于在CPB下行瓣膜置换术的病人，通过观察异丙酚对致炎细胞因子和呼吸功能等的影响，探讨致炎细胞因子在CPB相关急性肺损伤中的作用及异丙酚保护作用的机制，为心脏外科麻醉合理用药及改善术后肺功能提供理论依据。
方法：选取ASA Ⅱ～Ⅲ级，主动脉阻断时间在40分钟和体外循环时间在60分钟以上的风湿性心脏瓣膜病人20例。随机分成两组即异丙酚组和对照组(每组10例)。除异丙酚组在麻醉诱导和维持
郑州大学（2皿2）硕土学位论文 异丙酚对体外循环中致炎细胞因子＊＊卜u、！卜8及呼吸指数影响的临床研究
中加用异丙酚外，其它术中用药两组均相同。术中在监测病人血流
动力学的指标下，两组分别于麻醉诱导后CPB前汀；人主动脉阻
断后 30min（T。）、王动脉开放后 10min 汀。人 30 min（T。）、Zh（T。）。
4h叮介6h汀J分别采集肝素抗凝挠动脉血和上腔静脉血检测①
动脉血气分析计算呼吸指数；②肺循环前后（右房血－左房血）中性
粒细胞计数的变化；③采集动脉血浆标本用硫代巴比妥酸显色法检
测 MDA的含量和用酶联免疫吸附法检测 TNF＆和 IL七的含量。统
计数据用均数土标准差佰J）表示，采用 SPSS （ 0刀）统计软件
包处理，以P＜o刀5为显著性检验标准。
结果：
1．一般资料：两组病人年龄、体重、升主动脉阻断时间、体外
循环时间、手术时间及＊SA分级差异均无显著性（P＞0刀5人
2．围术期血流动力学的变化：围术期两组病人血流动力学指标
心率（Illl厂平均动脉压（MAP）和中心静脉压uVP）的变化差异
无显著性（P＞0刀5人
3．围术期呼吸指数的变化：两组病人在 T；和 TZ时间点的呼吸
土 数组间差异无显著性（0＊710．11 VS 0＊410 二 6、0．7010二 0 VS
0石7＝I＝0．09，P＞0刀5人 而在T。－T，时间点组间差异具有显著性
（P＜0刀 1人对照组大于异丙酚组。组内比较，两组 T3～T7时间点与
T；和 T。时间点差异具有显著性（P＜0刀5人 T；和 T。间差异无显著性
（0＊7土0．llVso＊0土0．10、0＊4士0二6vso＊7土0＊9，P＞0＊5）。
4．肺循环前后中性粒细胞计数的变化：对照组肺循环前后中性
粒细胞计数的变化于 T3点差异有显著性门．3013．21 10’／L VS
7．33迎．66X 1001，p＜0．of），右房血高于左房血，而异丙酚组于各时
－二－
郑州大学（222）硕士学位论文 异丙酚村休外循环中致炎细胞因子TNF－a、IL－8及呼吸指数邑响的临床研究
fMdMWWWWM｛x－xxxMWtefM－WdM：xWWW：MWwWWHMM7－；xWMMWMMWMMMMMMxw．xxMWWK（－～－～－－－－ca－－－－－－－－－－－－－．－－－－－－－－ram
间点的变化差异无显著性（P＞0刀5L．两组于T厂T，时间点的中性粒
细胞计数与T；和L的比较差异具有显著性（P功刀1人
5．血浆MDA水平的变化：两组病人在T；和 T。时间点 MDA的
含量组间差异无显著性（3．42ti．24 nmol／ml vs 3．39if·23 nmol／ml．
4．3910．86m。l／ml VS 4．3 110．87 flmol／mis P＞0刀5），而在 T3～ T7时间
点组间差异具有显著性（P＜0刀5人对照组高于异丙酚组。组内比较，
两组T；～T，时间点的MDA含量明显高于T；时间点，差异具有显著
性（P功刀1人并于＊点达峰值。而T；和L间差异无显著性u．42到．24
nmol／ml vs 4．39土0．86 nmol／ml、3．39土1．23 nmol／ml vs 4．31士0．87
nmol／ml，P＞0刀5）。
6．血浆致炎细胞因子’t’ii仑及IL毛水平的变化：两组病人血
浆TNF仓的含量组间比较，在T。～T。时间点两组间差异有显著性
（P＜0刀5人 而在L和L时间点两组间差异无显著性门8．44土6．门
＂g／ml vs 17．53t6．97 ＂g／ffil． 23．91t7＊8 ＂g／ffil vs ZI．96t6．87 tl，
P＞0刀5）；组内比较，两组 ’t’iv’《的含量在 TZ～T7时间点与L比较
差异具有显著性（P功刀 1人 体外循环时明显升高，并于 T3点达峰
值。两组病人血浆IL七的含量组间比较，在T。～T，时间点两组间差
异具有显著性（P＜0刀5人 而在乃和L时间点两组间差异无显著性
（4．55ti＊4 ＂g／ffil vs 4．39t0．93 ng／ml、4＊Ztl．15 ＂g／ml vs 4．49t0．80
＂g／ml， P＞0刀5）；组内比较，对照组 IL－8的含量在 T。～ T。时间点与
D
T；、T斤 乙?
