体外循环冠状动脉搭桥术中不同麻醉方法对S-100B、NSE蛋白水平及脑氧代谢影响的研究
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摘要
目的:观察不同麻醉方法下中低温体外循环(CPB)冠状动脉搭桥术(CABG)中各时点颈内静脉血S-100B、NSE蛋白水平表达,以及对脑氧代谢指标的影响,评价S-100B、NSE及脑氧代谢指标与术后脑损伤和精神神经功能改变的相关性。
方法:年龄≥50岁择期CPB下行CABG病人40例,随机均分为两组,丙泊酚组(n=20,P组)、芬太尼组(n=20,F组)。分别于麻醉诱导后(a点)、CPB开始(b点)、CPB结束(c点)、术后4h(d点)、24h(e点)、48h(f点)、72h(g点)采取右颈内静脉血,用ELISA方法检测血浆中的S-100B、NSE蛋白含量;于麻醉前(T_1)、麻醉后(T_2)、锯胸骨(T_3)、降温结束(T_4)、复温结束(T_5)、CPB结束(T_6)采取右颈内静脉球部血和桡动脉血进行血气分析、葡萄糖及乳酸测定,并计算脑血流量/脑氧耗比值(CBF/CMRO_2)、脑氧耗/脑糖耗比值(CMRO_2/CMRG_(Glu))及乳酸生成量(ADVL);术前、术后采用标准神经功能检查和简短精神状态量表(MMSE)检查,将病人分为存在精神神经系统并发症(POMD)和无精神神经系统并发症(NPMD)两组,并分别对以上指标进行统计学处理。
结果:(1)S-100B:P组、F组均在CPB开始(b点)时上升、CPB结束(c点)达到高峰、术后4h(d点)开始下降,术后48h(f点)恢复正常。两组内c、d、e点与a点比较差异显著(P<0.001);(2)NSE:P组、F组均在CPB开始(b点)时上升、术后4h(d点)达到高峰、术后24h(e点)开始下降,术后72h(g点)恢复正常。两组内b、c、d、e点与a点比较差异显著(P<0.001);(3)术后有8例病人发生POMD发生率为20%,其中P组有2例、F组有6例;(4)按照麻醉方式分组对不同T点脑氧代谢指标T检验,P组与F组SjO_2仅在T_5点有显著差异(P=0.019<0.05),P组明显高于F组;(5)根据术后出现POMD有否分为POMD组(n=8)、NPMD组(n=32),对两组不同T点的脑氧代谢指标进行比较,①SjO_2变化POMD组发生颈内静脉血氧去饱
Objective: To observe the changes of S-100B、 NSE protein level and their influences to cerebral oxygen metabolism at different phase point of various anesthetic methods cardiopulmonary bypass (CPB) coronary artery bypass graft(CABG) with moderate hypothermia. To evaluate the relationship between S-100B、 NSE, indexes of cerebral oxygen metabolism and postoperative cerebral injury, mental function.Methods: 40 cases of 50 years old and above patients for selective CABG under CPB were randomly divided into two groups: propofol group (n=20, group P) and fentanyl group(n=20, group F). Blood samples were taken from right internal jugular vein at different phase points: after anesthetic induction (point a), CPB start (point b), CPB over (point c),4 hours after operation(point d), 24 hours after operation (point e), 48 hours after operation (point f). 72 hours after operation (point g). S-100B、 NSE protein contents were measured by ELISA. Blood gas analysis, glucose and lactic acid determination were carried out by taking blood samples from right internal jugular vein bulb and radial artery at different phase points: before anesthesia (T_1). immediately after induction of anesthesia (T_2), sawing the sternum (T_3), hypothermia over (T_4), rewarming over (T_5), at the end of bypass (T_6). Cerebral blood flow/cerebral metabolic rate of O_2 (CBF/CMRO_2), cerebral metabolic rate of O_2/ cerebral metabolic rate of glucose (CMRO_2/ CMR_(Glu)) and advent volume of lactification (ADVL) were also calculated. Patients were divided into groups of postoperative mental disorders (POMD) and non-POMD (NPMD) according to standard neurological function examination and mental measuring scale (MMSE) preoperation, 1st, 3~(rd),7~(th) and 10~(th) day postoperation each. All the above indexes were analyzed by statistics to investigate the rule of S-100B, NSE and changes of cerebral oxygen metabolic indexes and their relationship with mental and neurological disorders.Result: (1)S-100B: group P and F all began to increase at CPB start point (point b), reached climax at CPB over point (point c), decrease at 4 hours after operation (point d), restore to normal at 48 hours after operation (point f). There were significant differences between two groups at point c, d, e compared with point a (P<0.001); (2) NSE: group P and F all began to
