心脏不停跳和心脏停跳下心内直视手术脑损害的临床对比研究
|
摘要
目的 观测浅低温体外循环(CPB)心脏不停跳与中浅低温体外循环心脏停跳下心内直视手术患者围手术期血浆中神经元特异性烯醇化酶(NSE)与S-100b蛋白的含量和手术前后脑电图(EEG)的变化，对心脏停跳与心脏不停跳条件下心内直视手术导致的脑损害进行临床对比研究。 方法 选择择期心内直视手术患者40例，其中先天性心脏病20例，风湿性心脏病20例。随机分为A组(n=20)，在中低温体外循环心脏停跳下施行心内直视手术，其中先天性心脏病(A1组)和风湿性心脏病(A2组)各10例；B组(n=20)，在浅低温体外循环心脏不停跳下施行心内直视手术，其中先天性心脏病(B1组)和风湿性心脏病(B2组)各10例。两组患者均在术前、CPB开始后20 min、CPB结束后60 min 和术后24 h采取血标本。运用酶联免疫吸附法(ELISA，单克隆双抗体夹心法)测定血浆中NSE和S-100b蛋白的含量；并在术前与术后7天对全组患者进行脑电图检查。对所得结果进行统计分析处理。 结果 CPB开始 20 min两组患者血浆中的S－100b均明显升高(p<0.01)，而且一直持续到术后第一天仍高于术前水平(p<0.01)；CPB 开始20 min , A组中先心病患者血浆S－100b升高程度高于B组中先心病患者(p<0.05)。在CPB 开始20 min A组患者血浆NSE升高的程度高于B组患者(p<0.05)；血浆NSE水平在CPB 开始20 min先心病组明显升高(p<0.01)，一直持续至CPB 结束后60 min达到最高点，以后NSE浓度逐渐下降，至术后24 h已降至术前水平(p>0.05)；风心病组患者在CPB 开始20 min NSE升高(p<0.05)，在CPB 结束后60 min明显高于术前，一直持续到术后24 h仍较术前高(p<0.01)。 其余各时相点血浆NSE和S－100b的变化两组间无显著差异(p>0.05)。术后两组患者EEG结果较术前明显变差(p<0.01)；但两组间的异常率无显著差别(p>0.05)。 结论 我们的结果表明体外循环心脏停跳与心脏不停跳心内直视手术患者血浆中NSE和S－100b蛋白均有明显升高；EEG较术前明显变差，说明体外循环心内直视手术会导致一定的脑组织损害。心脏不停跳组患者血浆NSE、S－100b蛋白的升高程度和术后EEG的变化并不比心脏停跳组显著，提示浅低温体外循环心脏不停跳心内直视手术导致的脑损伤并不比传统的心脏停跳心内直视手术更严重。
Objective The aim of this study was to compare the cerebral injury in on-pump beating-heart intracardiac procedures with that in traditional arrested heart intracardiac procedures. Methods Forty patients, including of twenty patients with congenital heart disease and twenty patients with rheumatic heart valve disease, were randomly divided into two groups: on-pump arrested heart group(Group A, n=20) and on-pump beating-heart group(Group B, n=20). There were ten cases of congenital heart disease and ten cases of rheumatic heart disease in each group. The patients in Group A underwent traditional arrested-heart intracardiac procedures, and the patients in Group B underwent on-pump beating-heart intracardiac procedures. Arterial blood was sampled at preoperation, twenty minutes after the start of CPB, one hour after CPB and twenty-four hours after operation. Levels of plasma neuron specific enolase(NSE) and protein S-100b were measured with ELISA. All the patients' electroencephalograms(EEGs) were examined before and one week after operations. The perioperative plasma NSE ,protein S-100b and EEG changes of the two groups were compared statistically. Results The levels of plasma protein S-100b increased significantly at twenty minutes after the start of CPB, and maintained high level till twenty four hours after operation(p<0.01). The level of plasma NSE in congenital heart disease group increased more significantly than that did in rheumatic heart disease group at twenty minutes after the start of CPB. The level of plasma NSE in congenital heart disease group returned to the nadir at twenty four hours after operation, but it was still higher than the preoperative level in rheumatic heart disease group at the same time(p<0.01). The level of plasma NSE in group A was significantly higher than that in group B at twenty minutes after the start of CPB. The protein S-100b of the patients with congenital heart disease in group A was significantly higher than that in group B at twenty minutes after the start of CPB (p<0.05).There was no significant difference between the twe groups at other times. The postoperative EEG abnormality rates were 65% in group A and 70% in group B respectively. There was no significant difference between two groups. Conclusion Our preliminary results showed that the levels of plasma NSE and S-100b
increased significantly during intracardic procedures both on-pump beating-heart and on traditional arrested heart; postoperative EEG became even worse than that before operation, which implicated that intracardic procedures under CPB might induce some cerebral injury. The increase of NSE and S-100b in the beating-heart group and the abnormality of the postoperative EEG are not more significant than those in the arrested-heart group, which recommend that the cerebral injury induced by on-pump beating heart intracardic procedures was not more severe than that by traditional arrested heart operations.
