前列腺素E_1脂微球载体制剂对围体外循环期患者脑损伤保护作用的研究
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摘要
【目的】探讨应用前列腺素E1脂微球载体制剂(liposomal prostaglandin E1,Lipo-PGE1)对围体外循环(cardiopulmonary bypass,CPB)期脑损伤的保护作用及其可能机制。
【方法】随机选取风湿性心脏瓣膜病手术患者30例,其中男性10例,女性20例,年龄32～60岁,平均年龄(41.7±7.7)。术前无心内膜炎、糖尿病、高血压、高脂血症、脑血管疾病、免疫系统疾病和神经精神疾病,无酗酒史,无明显肺、肝、肾功能异常。心功能分级Ⅱ～Ⅲ级(NYHA),未使用对免疫系统有明显影响的药物。其中主动脉瓣置换术(AVR)5例,二尖瓣置换术(MVR)13例,二尖瓣加主动脉瓣置换术(DVR)12例。随机分为Lipo-PGE1组(P组)和对照组(C组),每组15例。P组于麻醉诱导后、CPB转流前持续静脉泵滴入Lipo-PGE1(剂量3ng/kg·min)至手术结束;C组用相同的方法给予相同容量的生理盐水。两组患者均于麻醉后手术前(T1)、CPB后30min(T2)、开放升主动脉后1h(T3)、CPB后6h(T4)、CPB后24h(T5)时间点采颈静脉球血4ml,用ELISA法测S100β蛋白、NSE、TNF-α浓度,用硫代巴比妥法测定MDA浓度、用黄嘌呤氧化酶法测定SOD活性。
【结果】1.两组患者麻醉后手术前(T1) S100β蛋白、NSE含量差异无统计学意义(P>0.05)、CPB后30min(T2)上升(P<0.05)、开放升主动脉后1h(T3)达峰值(P<0.05)、CPB后6h(T4)开始下降(P<0.05)、CPB后24h(T5)仍高于术前水平,但无统计学意义(P>0.05)。组间比较T2-T4时点P组S100β蛋白、NSE浓度低于C组(P<0.05)。2.两组患者麻醉后手术前(T1) TNF-α含量差异无统计学意义(P>0.05)、CPB后30min(T2)上升(P<0.05)、开放升主动脉后1h(T3)达峰值(P<0.05)、CPB后6h(T4)开始下降(P<0.05)、CPB后24h(T5)仍高于术前水平,但无统计学意义(P>0.05)。组间比较T2-T4时点P组TNF-α浓度低于c组(P<0.05)。3.两组患者麻醉后手术前(T1) MDA、SOD含量差异无统计学意义(P>0.05)、T2-T4时点两组MDA浓度升高,SOD活性下降(P<0.05)。组间比较T2-T4时点P组MDA浓度低于C组,SOD活性高于C组(P<0.05)。
【结论】围CPB期血清中脑损伤的特异性生化标志物S100β蛋白、NSE水平均有一过性明显升高;Lipo-PGE1可以降低围CPB期S100β蛋白、NSE的水平升高,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活性有关。
【Objective】To discuss the protective effects and probable mechanism of liposomal prostaglandin E1 (Lipo-PGE1) on brain injury of patients during cardiopulmonary bypass (CPB).
【Methods】30 patients underwent rheumatic heart valve replacement were selected randomly, including 10 males and 20 females with ages from 32 to 60,and the average age was 41.7±7.7 years. None of them had endocarditis, diabetes, hypertension, hyperlipidemia, cerebrovascular diseases, immune system diseases or mental disorders before operation, and had no drinking hobby or obvious lung, liver, kidney dysfunction before operation. These patients’heart function were GradeⅡ～Ⅲon the basis of New York Heart Association (NYHA), and none of them used the drugs which have significant effects on the immune system.The study was composed of 5 cases of aortic valve replacement (AVR), 13 cases of mitral valve replacement (MVR) and 12 cases of double valve replacement (DVR). The 30 cases were divided into two groups randomly, including experimental group (Group P, n=15) and control group (Group C, n=15).In Group P, Lipo-PGE1 (dose of 3ng/kg?min) was continuously pumped intravenously into the patients after induction of anesthesia and before CPB, till to the end of operation. In Group C, the patients were given identical volume of normal saline instead of Lipo-PGE1 with the same methods. 4 ml of blood samples were taken from jugular bulb after induction of anesthesia and before operation (T1), 30 minutes after initiation of CPB (T2), 1 h after the ascending aortic off-clamping (T3), 6h (T4) and 24h (T5) after discontinuation of CPB to determine the concentrations of plasma S100βprotein, NSE and TNF-αwith ELISA, to determine the concentration of MDA with thio-barbitone, and to determine the activity of SOD with xanthinoxidase, respectively.