方法:年龄≥50岁择期CPB下行CABG病人40例,随机均分为两组,丙泊酚组(n=20,P组)、芬太尼组(n=20,F组)。分别于麻醉诱导后(a点)、CPB开始(b点)、CPB结束(c点)、术后4h(d点)、24h(e点)、48h(f点)、72h(g点)采取右颈内静脉血,用ELISA方法检测血浆中的S-100B、NSE蛋白含量;于麻醉前(T_1)、麻醉后(T_2)、锯胸骨(T_3)、降温结束(T_4)、复温结束(T_5)、CPB结束(T_6)采取右颈内静脉球部血和桡动脉血进行血气分析、葡萄糖及乳酸测定,并计算脑血流量/脑氧耗比值(CBF/CMRO_2)、脑氧耗/脑糖耗比值(CMRO_2/CMRG_(Glu))及乳酸生成量(ADVL);术前、术后采用标准神经功能检查和简短精神状态量表(MMSE)检查,将病人分为存在精神神经系统并发症(POMD)和无精神神经系统并发症(NPMD)两组,并分别对以上指标进行统计学处理。
结果:(1)S-100B:P组、F组均在CPB开始(b点)时上升、CPB结束(c点)达到高峰、术后4h(d点)开始下降,术后48h(f点)恢复正常。两组内c、d、e点与a点比较差异显著(P<0.001);(2)NSE:P组、F组均在CPB开始(b点)时上升、术后4h(d点)达到高峰、术后24h(e点)开始下降,术后72h(g点)恢复正常。两组内b、c、d、e点与a点比较差异显著(P<0.001);(3)术后有8例病人发生POMD发生率为20%,其中P组有2例、F组有6例;(4)按照麻醉方式分组对不同T点脑氧代谢指标T检验,P组与F组SjO_2仅在T_5点有显著差异(P=0.019<0.05),P组明显高于F组;(5)根据术后出现POMD有否分为POMD组(n=8)、NPMD组(n=32),对两组不同T点的脑氧代谢指标进行比较,①SjO_2变化POMD组发生颈内静脉血氧去饱
Objective: To observe the changes of S-100B、 NSE protein level and their influences to cerebral oxygen metabolism at different phase point of various anesthetic methods cardiopulmonary bypass (CPB) coronary artery bypass graft(CABG) with moderate hypothermia. To evaluate the relationship between S-100B、 NSE, indexes of cerebral oxygen metabolism and postoperative cerebral injury, mental function.Methods: 40 cases of 50 years old and above patients for selective CABG under CPB were randomly divided into two groups: propofol group (n=20, group P) and fentanyl group(n=20, group F). Blood samples were taken from right internal jugular vein at different phase points: after anesthetic induction (point a), CPB start (point b), CPB over (point c),4 hours after operation(point d), 24 hours after operation (point e), 48 hours after operation (point f). 72 hours after operation (point g). S-100B、 NSE protein contents were measured by ELISA. Blood gas analysis, glucose and lactic acid determination were carried out by taking blood samples from right internal jugular vein bulb and radial artery at different phase points: before anesthesia (T_1). immediately after induction of anesthesia (T_2), sawing the sternum (T_3), hypothermia over (T_4), rewarming over (T_5), at the end of bypass (T_6). Cerebral blood flow/cerebral metabolic rate of O_2 (CBF/CMRO_2), cerebral metabolic rate of O_2/ cerebral metabolic rate of glucose (CMRO_2/ CMR_(Glu)) and advent volume of lactification (ADVL) were also calculated. Patients were divided into groups of postoperative mental disorders (POMD) and non-POMD (NPMD) according to standard neurological function examination and mental measuring scale (MMSE) preoperation, 1st, 3~(rd),7~(th) and 10~(th) day postoperation each. All the above indexes were analyzed by statistics to investigate the rule of S-100B, NSE and changes of cerebral oxygen metabolic indexes and their relationship with mental and neurological disorders.Result: (1)S-100B: group P and F all began to increase at CPB start point (point b), reached climax at CPB over point (point c), decrease at 4 hours after operation (point d), restore to normal at 48 hours after operation (point f). There were significant differences between two groups at point c, d, e compared with point a (P<0.001); (2) NSE: group P and F all began to
引文
1. Rosen H, Sunnerhagen KS, Herlitz J, et al. Serum levels of the brain-derived protein S-100B and NSE predict long-term outcome after cardiac arrest. Resuscition, 2001, 49:183-191.