Objective The aim of this study was to compare the cerebral injury in on-pump beating-heart intracardiac procedures with that in traditional arrested heart intracardiac procedures. Methods Forty patients, including of twenty patients with congenital heart disease and twenty patients with rheumatic heart valve disease, were randomly divided into two groups: on-pump arrested heart group(Group A, n=20) and on-pump beating-heart group(Group B, n=20). There were ten cases of congenital heart disease and ten cases of rheumatic heart disease in each group. The patients in Group A underwent traditional arrested-heart intracardiac procedures, and the patients in Group B underwent on-pump beating-heart intracardiac procedures. Arterial blood was sampled at preoperation, twenty minutes after the start of CPB, one hour after CPB and twenty-four hours after operation. Levels of plasma neuron specific enolase(NSE) and protein S-100b were measured with ELISA. All the patients' electroencephalograms(EEGs) were examined before and one week after operations. The perioperative plasma NSE ,protein S-100b and EEG changes of the two groups were compared statistically. Results The levels of plasma protein S-100b increased significantly at twenty minutes after the start of CPB, and maintained high level till twenty four hours after operation(p<0.01). The level of plasma NSE in congenital heart disease group increased more significantly than that did in rheumatic heart disease group at twenty minutes after the start of CPB. The level of plasma NSE in congenital heart disease group returned to the nadir at twenty four hours after operation, but it was still higher than the preoperative level in rheumatic heart disease group at the same time(p<0.01). The level of plasma NSE in group A was significantly higher than that in group B at twenty minutes after the start of CPB. The protein S-100b of the patients with congenital heart disease in group A was significantly higher than that in group B at twenty minutes after the start of CPB (p<0.05).There was no significant difference between the twe groups at other times. The postoperative EEG abnormality rates were 65% in group A and 70% in group B respectively. There was no significant difference between two groups. Conclusion Our preliminary results showed that the levels of plasma NSE and S-100b
increased significantly during intracardic procedures both on-pump beating-heart and on traditional arrested heart; postoperative EEG became even worse than that before operation, which implicated that intracardic procedures under CPB might induce some cerebral injury. The increase of NSE and S-100b in the beating-heart group and the abnormality of the postoperative EEG are not more significant than those in the arrested-heart group, which recommend that the cerebral injury induced by on-pump beating heart intracardic procedures was not more severe than that by traditional arrested heart operations.