【Result】The difference of the plasma concentrations of S100βprotein, NSE and TNF-αwas not statistically significant between both groups at T1 (P>0.05). In contrast with Group C, the plasma concentrations of S100βprotein, NSE and TNF-αin Group P rose at T2 (P<0.05), reached to the peak at T3 (P<0.05), began to descend at T4 (P<0.05), and were still higher than pre-operation at T5, but the difference was not statistically between them (P>0.05). When contrasted between groups, the concentrations of Group P were lower than Group C in T2-T4 (P<0.05). 2. The difference of the plasma concentrations of MDA and activity of SOD was not statistically significant between both groups at T1 (P>0.05); in contrast with Group C, the plasma concentrations of MDA were higher than and the activity of SOD descended in Group P (P<0.05 ). When contrasted between groups, the plasma concentration of MDA in Group P was lower than Group C and the activity of SOD was higher than Group C in T2-T4 (P<0.05).
【Conclusion】The plasma concentrations of specific biochemical marker for brain injury, such as S100βprotein and NSE, all markedly rose transiently during CPB, Lipo-PGE1 can relieve the expression level of S100βprotein and NSE of peri-CPB. Its mechanism may principally be suppressing the release of inflammatory factor TNF-α, lessening the production of MDA and increasing the activity of SOD.
【方法】随机选取风湿性心脏瓣膜病手术患者30例,其中男性10例,女性20例,年龄32～60岁,平均年龄(41.7±7.7)。术前无心内膜炎、糖尿病、高血压、高脂血症、脑血管疾病、免疫系统疾病和神经精神疾病,无酗酒史,无明显肺、肝、肾功能异常。心功能分级Ⅱ～Ⅲ级(NYHA),未使用对免疫系统有明显影响的药物。其中主动脉瓣置换术(AVR)5例,二尖瓣置换术(MVR)13例,二尖瓣加主动脉瓣置换术(DVR)12例。随机分为Lipo-PGE1组(P组)和对照组(C组),每组15例。P组于麻醉诱导后、CPB转流前持续静脉泵滴入Lipo-PGE1(剂量3ng/kg·min)至手术结束;C组用相同的方法给予相同容量的生理盐水。两组患者均于麻醉后手术前(T1)、CPB后30min(T2)、开放升主动脉后1h(T3)、CPB后6h(T4)、CPB后24h(T5)时间点采颈静脉球血4ml,用ELISA法测S100β蛋白、NSE、TNF-α浓度,用硫代巴比妥法测定MDA浓度、用黄嘌呤氧化酶法测定SOD活性。
【结果】1.两组患者麻醉后手术前(T1) S100β蛋白、NSE含量差异无统计学意义(P>0.05)、CPB后30min(T2)上升(P<0.05)、开放升主动脉后1h(T3)达峰值(P<0.05)、CPB后6h(T4)开始下降(P<0.05)、CPB后24h(T5)仍高于术前水平,但无统计学意义(P>0.05)。组间比较T2-T4时点P组S100β蛋白、NSE浓度低于C组(P<0.05)。2.两组患者麻醉后手术前(T1) TNF-α含量差异无统计学意义(P>0.05)、CPB后30min(T2)上升(P<0.05)、开放升主动脉后1h(T3)达峰值(P<0.05)、CPB后6h(T4)开始下降(P<0.05)、CPB后24h(T5)仍高于术前水平,但无统计学意义(P>0.05)。组间比较T2-T4时点P组TNF-α浓度低于c组(P<0.05)。3.两组患者麻醉后手术前(T1) MDA、SOD含量差异无统计学意义(P>0.05)、T2-T4时点两组MDA浓度升高,SOD活性下降(P<0.05)。组间比较T2-T4时点P组MDA浓度低于C组,SOD活性高于C组(P<0.05)。
【结论】围CPB期血清中脑损伤的特异性生化标志物S100β蛋白、NSE水平均有一过性明显升高;Lipo-PGE1可以降低围CPB期S100β蛋白、NSE的水平升高,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活性有关。
【Objective】To discuss the protective effects and probable mechanism of liposomal prostaglandin E1 (Lipo-PGE1) on brain injury of patients during cardiopulmonary bypass (CPB).