2. Henribe S, Hilman WP, et al. Neuron specific enolase concentrations in blood as aprognostic parameter in cerebrovascular diseases[J]. Stroke, 1994, 24(3):558-565.
3. Lindberg l, et al. J Thorac Cardiovasc Surg, 1998:116:281.
4. Westaby S et al. Ann Thorae Surg, 1996:61:88.
5.王兴河、秦梅等,新生鼠缺氧缺血性脑损伤S-100B NSE mRNA和蛋白水平变化.中国当代儿科杂志.2000,2(6):381-385.
6. Beards SC, Yule S, Kassner A, et al. Automatic variation of cerebral venous damage: the theoretical effect on jugular bulb samples. Anaesthesia, 1998, 53:627-633.
7. Croughwell ND, Peter F, Blumenthal JA, et al. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg, 1994,58:702.
8. Caralei E, Peters B, Jasminka B, et al. Anesthetic concentration of propofol protect against oxidantive stress in primary astraeyte cultures. Anesth Analg, 1990;71:49.
9. Star SM, Hanifi-Moghaddam P, Gelb A, et al. Propofol prevents peroxide-induced inhibition of glutamate transport in cultured astrocyte. Anesthesiology, 1999, 90(5): 1446-1453.
10. Kadio Y, Saito S, Kumimoto F, et al. Comarative effects of propofol versus fentanyl on cerebral oxygenation state during normothermic cardiopulmonary bypass and postoperative cognitive dysfuntion. Ann Thorac Surg, 2003:75:840-846.
11. WongDH. Perioperativestroke. Part: Cardiacsurgeryandcardiogenicembolicstroke. CanJAn aesth, 1991, 38(4 Pt 1):471-488.
12. ClarkRE, BrillmanJ, DavisDA, etal. Microemboliduringecronaryarterybypassgrafting. Gene sisandeffectonoutcome. J Thorac Cardiovasc Surg, 1995, 109(2):249-258.
13. O'BrienJJ, ButterworthJ, HammonJW, etal. Cerebralemboliduringcardiacsurgeryinchildren. Anesthesiology, 1997,87(5): 1063-1069.
14. DeiwickM, TandlerR, MollhoffT, etal. Heartsurgeryinpa-tientsagedeightyyearsandabove:de terminantsofmorbidityandmortality. ThoracCardiovascSurg, 1997, 45(3): 119-126.
15. BarbutD, YaoFS,HagerDN,etal. ComparisonoftranscraniaDopplerultrasonographyandtrans esophagealechocardiographytomonitoremboliduringcoronaryarterybypasssurgery. Stroke, 1996, 27(1):87-90.
16. Jnsson H, Jonsson P, Alling C, et al. Significance of serum S-100 release after coronary artery bypass grafting. Ann Thorac Surg, 1998, 65:1639-1644.
17. Gao F, Harris DN, Sapaed-Byrne S. Time course of neurone-specific enolase and S-100B protein release during and after coronary artery bypass grafting. Br J Anaesth, 1999, 82:266-267.