Objective: Post-operative pulmonary function disturbance caused by acute lung injury (ALI) correlated with cardiopulmonary bypass (CPB) has been a common clinical issue in cardiovascular surgery ever since. As CPB is a nonphysiological circulation pattern, it can evoke system inflammotary response syndrome (SIRS), and the SIRS is an important reason for ALI correlated with CPB. Recent studies have revealed that the proinflammatory cytokines may play important role in ALI correlated with CPB. Propofol has been shown that it not only has the actions of anesthesia and antioxidation, but also can clear oxygen free radicals, inhibit the function of neutrophil and the release of proinflammatory cytokines etc. In this experiment, propofol was used to the patients undergone the valvular replacement under the CPB. By means of observing the effects of propofol on the proinflammatory cytokines and respiratory function in order to inquire into the significance of proinflammatory cytokines in ALI correlated with CPB and
the mechanism of propofol's protective action, provide theoretical basis for cardiac surgery anesthesia and improve post-operative pulmonary function.
Methods: Twenty patients with rheumatic heart valvular disease whose ASA scale was II-HI, aortic clamping time and bypass time were more than 40, 60 minutes (min) respectively were selected and divided randomly into two groups (n=10 each): control group and propofol group. There were no differences between two groups about medication during operation except that the propofol was used for anesthesia induction and maintenance in propofol group. Under the monitoring of hemodynamics at surgery, heparinized anticoagulant blood samples from radial artery and superior vena cava were taken after anesthesia induction and before CPB (Ti) , 30 min after aortic clamping (T2) and 10min(T3),30 min(T4),2h(T5),4h(T6),6h(T7)after aortic declamping for determining the following data: respiratory index (RI) derived from arterial blood gas analysis,(2)median cell difference(MCD) of neutrophil count derived from left and right atrium blood, arterial plasma levels of malondialdilyde (MDA) ,tumour necrosis factor-a (TNF-a) and interleukin-8 (IL-8) .No adjustment was made for hemodilution. The data were expressed as mean + SD. Statistical package (SPSS 10.0) was used for processing data. P<0.05 was considered statistically significant. Results:
1. General patient data
There were no significant differences between two groups in age, weight, ascending aorta clamping time, CPB time, operation time and ASA scale (P > 0.05).
2. Changes in hemodynamics
There were no significant differences between two groups in HR, MAP and CVP during the operation (P > 0.05).
3. Change in respiratory index
There were no significant differences between two groups in RI at the points of Ti and T2 (0.67+0.11 vs 0.64+0.16, 0.70+0.10 vs 0.67+0.09, P>0.05), but there were significant differences at the points of TS to T7 (P< 0.01 ), RI of control group was higher than that of propofol group. Compared in two groups, RI at the points of T3 to T? was higher than that at the points of T1 and T2 (TO.05), but there was no significant difference between the time points TI and T2 (0.67+0.11 vs 0.70+0.10, 0.64+0.16 vs 0.67+0.09, P>0.05).
4. Change in median cell difference (MCD) of pulmonary circulation
There was significant difference in MCD at the point of TS in control group (11.30+3.21X109/L vs 7.33+2.66X109/L, PO.01), neutrophil count of right atrium blood was higher than that of left one, but there was no significant difference in MCD at any time points in propofol group (P >0.05). Neutrophil counts at the points of TS to TI were higher than that at the points of TI and T2 and the difference was statistically significant (P O.01).
5. Change in the plasma levels of MDA
There were no significant differences between two groups in MDA levels at the points of TI and T2 (3.42+1.24 nmol/ml vs 3.39+1.23 nmol/ml, 4.39+0.86 nmol/ml vs 4.31+0.87 nmol/ml, P >0.05), but there were significan
方法：选取ASA Ⅱ～Ⅲ级，主动脉阻断时间在40分钟和体外循环时间在60分钟以上的风湿性心脏瓣膜病人20例。随机分成两组即异丙酚组和对照组(每组10例)。除异丙酚组在麻醉诱导和维持
郑州大学（2皿2）硕土学位论文 异丙酚对体外循环中致炎细胞因子＊＊卜u、！卜8及呼吸指数影响的临床研究
中加用异丙酚外，其它术中用药两组均相同。术中在监测病人血流
动力学的指标下，两组分别于麻醉诱导后CPB前汀；人主动脉阻
断后 30min（T。）、王动脉开放后 10min 汀。人 30 min（T。）、Zh（T。）。
4h叮介6h汀J分别采集肝素抗凝挠动脉血和上腔静脉血检测①