【Methods】30 patients underwent rheumatic heart valve replacement were selected randomly, including 10 males and 20 females with ages from 32 to 60,and the average age was 41.7±7.7 years. None of them had endocarditis, diabetes, hypertension, hyperlipidemia, cerebrovascular diseases, immune system diseases or mental disorders before operation, and had no drinking hobby or obvious lung, liver, kidney dysfunction before operation. These patients’heart function were GradeⅡ～Ⅲon the basis of New York Heart Association (NYHA), and none of them used the drugs which have significant effects on the immune system.The study was composed of 5 cases of aortic valve replacement (AVR), 13 cases of mitral valve replacement (MVR) and 12 cases of double valve replacement (DVR). The 30 cases were divided into two groups randomly, including experimental group (Group P, n=15) and control group (Group C, n=15).In Group P, Lipo-PGE1 (dose of 3ng/kg?min) was continuously pumped intravenously into the patients after induction of anesthesia and before CPB, till to the end of operation. In Group C, the patients were given identical volume of normal saline instead of Lipo-PGE1 with the same methods. 4 ml of blood samples were taken from jugular bulb after induction of anesthesia and before operation (T1), 30 minutes after initiation of CPB (T2), 1 h after the ascending aortic off-clamping (T3), 6h (T4) and 24h (T5) after discontinuation of CPB to determine the concentrations of plasma S100βprotein, NSE and TNF-αwith ELISA, to determine the concentration of MDA with thio-barbitone, and to determine the activity of SOD with xanthinoxidase, respectively.
【Result】The difference of the plasma concentrations of S100βprotein, NSE and TNF-αwas not statistically significant between both groups at T1 (P>0.05). In contrast with Group C, the plasma concentrations of S100βprotein, NSE and TNF-αin Group P rose at T2 (P<0.05), reached to the peak at T3 (P<0.05), began to descend at T4 (P<0.05), and were still higher than pre-operation at T5, but the difference was not statistically between them (P>0.05). When contrasted between groups, the concentrations of Group P were lower than Group C in T2-T4 (P<0.05). 2. The difference of the plasma concentrations of MDA and activity of SOD was not statistically significant between both groups at T1 (P>0.05); in contrast with Group C, the plasma concentrations of MDA were higher than and the activity of SOD descended in Group P (P<0.05 ). When contrasted between groups, the plasma concentration of MDA in Group P was lower than Group C and the activity of SOD was higher than Group C in T2-T4 (P<0.05).
【Conclusion】The plasma concentrations of specific biochemical marker for brain injury, such as S100βprotein and NSE, all markedly rose transiently during CPB, Lipo-PGE1 can relieve the expression level of S100βprotein and NSE of peri-CPB. Its mechanism may principally be suppressing the release of inflammatory factor TNF-α, lessening the production of MDA and increasing the activity of SOD.
引文
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[1] Rrow smith JE,Grocott HP,Reves JG,et a1.Central nervous system complications of cardiac surgery[J].Br J Anaesth,2000,84(3):387-393.
[2] Newman MF,Grocott HP,Mathew JP,et al.Report of the substudy assessing the impact of neurocognitive function on quality of life 5 years after cardiac surgery[J]. Stroke,2001,32,(12):2874-2881.