18. Ali MS, Harmer M, Vaughan RS, et al. Early release pattern of S-100B protein as a marker of brain damage after warm cardiopulmonary bypass. Anaesthesia, 2000, 55:L802-806.
19. Blomquist S, Johnsson P, Lubrs 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 Cardiothorac Vasc Anesth, 1997, 11:699-703.
20. Aberg T. Signs of brain cell injury during open heart operations: past and present. Ann Thorac Surg, 1995, 59:1312-1315.
21. Kumar P, Dhital K, Hossein-Nia M, et al. S-100B protein release in a range of cardiothoracic surgical procedures. J Thorac Cardiovasc Surg. 1997, 113:953-954.
22. Taggart DP, Mazel JW, Bhattacharya K, et al. Comparison of serum S-100B beta levels during CABG and intracardiac operations. Ann Thorac Surg, 1997, 63: 492-496.
23. Koide M, Kunii Y, Morikki N, et al. Clinical significance of serum S-100B beta protein level after pediatric cardiac surgery. Jpn J Thorac is it a rerliable marker for cerebral damage? Ann Thorac Surg, 2000, 69: 1515-1519.
24. Astudillo R, Van der Linden J, Radegran K, et al. Elevated serum levels after deep hypothemic arrest correlate with duration of circulatory arrest. Eur J Cardiothorac SURG, 1996, 10:1107-1112.
25. Lindberg L, Olsson AK, Anderson K, et al. Serum S-100B protein levels after pediatric cardiac operations: a possible new marker for postperfusion cerebral injury. J Thorac Cardiovasc Surg, 1998, 116: 281-285.
26.王兴河、秦梅、樊绍曾等.新生鼠缺氧缺血性脑损伤S-100B NSE mRNA和蛋白水平变化。中国当代儿科杂志.2000;2(6):381-385.
27. Taggart DP, Reece U, Wheathy DJ. Cerebral deficit after cardiac surgery. Lancet, 1987,1:47.
28. Borowicz LM, Goldsborough MA, Selnes OA, et al. Neuropsychological change after cardiac surgery: a critical review. J Cardiothorac Vasc Anesth, 1996,10:105-111.
29. Gao F,Harris DN, Sapaed Byrne S,et al . Neurone-specific enolase and Sangtec 100 assays during cardiac surgery: part I -the effects of heparin, protamine and propofol. Perfusion, 1997,12:163-165.
30. Derkach DN, Okamoto H, Takahashi S. Neuronal and astroglial injuries in patients undergoing coronary artery bypass grafting and aortic arch replacement during hypothermic cardiopulmonary bypass. Anesth Analg,2000,91:1066-1072.
31. Gao F.Harris DN, Sapaed Byrne S,et al . Neurone-specific enolase and Sangtec 100 assays during cardiac surgery: part I -the effects of heparin, protamine and propofol. Perfusion, 1997,12:163-165.
32. Wolman RL, Nussmeler NA, Aggarwal A,et al. Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Stroke, 1999,30:514-522.
33. Grocott HP, Croughwell ND.Verkerk GC,et al. Serum S-100B as a predic to neurologic and neuropsychologic outcome after cardiac surgery. Anesth Analg, 1998,86:S65.
34. Kanbak M, Avci A, Yener F,et al. Cerebral injury assessed by S-100B β protein and neuropsychologic test after coronary artery bypass surgery. Br J Anaesth, 1999,82(Suppl I ):A.292.
35. Kilminster S,Treasure T, McMillan T,et al. Neuropsychological Changes and S-100B protein release in 130 unselected patients undergoing cardiac surgery. Stroke, 1999,30:1869-1874.
36. Babin- Ebell J, Misoph M, Mullges W, et al. Intraoperative embolus formation during cardiopulmonary bypass effects the release of S-100B. Thorac Cardiovasc Surg, 1999,47:166-169.
37. Linderg L, Olsson AK, Anderson K,et al. Serum S-100B protein levels after pediatric cardiac operations: a possible new marker for postoperative cerebral injury. J Thorac Cardiovasc Surg,1998,116:281-285.
38. Borger MA, Peniston CM, Weisel RD, et al. Perioperative predictors of stroke following coronary bypass surgery. Perfusion, 1997,12:36.