动脉血气分析计算呼吸指数；②肺循环前后（右房血－左房血）中性
粒细胞计数的变化；③采集动脉血浆标本用硫代巴比妥酸显色法检
测 MDA的含量和用酶联免疫吸附法检测 TNF＆和 IL七的含量。统
计数据用均数土标准差佰J）表示，采用 SPSS （ 0刀）统计软件
包处理，以P＜o刀5为显著性检验标准。
结果：
1．一般资料：两组病人年龄、体重、升主动脉阻断时间、体外
循环时间、手术时间及＊SA分级差异均无显著性（P＞0刀5人
2．围术期血流动力学的变化：围术期两组病人血流动力学指标
心率（Illl厂平均动脉压（MAP）和中心静脉压uVP）的变化差异
无显著性（P＞0刀5人
3．围术期呼吸指数的变化：两组病人在 T；和 TZ时间点的呼吸
土 数组间差异无显著性（0＊710．11 VS 0＊410 二 6、0．7010二 0 VS
0石7＝I＝0．09，P＞0刀5人 而在T。－T，时间点组间差异具有显著性
（P＜0刀 1人对照组大于异丙酚组。组内比较，两组 T3～T7时间点与
T；和 T。时间点差异具有显著性（P＜0刀5人 T；和 T。间差异无显著性
（0＊7土0．llVso＊0土0．10、0＊4士0二6vso＊7土0＊9，P＞0＊5）。
4．肺循环前后中性粒细胞计数的变化：对照组肺循环前后中性
粒细胞计数的变化于 T3点差异有显著性门．3013．21 10’／L VS
7．33迎．66X 1001，p＜0．of），右房血高于左房血，而异丙酚组于各时
－二－
郑州大学（222）硕士学位论文 异丙酚村休外循环中致炎细胞因子TNF－a、IL－8及呼吸指数邑响的临床研究
fMdMWWWWM｛x－xxxMWtefM－WdM：xWWW：MWwWWHMM7－；xWMMWMMWMMMMMMxw．xxMWWK（－～－～－－－－ca－－－－－－－－－－－－－．－－－－－－－－ram
间点的变化差异无显著性（P＞0刀5L．两组于T厂T，时间点的中性粒
细胞计数与T；和L的比较差异具有显著性（P功刀1人
5．血浆MDA水平的变化：两组病人在T；和 T。时间点 MDA的
含量组间差异无显著性（3．42ti．24 nmol／ml vs 3．39if·23 nmol／ml．
4．3910．86m。l／ml VS 4．3 110．87 flmol／mis P＞0刀5），而在 T3～ T7时间
点组间差异具有显著性（P＜0刀5人对照组高于异丙酚组。组内比较，
两组T；～T，时间点的MDA含量明显高于T；时间点，差异具有显著
性（P功刀1人并于＊点达峰值。而T；和L间差异无显著性u．42到．24
nmol／ml vs 4．39土0．86 nmol／ml、3．39土1．23 nmol／ml vs 4．31士0．87
nmol／ml，P＞0刀5）。
6．血浆致炎细胞因子’t’ii仑及IL毛水平的变化：两组病人血
浆TNF仓的含量组间比较，在T。～T。时间点两组间差异有显著性
（P＜0刀5人 而在L和L时间点两组间差异无显著性门8．44土6．门
＂g／ml vs 17．53t6．97 ＂g／ffil． 23．91t7＊8 ＂g／ffil vs ZI．96t6．87 tl，
P＞0刀5）；组内比较，两组 ’t’iv’《的含量在 TZ～T7时间点与L比较
差异具有显著性（P功刀 1人 体外循环时明显升高，并于 T3点达峰
值。两组病人血浆IL七的含量组间比较，在T。～T，时间点两组间差
异具有显著性（P＜0刀5人 而在乃和L时间点两组间差异无显著性
（4．55ti＊4 ＂g／ffil vs 4．39t0．93 ng／ml、4＊Ztl．15 ＂g／ml vs 4．49t0．80
＂g／ml， P＞0刀5）；组内比较，对照组 IL－8的含量在 T。～ T。时间点与
D
T；、T斤 乙?
Objective: Post-operative pulmonary function disturbance caused by acute lung injury (ALI) correlated with cardiopulmonary bypass (CPB) has been a common clinical issue in cardiovascular surgery ever since. As CPB is a nonphysiological circulation pattern, it can evoke system inflammotary response syndrome (SIRS), and the SIRS is an important reason for ALI correlated with CPB. Recent studies have revealed that the proinflammatory cytokines may play important role in ALI correlated with CPB. Propofol has been shown that it not only has the actions of anesthesia and antioxidation, but also can clear oxygen free radicals, inhibit the function of neutrophil and the release of proinflammatory cytokines etc. In this experiment, propofol was used to the patients undergone the valvular replacement under the CPB. By means of observing the effects of propofol on the proinflammatory cytokines and respiratory function in order to inquire into the significance of proinflammatory cytokines in ALI correlated with CPB and
the mechanism of propofol's protective action, provide theoretical basis for cardiac surgery anesthesia and improve post-operative pulmonary function.
Methods: Twenty patients with rheumatic heart valvular disease whose ASA scale was II-HI, aortic clamping time and bypass time were more than 40, 60 minutes (min) respectively were selected and divided randomly into two groups (n=10 each): control group and propofol group. There were no differences between two groups about medication during operation except that the propofol was used for anesthesia induction and maintenance in propofol group. Under the monitoring of hemodynamics at surgery, heparinized anticoagulant blood samples from radial artery and superior vena cava were taken after anesthesia induction and before CPB (Ti) , 30 min after aortic clamping (T2) and 10min(T3),30 min(T4),2h(T5),4h(T6),6h(T7)after aortic declamping for determining the following data: respiratory index (RI) derived from arterial blood gas analysis,(2)median cell difference(MCD) of neutrophil count derived from left and right atrium blood, arterial plasma levels of malondialdilyde (MDA) ,tumour necrosis factor-a (TNF-a) and interleukin-8 (IL-8) .No adjustment was made for hemodilution. The data were expressed as mean + SD. Statistical package (SPSS 10.0) was used for processing data. P<0.05 was considered statistically significant. Results:
1. General patient data
There were no significant differences between two groups in age, weight, ascending aorta clamping time, CPB time, operation time and ASA scale (P > 0.05).
2. Changes in hemodynamics
There were no significant differences between two groups in HR, MAP and CVP during the operation (P > 0.05).