引文
1. Barbut D, Caplan I. R. Brain complications of cardiac surgery[J]. Curr Probl Cardiol, 1997,22: 449-480
2. Christina T. Mora Cardiopulmonary Bypass[M]. Springer-Verlag New York Inc.USA. 1995,114-146
3. G.Wimmer-Greinecker, G.Matheis, M. Brieden, et,al. Neuropsychological Changes after Cardiopulmonary Bypass for Coronary Artery Bypass Grafting[J]. Thorac. Cardiovasc. Surg, 1998,46:207-212
4. Ahlgren E, Aren C. Cerebral dysfunction a feared complication of cardiac surgery[J]. Perfusion, 1997, 12:32
5. O’Brien JJ, Butterworth J, Hammon JW, et al. Cerebral emboli during cardiac surgery in children[J]. Anesthesiology 1997;87:1063-1069
6. 肖颖彬，陈林，王学锋，等. 浅低温体外循环心脏跳动中心内直视手术1032例临床分析[J].第三军医大学学报, 2001, 23(5)：502－504
7. 陈林, 肖颖彬, 王学锋, 等. 浅低温体外循环心脏跳动中手术矫治先心病合并重度肺动脉高压[J].第三军医大学学报, 2001, 23(5)：505－507
8. 王学锋，肖颖彬，陈林，等. 心脏跳动中二尖瓣置换术234例临床分析[J］.第三军医大学学报, 2001, 23(5)：511－512
9. 何巍，林辉，陈铭伍，等. 心脏跳动中二尖瓣置换术(附137例报告)[J］.中华外科杂志, 1996,34(11)：678-680
10. Perrault L P, Menasche P, Peynet J, et al. On-pump beating-heart coronary operations in high-risk patients: An acceptable trade-off?[J]. Ann Thorac Surg, 1997,64(5): 1368-1373
11. Firlik AD, Yonas H, Kaufmann AM, et al. Relationship between cerebral blood flow and the development of swelling and lifethreatening herniation in acute ischemic stroke[J]. J Neurosurg, 1998,89(2)243-249
12. 金沐，孙来保，黄文起，等. S-100蛋白与脑损伤[J］.国外医学. 麻醉学与复苏分册，1999，20(3)：160－162
13. 徐卫平，谢飞，朱忠勇. S-100蛋白检测及其临床运用[J］.国外医学. 临床生物化学与检验学分册，2001，22(4)：173－174
14. 戴黎萌，李力仙，王天佑，等. NF－κB与中枢神经系统疾病[J］. 国外医学神经病学神经外科学分册，1998，25(5)：267－69
15. O'Neil LAJ, Kaltschmidt C. NF－κB acrucial transcription factor for glial and neuronal cell function[J]. Tins, 1997;20:252-55
16. Goldsborough MA, Boronicz LM, McKhann GM, Baumgartner. Variation in stroke occurrence by cardiac procedures[J]. Perfusion, 1997, 12:47
17. William A, Baumgartner, Peter L, Jorge D.Salazar, et al. Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury[J]. Ann Thorac Surg 1999, 67:1871-1873
18. Jonas,RA. Myocardial protection for neonates and infants[J]. Thorac Cardiovasc Surg. 1998, 46 (Suppl 2): 288-291.
19. Silverstein FS, Barks JD, Hagan P, et al. Cytokines and perinatal brain injury[J]. Neurochem Int, 1997;30(4):375-83
20. 张德英. 动态脑电图检查在神经系统疾病中的应用与评价[J]. 辽宁医学，1993，7(2)：66
21. 卢涛, 边连防, 杨渝, 等. 脑电波变化对急性脑损害预后的判断作用[J]. 中国神经精神疾病杂志, 2002，28(3): 216-217
22. Gutling E, Gonser A, Imhof H G, et al. EEG reactivity in the prognosis of severe haad injury[J]. Neurology, 1995, 45(5): 915-20
23. 王建军, 李作汉. 连续脑电图监测在神经科重症监护病房中的应用[J]. 临床神经电生理杂志, 2002, 11(1): 57-60
24. Vespa PM, Nuwer MR, Juhasz C, et al. Early detection of vasospasm after acute subarachnoid hemorrhage[J]. Electroencephalogr Clin Neurophysiol, 1997, 103: 606-615
25. Carl H Wong, Stephen. J, Rooney, Robert S. Bonser. S-100b release in hypothermic circulatory arrest and coronary artery surgery[J]. Ann Thorac Surg. 1999, 67:1911-1914
26. Buttner T, Weyers S, Postert T, et al. S-100b protein: serum marker of focal brain damage after ischeamic territorial MCA infarction[J]. Stroke. 1997, 28:1961-1965
27. Taggart DP, Bhattcharya K, Meston N, et al. Serum s-100 protein concentration after cardiac surgery: a ramdomized trial of arterial line filtration[J]. Eur J Cardio-Thorac Surg. 1997, 11:645-649
28. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Che-noweth DE, Pacifico AD. Complement and the damaging effects of cardiopulmonary bypass[J]. Thorac Cardiovasc Surg 1983;86:845-857
Taylor KM. SIRS-the systemic inflammatory response syndrome after cardiac
29. operations [Editorial][J]. Ann Thorac Surg 1996,61:1607-1608.