[3] Llinas R,Barbut D,Caplan LR. Neurologic complications of cardiac surgery [J]. Prog Cardiovasc Dis,2000,43(2):101-ll2.
[4] Ahonen J,Salmenpera M. Brain injury after adult cardiac surgery[J].Acta Anaesthesiologica Scandinavica, 2004, 48(1):4-19.
[5] Conlon N,Grocott HP,Mackensen GB, Neuroprotection during cardiac surgery[J]. Expert Rev Cardiovasc Ther,2008,6(4):503-520.
[6] Taylor KM.Central nervous system effects of cardiopulmonary bypass[J].Ann Thorac Surg.1998,66(5 Suppl): S20-4, discussion:S25-8.
[7] Djaiani G,Fedorko L, Borger M, et al. Mild-to-moderate atheromatous disease of the thoracic aorta and new ischemic brain lesions after conventional coronary artery bypass graftsurgery[J]. Stroke,2004,35(9):E356–358.
[8] Hogue CW Jr,Palin CA,Arrowsmith JA. Cardiopulmonary bypass management and neurologic outcomes: an evidence-based appraisal of current practices[J]. Anesth Analg 2006,103(1):21-37.
[9] Blauth CI,Cosgrove DM,Webb BW, et al. Atheroembolism from the ascending aorta: an emerging problem in cardiac surgery[J]. J Thorac Cardiovasc Surg 1992,103(6):1104–1112.
[10] Nollert G,Reichart B,Cardiopulmonary bypass and cerebral injury in adults[J]. Shock,2001,16Suppl 1:16-19.
[11] Harris DNF,Bailey SM,Smith PLC,et a1.Brain swelling in the first hour after coronary artery bypass surgery[J].Lancet,1993,342(8871):586-587.
[12] Krishnadasan B,Craig R, Hampton,et al. Molecular Mechanisms of Neurologic Injury Following Cardiopulmonary Bypass[J]. Semin Cardiothorac Vasc Anesth 2002,6,(1): 43-45.
[13] Nakamura K,Ueno T,Yamamoto H,et a1.Relationship between cerebral injury and inflammatory responses in patients undergoing cardiac surgery with cardiopulmonary bypass[J].Cytokine,2005,29(3):95-104.
[14] Stroick M,Fatar M,Ragoschke-Schumm,et al.Protein S-100B - A Prognostic Marker for Cerebral Damage[J].Curt Med Chem,2006,13(25):3053 -3060.
[15] Blomqist S,Johnsson P,Luhrs C,et al. The appearance of S-100 protein in serum during and immediately after cardiopulmonary bypass surgery: a possible marker for cerebral injury [J].J Cardiothorac Vasc Anesth,1997,11(6):699-703.
[16] Ali MS,Harmer M,Vaughan R.Serum S100 protein as a marker of cerebral damage during cardiac surgery[J].Bri Anaesth,2000,85(2):287-298.
[17] Farsak B,Gunaydin S,Yorgancioglu C,et al. Elevated levels of s-100beta correlate with neurocognitive outcome after cardiac surgery [J].J Cardiovasc Surg(Tori no)2003,44(1):31-35.
[18] Svenmarker S,Sandstrom E,Karlsson T,et al .Is there an association between release of protein S100B during cardiopulmonary bypass and memory disturbances [J] .Scand Cardiovasc J,2002,36(2):117-122.
[19]Jonsson H,Johnssonp,Hoglund P,et al. Elimination of S100B and renal function after cardiac surgery [J]. J Cardiothorac Vasc Anesth,2000,14(6):698-701.
[20] Parolari A,Alamanni F,Naliato M,et al.Adult cardiac surgery outcomes:role of the pump type [J].Eur J Cardiothral Surg,2000,18(5):575-582.
[21]杨绍文,曹国彬,李波等.血清S100B、NSE和MBP在颅脑损伤患者中的检测及其临床意义[J].广州医药,2007,38(3):3-5.