3. Change in respiratory index
There were no significant differences between two groups in RI at the points of Ti and T2 (0.67+0.11 vs 0.64+0.16, 0.70+0.10 vs 0.67+0.09, P>0.05), but there were significant differences at the points of TS to T7 (P< 0.01 ), RI of control group was higher than that of propofol group. Compared in two groups, RI at the points of T3 to T? was higher than that at the points of T1 and T2 (TO.05), but there was no significant difference between the time points TI and T2 (0.67+0.11 vs 0.70+0.10, 0.64+0.16 vs 0.67+0.09, P>0.05).
4. Change in median cell difference (MCD) of pulmonary circulation
There was significant difference in MCD at the point of TS in control group (11.30+3.21X109/L vs 7.33+2.66X109/L, PO.01), neutrophil count of right atrium blood was higher than that of left one, but there was no significant difference in MCD at any time points in propofol group (P >0.05). Neutrophil counts at the points of TS to TI were higher than that at the points of TI and T2 and the difference was statistically significant (P O.01).
5. Change in the plasma levels of MDA
There were no significant differences between two groups in MDA levels at the points of TI and T2 (3.42+1.24 nmol/ml vs 3.39+1.23 nmol/ml, 4.39+0.86 nmol/ml vs 4.31+0.87 nmol/ml, P >0.05), but there were significan
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19． Colman RW.Surface-mediated defence reactions:the plasma contact activation system.J Clin Invest,1984,73(5) :1249-1253
20． Dang CV,Bell WR,Kaiser D,et al.Disorganization of cultured endothelial call monolayers by fibrinogen fragment D.Science,1985,227(4693) :1487-1490
21． Andersen LW,Beak L,Degn H,et al.Presence of circulating endotoxins during cardiac operation.J Thorac cardiovasc Surg,1987,93(1) : 115-119
22． Rocke DA,Gaffin SL,Wells MT,et al.Endotoxemia associatied with cardiopulmonary
bypass.J Thorac Cardiovasc Surg,1987,93(6) :832-837
23． Dinarello CA,Gelfand JA.Wolff SM.Anticytokine strategies in the treament of tho systemic inflammatory response syndrome.JAMA,1993,269(10) :1829-1835
24． Cremer J,Martin M,Redl H,et al.Systernic inflammatory response syndrome after cardiac operation.Ann Thorac Surg,1996,61(5) : 1714-1722
25． Klebanoff S,Vadas MA,Harlan JM,et al.Stimulation of neutrophils by tumor necrosis factor.J Immunol,1986,136(11) :4220-4225
26． TraceyKJ,VlassaraH,CeramiA.Cachctin/tumornecrosisfactor.Lancet,1989,1 (8647) : 1122-1126
27． Perlmutter DH,Dinarello CA,Punsal PI,et al.Cachetin/tumor necrosis factor regulates hepatic acute phase gene expression.J Clin Invest,1986,78(5) : 1349-1354
28． Dinarello CA.Interleukin-1． Rev Infect Dis,1984,6(1) :51-95
29． Beutler B,Cerami A.Cachectin:more than a tumor necrosis factor.N Engl J Med,1987,316(2) :379-385
30． Hill GE,Whitten CW,Landers DF,et al.The influence of cardiopulmonary bypass on cytokines and cell-cell communication.J Cardiothorac Vase Anesth.1997 ,11(3) :367-75．
31． Deng MC,Dasch B,Erren M,et al.Impact of left ventricular dysfunction on cytokines,hemodynamics and outcome in bypass grafting.Ann Thorac Surg,1996,62(1) : 184-188
32． Hebert CA,Luscinskas FW,Kiely JM,et al.Endothelial and leukocyte forms of IL-8． conversion by thrombin and interactions with neutrophils.J Immunol,1990,145(9) :3033-3040
33． Finn A,Naik S,Klein N,et al.Interleukin-8 release and neutrophil degranulation after pediatric cardiopulmonary bypass.J Thorac Cardiovasc Surg,1993,105(2) :234-241
34． Cassatella MA,Medal,Bonora s,et al.Interleukin-10(IL-10) inhibits the release of proinflammatory cytokines from human polymorphonuclear leukocytes,evidence of an autocrine role of tumor necrosis factor and IL-1β in the production of IL-8 triggered by lipopolysaccharids.J Exp Med,1993,178(6) :2207-2211
35． Cassatella MA,Medal,Gasperini S,et al.IL-10 upregulates IL-1β receptor antagonist production from lipopolysaccharide-stimulated human polymorphonuclear leucocytes by delaying mRNA degradation.J Exp Med,1994,179(5) :1695-1699
36． Eppinger MJ,Ward PA,Bolling JR,et al.Regulatory effects of interleukin-10 on lung ischemia-reperfusion injury.J Thorac Cardiovasc Surg.1996,112(5) : 1301-5
37． Hill GE,Diego RP,Stammers AH,et al.Aprotinin enhances the endogenous release of interleukin-10 after cardiac operations.Ann Thorac Surg,1998,65(1) :66-69