39. Matta B, Beards SC, Yule S. Advances in monitoring cerebral oxygenation. Current Opinion in Anaesthesiology, 1996, 365-370.
40. Nakajima T, Kuro M, Hayashi K, et al. Clinical evaluation of cerebral oxygen balance during cardiopulmonary bypass: on-line continuous monitoring of jugular venous oxyhemoglobin saturation. Anesth and Analg, 1992,74:630-635.
2. Henribe S, Hilman WP, et al. Neuron specific enolase concentrations in blood as aprognostic parameter in cerebrovascular diseases[J]. Stroke, 1994, 24(3):558-565.
3. Lindberg l, et al. J Thorac Cardiovasc Surg, 1998:116:281.
4. Westaby S et al. Ann Thorae Surg, 1996:61:88.
5.王兴河、秦梅等,新生鼠缺氧缺血性脑损伤S-100B NSE mRNA和蛋白水平变化.中国当代儿科杂志.2000,2(6):381-385.
6. Beards SC, Yule S, Kassner A, et al. Automatic variation of cerebral venous damage: the theoretical effect on jugular bulb samples. Anaesthesia, 1998, 53:627-633.
7. Croughwell ND, Peter F, Blumenthal JA, et al. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg, 1994,58:702.
8. Caralei E, Peters B, Jasminka B, et al. Anesthetic concentration of propofol protect against oxidantive stress in primary astraeyte cultures. Anesth Analg, 1990;71:49.
9. Star SM, Hanifi-Moghaddam P, Gelb A, et al. Propofol prevents peroxide-induced inhibition of glutamate transport in cultured astrocyte. Anesthesiology, 1999, 90(5): 1446-1453.
10. Kadio Y, Saito S, Kumimoto F, et al. Comarative effects of propofol versus fentanyl on cerebral oxygenation state during normothermic cardiopulmonary bypass and postoperative cognitive dysfuntion. Ann Thorac Surg, 2003:75:840-846.
11. WongDH. Perioperativestroke. Part: Cardiacsurgeryandcardiogenicembolicstroke. CanJAn aesth, 1991, 38(4 Pt 1):471-488.
12. ClarkRE, BrillmanJ, DavisDA, etal. Microemboliduringecronaryarterybypassgrafting. Gene sisandeffectonoutcome. J Thorac Cardiovasc Surg, 1995, 109(2):249-258.
13. O'BrienJJ, ButterworthJ, HammonJW, etal. Cerebralemboliduringcardiacsurgeryinchildren. Anesthesiology, 1997,87(5): 1063-1069.
14. DeiwickM, TandlerR, MollhoffT, etal. Heartsurgeryinpa-tientsagedeightyyearsandabove:de terminantsofmorbidityandmortality. ThoracCardiovascSurg, 1997, 45(3): 119-126.
15. BarbutD, YaoFS,HagerDN,etal. ComparisonoftranscraniaDopplerultrasonographyandtrans esophagealechocardiographytomonitoremboliduringcoronaryarterybypasssurgery. Stroke, 1996, 27(1):87-90.
16. Jnsson H, Jonsson P, Alling C, et al. Significance of serum S-100 release after coronary artery bypass grafting. Ann Thorac Surg, 1998, 65:1639-1644.
17. Gao F, Harris DN, Sapaed-Byrne S. Time course of neurone-specific enolase and S-100B protein release during and after coronary artery bypass grafting. Br J Anaesth, 1999, 82:266-267.
18. Ali MS, Harmer M, Vaughan RS, et al. Early release pattern of S-100B protein as a marker of brain damage after warm cardiopulmonary bypass. Anaesthesia, 2000, 55:L802-806.
19. Blomquist S, Johnsson P, Lubrs 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 Cardiothorac Vasc Anesth, 1997, 11:699-703.
20. Aberg T. Signs of brain cell injury during open heart operations: past and present. Ann Thorac Surg, 1995, 59:1312-1315.