[22]Gao F,Harris DN,Sapsed-Byrne S. Time course of neurone-specific enolase and S-100 protein release during and after coronary artery bypass grafting. Br J Anaesth,1999,82(2):266-267.
[23] Herrmann M,Ebert AD,Galazky I,et al.Neurobehavioral outcome prediction after cardiac surgery: role of neurobiochemical markers of damage to neuronal and glial brain tissue[J]. Stroke,2000,31(3):645-650.
[24] Cooper EH.Neuron-specific enolase[J]. Int J Biol Markers,1994,9(4):205-210.
[25] Rasmussen LS,Christiansen M,Eliasen K,et a1.Biochemical markers for brain damage after cardiac surgery -- time profile and correlation with cognitive dysfunction[J]. Acta Anaesthesiol Scand,2002,46(5):547-551.
[26] Ramlawi B,Rudolph JL,Mieno S, et al.C-Reactive protein and inflammatory response associated to neurocognitive decline following cardiac surgery. Surgery,2006,140(2):221-226.
[27] Ramlawi B,Rudolph JL,Mieno S,et al. Serologic markers of brain injury and cognitive function after cardiopulmonary bypass. Ann Surg,2006,244(4):593-601.
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[30] Engelman RM,Verrier ED.Optimal temperature for routine cardiopulmonary bypass[J] Adv Card Surg,2001,13:121-141.
[31] Bernard SA,Gray TW,Buist MD et al. Treatment of comatose survivors of out - of- hospital cardiac arrest with induced hypothermia [J]. N Engl J Med,2002,346(8),557–563.
[32]Cook DJ,Orszulak TA,Zehr KJ,et al.Effectiveness of the Cobra catheter for dual-temanagement during adult cardiac surgery[J].J Thorac Cardiovasc Surg,2003,125:378-384.
[33] Joras RA.Optical pH Strategy for hypothermic circulatory arrest[J].J Thorac Cardiovasc Surg,2001,121(2):204-205.
[34]Bellinger DC,Wypij D, et al. Developmental and neurologicof alpha-stat versus pH-stat strategies for deep hypothermic cardiopulmonary bypass in infants[J].J Thorac Cardiovasc Surg,2001,121: 374-383.
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[36]Whitaker D,Newman SP,Harrison MJ,et a1.Leucocyte depleting arterial line filtration during CABG reduces microemboli but not S100.[J].Perfusion,2001,16(2):264
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[1] Rrow smith JE,Grocott HP,Reves JG,et a1.Central nervous system complications of cardiac surgery[J].Br J Anaesth,2000,84(3):387-393.
[2] Newman MF,Grocott HP,Mathew JP,et al.Report of the substudy assessing the impact of neurocognitive function on quality of life 5 years after cardiac surgery[J]. Stroke,2001,32,(12):2874-2881.
[3] Llinas R,Barbut D,Caplan LR. Neurologic complications of cardiac surgery [J]. Prog Cardiovasc Dis,2000,43(2):101-ll2.
[4] Ahonen J,Salmenpera M. Brain injury after adult cardiac surgery[J].Acta Anaesthesiologica Scandinavica, 2004, 48(1):4-19.
[5] Conlon N,Grocott HP,Mackensen GB, Neuroprotection during cardiac surgery[J]. Expert Rev Cardiovasc Ther,2008,6(4):503-520.
[6] Taylor KM.Central nervous system effects of cardiopulmonary bypass[J].Ann Thorac Surg.1998,66(5 Suppl): S20-4, discussion:S25-8.
[7] Djaiani G,Fedorko L, Borger M, et al. Mild-to-moderate atheromatous disease of the thoracic aorta and new ischemic brain lesions after conventional coronary artery bypass graftsurgery[J]. Stroke,2004,35(9):E356–358.
[8] Hogue CW Jr,Palin CA,Arrowsmith JA. Cardiopulmonary bypass management and neurologic outcomes: an evidence-based appraisal of current practices[J]. Anesth Analg 2006,103(1):21-37.