38． Butler J,Parker D,Pillai R,er al.Effect of cardiopulmonary bypass on systemic release of neutrophil elastase and tumor necrosis factor.J Thorac Cardiovasc Surg.1993,105(1) :25-30
39． Tonz M,Mihaljevic T,Von Segesser LK,et al.Acute lung injury during cardiopulmonary bypass.Are the neutrophils responsible?.Chest.1995,108(6) : 1551-1556
40． Albelda SM,Smith CW,Ward PA,et al.Adhesion molecules and inflammatory injury.FASEB J,1994,8(8) :504-512
41． Weiss SJ.Tissue destruction by neutrophils.N Engl J Med,1989,320(6) :365-376
42． Gadaleta D,Fahey AL,Verma M,et al.Neutraphil leukotriene generation increases after cardiopulmonary bypass.J Thorac Cardiovasc Surg,1994,108(4) :642-647
43． Hashimoto K,Miyamoto H,Suzuki K,et al.Evidence of organ damage after cardiopulmonary bypass:The role of elastase and vasoactive mediators.J Thorac Cardiovasc Surg,1992,104(3) :666-673
44． Tonz M,Mihaljeric T,Von Segesser LK,et al.Acute lung injury during cardiopulmonary bypass:Are the neutrophils responsible?.Chest,1995,108(6) :1551-1556
45． Mihaljeric T,Tonz M,Von Segesser LK.et al.The influence of leukocyte filtration during cardiopulmonary bypass on postoperative lung function.A clinical study.J Thorac Cardiovasc Surg.1995 ,109(6) : 1138-45．
46． Steinberg JB,David P,Kapelanski,et al.Cytokine and complement levels in patients undergoing cardiopulmonary bypass.J Thorac cardiovasc surg,1993,106(6) :1008-1016
47． Fessatidis IT,Brannan JJ,Taylor KM,et al.Effect of prostacyclin PGI2 on cardiopulmonary bypass-induced lung injury.Perfusion,1994,9(1) :23-33
48． Gillinov AM,Redmond JM.Inhibition of neutrophil adhesion during cardiopulmonary bypass.Ann Thorac Surg,1994,57(1) :126-133
49． Andersen LW,Beak L.Degn H,et al.Presence of circulating endotoxins during cardiac operation.J Thorac cardiovasc Surg,1987,93(1) :115-119
50． Rocke DA,Gaffin SL,Wells MT,et al.Endotoxemia associatied with cardiopulmonary bypass.J Thorac Cardiovasc Surg,1987,93(6) :832-837
51． Nolan JP.Endotoxin,recticuloendothelial function,and liver injury.Hepatology,1981,1 (5) :458-465
52． Jansen NT,Van Oeveren W,Gu YJ,et al.Endotoxin release and tumor necrosis factor formation during cardiopulmonary bypass.Ann Thorac Surg,1992,54(4) :744-748
53． Craddock PR,Fehr J,Brigham KL,et al.Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis.N Engl J Med,1977,296(14) :769-774
54． Albelda SM,Smith CW,Ward PA,et al.Adhesion molecules and inflammatory injury.FASEB J,1994,8(8) :504-512
55． Weiss SJ.Tissue destruction by neutrophils.N Engl J Med,1989,320(6) :365-376
56． Gadaleta D,Fahey AL,Verma M,et al.Neutraphil leukotriene generation increases after cardiopulmonary bypass.J Thorac Cardiovasc Surg,1994,108(4) :642-647
57． Davies SW,Duffy JP.Wickens DG,et al.Time-course of free radical activity during coronary artery operations with cardiopulmonaty bypass.J Thorac Cardiovasc Surg,1997,105(6) :979-987
58． Magnuson DK,Maier RV,Pohlman TH.Protein kinase C:a potential pathway of endothelial cell activation by endotoxin,tumor necrosis factor.and interleukin-1． Surgery,1989,106(2) :216-223
59． Karin M.Singal transduction from cell surface to nucleus in development and disease.FASEB J,1992,6(8) :2581-2590
60． Collins T,Read MA,Neish AS,et al.Transcriptional regulation of endothelial cell adhesion molecules:NF-K B and cytokine-inducible enhancers.FASEB J,1995,9(10) :899-909
61． Canty TG Jr,Boyle EM Jr,Farr A,et al.Oxidative stress induces NF-kappaB nuclear translocation without degradation of IkappaBalpha.Circulation,1999,100(19 suppl):II361-364
62． 李庆新，易定华，宿学家。NF-кB的活化表达与体外循环未成熟肺损伤。细胞与分子免疫学杂志,2000,16 (4) : 298-299
63． Wan S,Leclerc JL,Antoine M,et al.Heparin-coated circuit reduce myocardial injury in heart or heart-lung transplantation: a prospective randomized study.Ann Thorac Surg,1999,68(4) : 1230-1235
64． Ranucci M,Cirri S,Conti D,et al.Beneficial effects of Durafflo Ⅱ heparin-coated circuits on postperfusion lung dysfunction.Ann Thorac Surg,1996,61(1) :76-81
65． Gu YJ,de Vries AJ,Boonstra PW,er al.Leukocyte depletion results in improved lung
function and reduced inflammatory response after cardiac surgery.J Thorac Cardiovasc Surg.1996,112(2) :494-500
66． Gillinov AM,Bator JM,Zehr KJ,et al.Neutrophil adhesion molecule expression during cardiopulmonary bypass with bubble and membrane oxygenators.Ann Thorac Surg,1993,56(4) :847-853
67． Mendler N,Hemisch W,Schad H.Pulmonary function after biventricular bypass for autologous lung oxygenation.Eur J Cardiothorac surg,2000,17(3) :325-330