30. Knoblach SM, Faden AI. Interleukin-10 improve outcome and alters proinflammatory cytokine-expression after experimental traumatic brain injury[J]. Experiment Neurology,1998,153(1):143-151
31. Olney JW, Ho OL, Rhee V, et al. Neurotoxic effects of glutamate[J]. N Engl J Med 1973;289,1374-75.
32. Choi DW. Glutamate neurotoxicity and diseases of the nervous system[J]. Neuron 1988,15:41-70.
33. Redmond JM, Zehr KJ, Blue ME, et al. AMPA glutamate receptor antagonism reduces neurologic injury after hypothermic circulatory arrest[J]. Ann Thorac Surg 1995,59:579- 84.
34. Tseng EE, Brock MV, Kwon CC, et al. Quantitative analyses of intracerebral excitatory amino acids and citrulline following hypothermic circulatory arrest [J] . Surg Forum 1997,48:297-99.
35. Brock MV, Blue ME, Lowenstein CJ, et al. Induction of neuronal nitric oxide following hypothermic circulatory arrest[J]. Ann Thorac Surg 1996;62:1313-20.
36. Kenneth M Taylor. Brain damage during cardiopulmonary bypass[J]. Ann Thorac Surg 1998,65(1):20-26
37. Ulrich Missler, Nicola Orlowski, Axel Notzold, et al. Early elevation of S-100b protein in blood after cardiac surgery is not a predictor of ischemic cerebral injury[J]. Clinical Chimica Acta 2002, 321(1-2):29-33
38. Evgenij V. Potapov, Matthias Loebe, Hashim Abdul-Khaliq, et al. Postoperative course of S-100b protein and neuron-specific enolase in patients after implantation of continuous and pulsatile flow lvads[J]. The Journal of Heart and Lung Transplantation, 2001,20(12):1310-1316
39. Selawi Dogan, Kai Graubitz, Tayfun Aybek, Mohammad Fawad Khan, et al. How safe is the port access technique in minimally invasive coronary artery bypass grafting?[J]. The Annals of Thoracic Surgery, 2002,74(5),1537-1543
40. Scholz, Martin Wimmen Greninecker, Gerhard Kleine, Peter Dzemali. Cariporide(HOE642) Limits S-100b release during cardiac surgery[J]. Journal of Cardiovascular Pharmacology, 2003, 41(3): 468-473
41. Schmidt, Reinelt. Differences in the release of S-100b protein during cardiopulmonary bypass[J]. Anaesthesia, 2002, 57(1): 91-92
2. Christina T. Mora Cardiopulmonary Bypass[M]. Springer-Verlag New York Inc.USA. 1995,114-146
3. G.Wimmer-Greinecker, G.Matheis, M. Brieden, et,al. Neuropsychological Changes after Cardiopulmonary Bypass for Coronary Artery Bypass Grafting[J]. Thorac. Cardiovasc. Surg, 1998,46:207-212
4. Ahlgren E, Aren C. Cerebral dysfunction a feared complication of cardiac surgery[J]. Perfusion, 1997, 12:32
5. O’Brien JJ, Butterworth J, Hammon JW, et al. Cerebral emboli during cardiac surgery in children[J]. Anesthesiology 1997;87:1063-1069
6. 肖颖彬，陈林，王学锋，等. 浅低温体外循环心脏跳动中心内直视手术1032例临床分析[J].第三军医大学学报, 2001, 23(5)：502－504
7. 陈林, 肖颖彬, 王学锋, 等. 浅低温体外循环心脏跳动中手术矫治先心病合并重度肺动脉高压[J].第三军医大学学报, 2001, 23(5)：505－507
8. 王学锋，肖颖彬，陈林，等. 心脏跳动中二尖瓣置换术234例临床分析[J］.第三军医大学学报, 2001, 23(5)：511－512
9. 何巍，林辉，陈铭伍，等. 心脏跳动中二尖瓣置换术(附137例报告)[J］.中华外科杂志, 1996,34(11)：678-680
10. Perrault L P, Menasche P, Peynet J, et al. On-pump beating-heart coronary operations in high-risk patients: An acceptable trade-off?[J]. Ann Thorac Surg, 1997,64(5): 1368-1373