[9] Blauth CI,Cosgrove DM,Webb BW, et al. Atheroembolism from the ascending aorta: an emerging problem in cardiac surgery[J]. J Thorac Cardiovasc Surg 1992,103(6):1104–1112.
[10] Nollert G,Reichart B,Cardiopulmonary bypass and cerebral injury in adults[J]. Shock,2001,16Suppl 1:16-19.
[11] Harris DNF,Bailey SM,Smith PLC,et a1.Brain swelling in the first hour after coronary artery bypass surgery[J].Lancet,1993,342(8871):586-587.
[12] Krishnadasan B,Craig R, Hampton,et al. Molecular Mechanisms of Neurologic Injury Following Cardiopulmonary Bypass[J]. Semin Cardiothorac Vasc Anesth 2002,6,(1): 43-45.
[13] Nakamura K,Ueno T,Yamamoto H,et a1.Relationship between cerebral injury and inflammatory responses in patients undergoing cardiac surgery with cardiopulmonary bypass[J].Cytokine,2005,29(3):95-104.
[14] Stroick M,Fatar M,Ragoschke-Schumm,et al.Protein S-100B - A Prognostic Marker for Cerebral Damage[J].Curt Med Chem,2006,13(25):3053 -3060.
[15] Blomqist S,Johnsson P,Luhrs C,et al. The appearance of S-100 protein in serum during and immediately after cardiopulmonary bypass surgery: a possible marker for cerebral injury [J].J Cardiothorac Vasc Anesth,1997,11(6):699-703.
[16] Ali MS,Harmer M,Vaughan R.Serum S100 protein as a marker of cerebral damage during cardiac surgery[J].Bri Anaesth,2000,85(2):287-298.
[17] Farsak B,Gunaydin S,Yorgancioglu C,et al. Elevated levels of s-100beta correlate with neurocognitive outcome after cardiac surgery [J].J Cardiovasc Surg(Tori no)2003,44(1):31-35.
[18] Svenmarker S,Sandstrom E,Karlsson T,et al .Is there an association between release of protein S100B during cardiopulmonary bypass and memory disturbances [J] .Scand Cardiovasc J,2002,36(2):117-122.
[19]Jonsson H,Johnssonp,Hoglund P,et al. Elimination of S100B and renal function after cardiac surgery [J]. J Cardiothorac Vasc Anesth,2000,14(6):698-701.
[20] Parolari A,Alamanni F,Naliato M,et al.Adult cardiac surgery outcomes:role of the pump type [J].Eur J Cardiothral Surg,2000,18(5):575-582.
[21]杨绍文,曹国彬,李波等.血清S100B、NSE和MBP在颅脑损伤患者中的检测及其临床意义[J].广州医药,2007,38(3):3-5.
[22]Gao F,Harris DN,Sapsed-Byrne S. Time course of neurone-specific enolase and S-100 protein release during and after coronary artery bypass grafting. Br J Anaesth,1999,82(2):266-267.
[23] Herrmann M,Ebert AD,Galazky I,et al.Neurobehavioral outcome prediction after cardiac surgery: role of neurobiochemical markers of damage to neuronal and glial brain tissue[J]. Stroke,2000,31(3):645-650.
[24] Cooper EH.Neuron-specific enolase[J]. Int J Biol Markers,1994,9(4):205-210.
[25] Rasmussen LS,Christiansen M,Eliasen K,et a1.Biochemical markers for brain damage after cardiac surgery -- time profile and correlation with cognitive dysfunction[J]. Acta Anaesthesiol Scand,2002,46(5):547-551.
[26] Ramlawi B,Rudolph JL,Mieno S, et al.C-Reactive protein and inflammatory response associated to neurocognitive decline following cardiac surgery. Surgery,2006,140(2):221-226.
[27] Ramlawi B,Rudolph JL,Mieno S,et al. Serologic markers of brain injury and cognitive function after cardiopulmonary bypass. Ann Surg,2006,244(4):593-601.
[28] 谷兴华,张供,张希全,等.血清蛋白B亚型和神经元特异性烯醇化酶对早期判断体外循环术后脑损伤的意义[J].中华医学杂志,2007,87(14):975-977.