68． Richter JA,Meisner H,Tassani P,et al.Drew-Anderson technique attenuates systemic inflammatory response syndrome and improves respiratory function after coronary artery bypass grafting.Ann Thorac Surg,2000,69(1) :77-83
69． Suzuki T,Fukuda T,Ito T,et al.Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants.Ann Thorac Surg,2000,69(2) :602-606
70． Soncul H,Oz E,Kalaycioglu S.Role of ischemia preconditioning on ischemic-reperfusion injury of the lung.Chest.1999,115(6) :1672-1677
71． Jorens PG,De Jongh R,De Backer W,et al.Interlukin-8 production in patients undergoing cardiopulmonary bypass :the influence of pretreatment with methylprednisolone.Am Rev Respir Dis,1993,148(4pt1) :890-895
72． Diego RP,Mihalakakos PJ,Hexum TD.Methlyprednisolone and full-dose aprotinin ' reduce reperfusion injury after cardiopulmonary bypass.J Cardiothorac Vasc Anesth,1997,11(1) :29-31
73． Wan S,DeSmet JM,Antoine M,et al.Steroid adminstration in heart and heart-lung transplantation :is the timing adequate?.Ann Thorac surg,1996,61(2) :674-678
74． Tracey KJ,Fong Y,Hesse DG,et al.Anti-cachetin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia.Nature,1987,330(6149) :662-664
75. Friedman M,Wang SY, Sellke FW, et al.Neutrophil adhension blockade with NPC15669 decreases pulmonary injury after total cardiopulmonary bypass.J Thorac Cardiovasc Surg. 1996,111(2):460-468
76. Gorman JH,Edmunds LH.Blood anesthesia for cardiopulmonary bypass.J Card Surg, 1995,10(3):270-279
77．钱有辉，高尚志，姚震，等。体外循环中丹参、别嘌呤醇、川芎嗪的氧自由基清除作用。中华胸心血管外科杂志，1993，9(3)：224-226
78．胡志伟，蔡俊坚，孙宗全。体外循环中机体脂质过氧化损伤和抗氧化能力的变化。同济医科大学学报，1996，25(5)：406-407
79. Murphy PG,Myers PS,Davise MJ,et al.The antioxidant potential of propofol(2,6-Dissopropylphenol).Br J Anesth, 1992,68(6):613-618
80. Green TR,Bennett SR,Nelson VM, et al. Specificity and properties of propofol as an antioxidant free radical scavenger. Toxicol Appl Pharmacol, 1994,129(1): 163-169
81．流红亮，戴体俊，王钧，等。利多卡因、异丙酚对缺血再灌注心肌细胞膜Na_+-K~+-ATP酶、肌浆网Ca~(2+)-ATP酶活性的影响。中国临床药理学与治疗学杂志，1999，4(2)：140-143
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84. Heine J,Leuwer M,Scheinichen D,et al.Flow cytometry evaluation of the in vitro influence of four iv anaesthetics on respiratory burst of neutrophils.Br J Anesth, 1996,77(3):387-392
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86. Hofbauer R, Frass M,Salfinger H,et al.Propofol reduces the migration of human leukocytes through endothelial cell monolayers.Crit Care Med, 1999,27(9): 1843-1847
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2． Kirklin JK,Westaby S,Blackstone EH,et al.Complement and the damaging effects of cardiopulmonary bypass.J Thorac Cardiovasc Surg ,1983,86(6) :845-857
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8． Ward PA.A plasmin-split fragment of C3 as a new chemotactic factor.J Exp Med,1967,126(2) : 189-206
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12． Rinder C,Fithch J.Amplification of the inflammatory response:adhesion molecules associated with platelet/white cell responses.J Cardiovasc Pharmacol,1996,27(81) :S6-12
13． Charo IF,Yune C,Perez HD,et al.Chemotactic peptides modulate adherence of human polymorphonuclear leukocytes to monolayers of cultured endothelial cells.J Immunol,1986,136(9) :3412-3419
14． Larry C,Casey A.Role of cytokines in the pathogenesis of cardiopulmonary-induced multisystem organ failure.Ann Thorac Surg,1993,56(5) :S92-96
15． Cochrane CG,Griffin JH.The biochemistry and pathophysiology of the contact system of plasma.Adv Immunol,1982,33(1) :241-306
16． Brister SJ,Ofosu FA,Buchanan MR,et al.Thrombin generation during cardiac surgery:Is heparin the ideal anticoagulant?.Thromb Haemost,1993,70(2) :259-262
17． Wachtfogel YT,Pixley RA,Kucich U,et al.Purified plasma factor XIIa aggregates human neutrophils and causes degranulation.Blood,1986,67(6) : 1731-1737
18． Kaplan AP,Kay AB,Austen KF,et al.A prealbumin activator of prekallikrein Ⅲ:Appearance of chemotactic activity for human neutrophils by the conversion of human prekallikrein to kallikrein.J Exp Med,1972,135(1) :81-97
19． Colman RW.Surface-mediated defence reactions:the plasma contact activation system.J Clin Invest,1984,73(5) :1249-1253
20． Dang CV,Bell WR,Kaiser D,et al.Disorganization of cultured endothelial call monolayers by fibrinogen fragment D.Science,1985,227(4693) :1487-1490