21. Kumar P, Dhital K, Hossein-Nia M, et al. S-100B protein release in a range of cardiothoracic surgical procedures. J Thorac Cardiovasc Surg. 1997, 113:953-954.
22. Taggart DP, Mazel JW, Bhattacharya K, et al. Comparison of serum S-100B beta levels during CABG and intracardiac operations. Ann Thorac Surg, 1997, 63: 492-496.
23. Koide M, Kunii Y, Morikki N, et al. Clinical significance of serum S-100B beta protein level after pediatric cardiac surgery. Jpn J Thorac is it a rerliable marker for cerebral damage? Ann Thorac Surg, 2000, 69: 1515-1519.
24. Astudillo R, Van der Linden J, Radegran K, et al. Elevated serum levels after deep hypothemic arrest correlate with duration of circulatory arrest. Eur J Cardiothorac SURG, 1996, 10:1107-1112.
25. Lindberg L, Olsson AK, Anderson K, et al. Serum S-100B protein levels after pediatric cardiac operations: a possible new marker for postperfusion cerebral injury. J Thorac Cardiovasc Surg, 1998, 116: 281-285.
26.王兴河、秦梅、樊绍曾等.新生鼠缺氧缺血性脑损伤S-100B NSE mRNA和蛋白水平变化。中国当代儿科杂志.2000;2(6):381-385.
27. Taggart DP, Reece U, Wheathy DJ. Cerebral deficit after cardiac surgery. Lancet, 1987,1:47.
28. Borowicz LM, Goldsborough MA, Selnes OA, et al. Neuropsychological change after cardiac surgery: a critical review. J Cardiothorac Vasc Anesth, 1996,10:105-111.
29. Gao F,Harris DN, Sapaed Byrne S,et al . Neurone-specific enolase and Sangtec 100 assays during cardiac surgery: part I -the effects of heparin, protamine and propofol. Perfusion, 1997,12:163-165.
30. Derkach DN, Okamoto H, Takahashi S. Neuronal and astroglial injuries in patients undergoing coronary artery bypass grafting and aortic arch replacement during hypothermic cardiopulmonary bypass. Anesth Analg,2000,91:1066-1072.
31. Gao F.Harris DN, Sapaed Byrne S,et al . Neurone-specific enolase and Sangtec 100 assays during cardiac surgery: part I -the effects of heparin, protamine and propofol. Perfusion, 1997,12:163-165.
32. Wolman RL, Nussmeler NA, Aggarwal A,et al. Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Stroke, 1999,30:514-522.
33. Grocott HP, Croughwell ND.Verkerk GC,et al. Serum S-100B as a predic to neurologic and neuropsychologic outcome after cardiac surgery. Anesth Analg, 1998,86:S65.
34. Kanbak M, Avci A, Yener F,et al. Cerebral injury assessed by S-100B β protein and neuropsychologic test after coronary artery bypass surgery. Br J Anaesth, 1999,82(Suppl I ):A.292.
35. Kilminster S,Treasure T, McMillan T,et al. Neuropsychological Changes and S-100B protein release in 130 unselected patients undergoing cardiac surgery. Stroke, 1999,30:1869-1874.
36. Babin- Ebell J, Misoph M, Mullges W, et al. Intraoperative embolus formation during cardiopulmonary bypass effects the release of S-100B. Thorac Cardiovasc Surg, 1999,47:166-169.
37. Linderg L, Olsson AK, Anderson K,et al. Serum S-100B protein levels after pediatric cardiac operations: a possible new marker for postoperative cerebral injury. J Thorac Cardiovasc Surg,1998,116:281-285.
38. Borger MA, Peniston CM, Weisel RD, et al. Perioperative predictors of stroke following coronary bypass surgery. Perfusion, 1997,12:36.
39. Matta B, Beards SC, Yule S. Advances in monitoring cerebral oxygenation. Current Opinion in Anaesthesiology, 1996, 365-370.
40. Nakajima T, Kuro M, Hayashi K, et al. Clinical evaluation of cerebral oxygen balance during cardiopulmonary bypass: on-line continuous monitoring of jugular venous oxyhemoglobin saturation. Anesth and Analg, 1992,74:630-635.