[29] Rasmussen LS,Christiansen M,Bliasen k,et al.Biochemical markers for brain damage afte cadiac surgery-time profile and correlation with cognitive dysfunction[J].Acta Anaesthesiol Scand 2002,46(5):547-551.
[30] Engelman RM,Verrier ED.Optimal temperature for routine cardiopulmonary bypass[J] Adv Card Surg,2001,13:121-141.
[31] Bernard SA,Gray TW,Buist MD et al. Treatment of comatose survivors of out - of- hospital cardiac arrest with induced hypothermia [J]. N Engl J Med,2002,346(8),557–563.
[32]Cook DJ,Orszulak TA,Zehr KJ,et al.Effectiveness of the Cobra catheter for dual-temanagement during adult cardiac surgery[J].J Thorac Cardiovasc Surg,2003,125:378-384.
[33] Joras RA.Optical pH Strategy for hypothermic circulatory arrest[J].J Thorac Cardiovasc Surg,2001,121(2):204-205.
[34]Bellinger DC,Wypij D, et al. Developmental and neurologicof alpha-stat versus pH-stat strategies for deep hypothermic cardiopulmonary bypass in infants[J].J Thorac Cardiovasc Surg,2001,121: 374-383.
[35] Pufsley WB,Klinger L,Paschalis C,et a1.The impact of microemboli during cardiopulmonary bypass neuro-psychological functioning [J].Stroke,1994,25(7):1393-1399.
[36]Whitaker D,Newman SP,Harrison MJ,et a1.Leucocyte depleting arterial line filtration during CABG reduces microemboli but not S100.[J].Perfusion,2001,16(2):264
[37]Chew MS.Does modified ultrafiltration reduce the systemic inflammatory response to cardiac surgery wich cardiopulmonary bypass? [J].Perfusion.2004,19(Suppl 1):S57-60.
[38] De Vroge R,Stooker W,Van Oeveren W,et a1.The impact of heparin coated circuits upon metabolism in vital organs:effect upon cerebral and renal function during and after cardiopulmonary bypass[J].ASAIO J,2005,51(1):103-109.
[39] Johansson-Synnergren M,Nilsson F,Bengtsson A,et al.Off-pump CABG reduces complement but does not significantly affect peripheral endothelial function:a prospective randominzed study[J].Scand Cardiovasc J,2004,38(1):53-58.
[40] Al-Ruzzeh S,Ambler G,Asimakopoulos G,et al.Off-pump coronary artery bypass surgery reduces risk-striatified mabidity and mortality:A United Kingdom multi-center comparative analysis of early clinical outcome[J].Circulation,2003,108(Suppl 1):II-1-II-8.
[41] Jarvinen O,Saarinen T,Julkunen J,et al.Improved health-related quality of life after coronary artery bypass grafting is unrelated to use of cardiopulmonary bypass[J].World J Surg,2004,28(10):1030-1035.
[42]Celik JB,Gormus N,Okesli S,et al.Methylprednisolone prevents inflammatory reaction occurring during cardiopulmonary bypass : effects on TNF-alpha , IL-6 , IL-8 ,IL-10[J]. Perfusion,2004,19(3):185-191.
[43] Cagli K,Ulas MM,Ozisik K,et al.The intraoperative effect of pentoxifylline in the inflammatory process and leukocytes in cardiac surgery patients undergoing cardiopulmonary bypass[J].Perfusion,2005,20(1):45-51.
[44]Arrowsmith JE,Harrison MJ,Newman SP,et a1.Neuroprotection of the brain during cardiopulmonary bypass:a randomised trial of remacemide during coronary artery bypass in 171 patients[J].Stroke,1998,29(11):2357-2362.
[45]Kadoi Y,Saito S,Goto F,et al.Effects of small doses of prostaglandin E(1) on systemic hemodynamics and jugular venous oxygen saturation during cardiopulmonary bypass[J].J Clin Anesth,2001,13(6):417-421.