21． Andersen LW,Beak L,Degn H,et al.Presence of circulating endotoxins during cardiac operation.J Thorac cardiovasc Surg,1987,93(1) : 115-119
22． Rocke DA,Gaffin SL,Wells MT,et al.Endotoxemia associatied with cardiopulmonary
bypass.J Thorac Cardiovasc Surg,1987,93(6) :832-837
23． Dinarello CA,Gelfand JA.Wolff SM.Anticytokine strategies in the treament of tho systemic inflammatory response syndrome.JAMA,1993,269(10) :1829-1835
24． Cremer J,Martin M,Redl H,et al.Systernic inflammatory response syndrome after cardiac operation.Ann Thorac Surg,1996,61(5) : 1714-1722
25． Klebanoff S,Vadas MA,Harlan JM,et al.Stimulation of neutrophils by tumor necrosis factor.J Immunol,1986,136(11) :4220-4225
26． TraceyKJ,VlassaraH,CeramiA.Cachctin/tumornecrosisfactor.Lancet,1989,1 (8647) : 1122-1126
27． Perlmutter DH,Dinarello CA,Punsal PI,et al.Cachetin/tumor necrosis factor regulates hepatic acute phase gene expression.J Clin Invest,1986,78(5) : 1349-1354
28． Dinarello CA.Interleukin-1． Rev Infect Dis,1984,6(1) :51-95
29． Beutler B,Cerami A.Cachectin:more than a tumor necrosis factor.N Engl J Med,1987,316(2) :379-385
30． Hill GE,Whitten CW,Landers DF,et al.The influence of cardiopulmonary bypass on cytokines and cell-cell communication.J Cardiothorac Vase Anesth.1997 ,11(3) :367-75．
31． Deng MC,Dasch B,Erren M,et al.Impact of left ventricular dysfunction on cytokines,hemodynamics and outcome in bypass grafting.Ann Thorac Surg,1996,62(1) : 184-188
32． Hebert CA,Luscinskas FW,Kiely JM,et al.Endothelial and leukocyte forms of IL-8． conversion by thrombin and interactions with neutrophils.J Immunol,1990,145(9) :3033-3040
33． Finn A,Naik S,Klein N,et al.Interleukin-8 release and neutrophil degranulation after pediatric cardiopulmonary bypass.J Thorac Cardiovasc Surg,1993,105(2) :234-241
34． Cassatella MA,Medal,Bonora s,et al.Interleukin-10(IL-10) inhibits the release of proinflammatory cytokines from human polymorphonuclear leukocytes,evidence of an autocrine role of tumor necrosis factor and IL-1β in the production of IL-8 triggered by lipopolysaccharids.J Exp Med,1993,178(6) :2207-2211
35． Cassatella MA,Medal,Gasperini S,et al.IL-10 upregulates IL-1β receptor antagonist production from lipopolysaccharide-stimulated human polymorphonuclear leucocytes by delaying mRNA degradation.J Exp Med,1994,179(5) :1695-1699
36． Eppinger MJ,Ward PA,Bolling JR,et al.Regulatory effects of interleukin-10 on lung ischemia-reperfusion injury.J Thorac Cardiovasc Surg.1996,112(5) : 1301-5
37． Hill GE,Diego RP,Stammers AH,et al.Aprotinin enhances the endogenous release of interleukin-10 after cardiac operations.Ann Thorac Surg,1998,65(1) :66-69
38． Butler J,Parker D,Pillai R,er al.Effect of cardiopulmonary bypass on systemic release of neutrophil elastase and tumor necrosis factor.J Thorac Cardiovasc Surg.1993,105(1) :25-30
39． Tonz M,Mihaljevic T,Von Segesser LK,et al.Acute lung injury during cardiopulmonary bypass.Are the neutrophils responsible?.Chest.1995,108(6) : 1551-1556
40． Albelda SM,Smith CW,Ward PA,et al.Adhesion molecules and inflammatory injury.FASEB J,1994,8(8) :504-512
41． Weiss SJ.Tissue destruction by neutrophils.N Engl J Med,1989,320(6) :365-376
42． Gadaleta D,Fahey AL,Verma M,et al.Neutraphil leukotriene generation increases after cardiopulmonary bypass.J Thorac Cardiovasc Surg,1994,108(4) :642-647
43． Hashimoto K,Miyamoto H,Suzuki K,et al.Evidence of organ damage after cardiopulmonary bypass:The role of elastase and vasoactive mediators.J Thorac Cardiovasc Surg,1992,104(3) :666-673
44． Tonz M,Mihaljeric T,Von Segesser LK,et al.Acute lung injury during cardiopulmonary bypass:Are the neutrophils responsible?.Chest,1995,108(6) :1551-1556
45． Mihaljeric T,Tonz M,Von Segesser LK.et al.The influence of leukocyte filtration during cardiopulmonary bypass on postoperative lung function.A clinical study.J Thorac Cardiovasc Surg.1995 ,109(6) : 1138-45．
46． Steinberg JB,David P,Kapelanski,et al.Cytokine and complement levels in patients undergoing cardiopulmonary bypass.J Thorac cardiovasc surg,1993,106(6) :1008-1016
47． Fessatidis IT,Brannan JJ,Taylor KM,et al.Effect of prostacyclin PGI2 on cardiopulmonary bypass-induced lung injury.Perfusion,1994,9(1) :23-33
48． Gillinov AM,Redmond JM.Inhibition of neutrophil adhesion during cardiopulmonary bypass.Ann Thorac Surg,1994,57(1) :126-133
49． Andersen LW,Beak L.Degn H,et al.Presence of circulating endotoxins during cardiac operation.J Thorac cardiovasc Surg,1987,93(1) :115-119
50． Rocke DA,Gaffin SL,Wells MT,et al.Endotoxemia associatied with cardiopulmonary bypass.J Thorac Cardiovasc Surg,1987,93(6) :832-837
51． Nolan JP.Endotoxin,recticuloendothelial function,and liver injury.Hepatology,1981,1 (5) :458-465
52． Jansen NT,Van Oeveren W,Gu YJ,et al.Endotoxin release and tumor necrosis factor formation during cardiopulmonary bypass.Ann Thorac Surg,1992,54(4) :744-748
53． Craddock PR,Fehr J,Brigham KL,et al.Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis.N Engl J Med,1977,296(14) :769-774
54． Albelda SM,Smith CW,Ward PA,et al.Adhesion molecules and inflammatory injury.FASEB J,1994,8(8) :504-512
55． Weiss SJ.Tissue destruction by neutrophils.N Engl J Med,1989,320(6) :365-376
56． Gadaleta D,Fahey AL,Verma M,et al.Neutraphil leukotriene generation increases after cardiopulmonary bypass.J Thorac Cardiovasc Surg,1994,108(4) :642-647
57． Davies SW,Duffy JP.Wickens DG,et al.Time-course of free radical activity during coronary artery operations with cardiopulmonaty bypass.J Thorac Cardiovasc Surg,1997,105(6) :979-987
58． Magnuson DK,Maier RV,Pohlman TH.Protein kinase C:a potential pathway of endothelial cell activation by endotoxin,tumor necrosis factor.and interleukin-1． Surgery,1989,106(2) :216-223
59． Karin M.Singal transduction from cell surface to nucleus in development and disease.FASEB J,1992,6(8) :2581-2590
60． Collins T,Read MA,Neish AS,et al.Transcriptional regulation of endothelial cell adhesion molecules:NF-K B and cytokine-inducible enhancers.FASEB J,1995,9(10) :899-909
61． Canty TG Jr,Boyle EM Jr,Farr A,et al.Oxidative stress induces NF-kappaB nuclear translocation without degradation of IkappaBalpha.Circulation,1999,100(19 suppl):II361-364
62． 李庆新，易定华，宿学家。NF-кB的活化表达与体外循环未成熟肺损伤。细胞与分子免疫学杂志,2000,16 (4) : 298-299
63． Wan S,Leclerc JL,Antoine M,et al.Heparin-coated circuit reduce myocardial injury in heart or heart-lung transplantation: a prospective randomized study.Ann Thorac Surg,1999,68(4) : 1230-1235
64． Ranucci M,Cirri S,Conti D,et al.Beneficial effects of Durafflo Ⅱ heparin-coated circuits on postperfusion lung dysfunction.Ann Thorac Surg,1996,61(1) :76-81
65． Gu YJ,de Vries AJ,Boonstra PW,er al.Leukocyte depletion results in improved lung
function and reduced inflammatory response after cardiac surgery.J Thorac Cardiovasc Surg.1996,112(2) :494-500
66． Gillinov AM,Bator JM,Zehr KJ,et al.Neutrophil adhesion molecule expression during cardiopulmonary bypass with bubble and membrane oxygenators.Ann Thorac Surg,1993,56(4) :847-853
67． Mendler N,Hemisch W,Schad H.Pulmonary function after biventricular bypass for autologous lung oxygenation.Eur J Cardiothorac surg,2000,17(3) :325-330
68． Richter JA,Meisner H,Tassani P,et al.Drew-Anderson technique attenuates systemic inflammatory response syndrome and improves respiratory function after coronary artery bypass grafting.Ann Thorac Surg,2000,69(1) :77-83
69． Suzuki T,Fukuda T,Ito T,et al.Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants.Ann Thorac Surg,2000,69(2) :602-606
70． Soncul H,Oz E,Kalaycioglu S.Role of ischemia preconditioning on ischemic-reperfusion injury of the lung.Chest.1999,115(6) :1672-1677
71． Jorens PG,De Jongh R,De Backer W,et al.Interlukin-8 production in patients undergoing cardiopulmonary bypass :the influence of pretreatment with methylprednisolone.Am Rev Respir Dis,1993,148(4pt1) :890-895
72． Diego RP,Mihalakakos PJ,Hexum TD.Methlyprednisolone and full-dose aprotinin ' reduce reperfusion injury after cardiopulmonary bypass.J Cardiothorac Vasc Anesth,1997,11(1) :29-31
73． Wan S,DeSmet JM,Antoine M,et al.Steroid adminstration in heart and heart-lung transplantation :is the timing adequate?.Ann Thorac surg,1996,61(2) :674-678
74． Tracey KJ,Fong Y,Hesse DG,et al.Anti-cachetin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia.Nature,1987,330(6149) :662-664
75. Friedman M,Wang SY, Sellke FW, et al.Neutrophil adhension blockade with NPC15669 decreases pulmonary injury after total cardiopulmonary bypass.J Thorac Cardiovasc Surg. 1996,111(2):460-468
76. Gorman JH,Edmunds LH.Blood anesthesia for cardiopulmonary bypass.J Card Surg, 1995,10(3):270-279
77．钱有辉，高尚志，姚震，等。体外循环中丹参、别嘌呤醇、川芎嗪的氧自由基清除作用。中华胸心血管外科杂志，1993，9(3)：224-226
78．胡志伟，蔡俊坚，孙宗全。体外循环中机体脂质过氧化损伤和抗氧化能力的变化。同济医科大学学报，1996，25(5)：406-407
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