11. Firlik AD, Yonas H, Kaufmann AM, et al. Relationship between cerebral blood flow and the development of swelling and lifethreatening herniation in acute ischemic stroke[J]. J Neurosurg, 1998,89(2)243-249
12. 金沐，孙来保，黄文起，等. S-100蛋白与脑损伤[J］.国外医学. 麻醉学与复苏分册，1999，20(3)：160－162
13. 徐卫平，谢飞，朱忠勇. S-100蛋白检测及其临床运用[J］.国外医学. 临床生物化学与检验学分册，2001，22(4)：173－174
14. 戴黎萌，李力仙，王天佑，等. NF－κB与中枢神经系统疾病[J］. 国外医学神经病学神经外科学分册，1998，25(5)：267－69
15. O'Neil LAJ, Kaltschmidt C. NF－κB acrucial transcription factor for glial and neuronal cell function[J]. Tins, 1997;20:252-55
16. Goldsborough MA, Boronicz LM, McKhann GM, Baumgartner. Variation in stroke occurrence by cardiac procedures[J]. Perfusion, 1997, 12:47
17. William A, Baumgartner, Peter L, Jorge D.Salazar, et al. Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury[J]. Ann Thorac Surg 1999, 67:1871-1873
18. Jonas,RA. Myocardial protection for neonates and infants[J]. Thorac Cardiovasc Surg. 1998, 46 (Suppl 2): 288-291.
19. Silverstein FS, Barks JD, Hagan P, et al. Cytokines and perinatal brain injury[J]. Neurochem Int, 1997;30(4):375-83
20. 张德英. 动态脑电图检查在神经系统疾病中的应用与评价[J]. 辽宁医学，1993，7(2)：66
21. 卢涛, 边连防, 杨渝, 等. 脑电波变化对急性脑损害预后的判断作用[J]. 中国神经精神疾病杂志, 2002，28(3): 216-217
22. Gutling E, Gonser A, Imhof H G, et al. EEG reactivity in the prognosis of severe haad injury[J]. Neurology, 1995, 45(5): 915-20
23. 王建军, 李作汉. 连续脑电图监测在神经科重症监护病房中的应用[J]. 临床神经电生理杂志, 2002, 11(1): 57-60
24. Vespa PM, Nuwer MR, Juhasz C, et al. Early detection of vasospasm after acute subarachnoid hemorrhage[J]. Electroencephalogr Clin Neurophysiol, 1997, 103: 606-615
25. Carl H Wong, Stephen. J, Rooney, Robert S. Bonser. S-100b release in hypothermic circulatory arrest and coronary artery surgery[J]. Ann Thorac Surg. 1999, 67:1911-1914
26. Buttner T, Weyers S, Postert T, et al. S-100b protein: serum marker of focal brain damage after ischeamic territorial MCA infarction[J]. Stroke. 1997, 28:1961-1965
27. Taggart DP, Bhattcharya K, Meston N, et al. Serum s-100 protein concentration after cardiac surgery: a ramdomized trial of arterial line filtration[J]. Eur J Cardio-Thorac Surg. 1997, 11:645-649
28. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Che-noweth DE, Pacifico AD. Complement and the damaging effects of cardiopulmonary bypass[J]. Thorac Cardiovasc Surg 1983;86:845-857
Taylor KM. SIRS-the systemic inflammatory response syndrome after cardiac
29. operations [Editorial][J]. Ann Thorac Surg 1996,61:1607-1608.
30. Knoblach SM, Faden AI. Interleukin-10 improve outcome and alters proinflammatory cytokine-expression after experimental traumatic brain injury[J]. Experiment Neurology,1998,153(1):143-151
31. Olney JW, Ho OL, Rhee V, et al. Neurotoxic effects of glutamate[J]. N Engl J Med 1973;289,1374-75.
32. Choi DW. Glutamate neurotoxicity and diseases of the nervous system[J]. Neuron 1988,15:41-70.
33. Redmond JM, Zehr KJ, Blue ME, et al. AMPA glutamate receptor antagonism reduces neurologic injury after hypothermic circulatory arrest[J]. Ann Thorac Surg 1995,59:579- 84.
34. Tseng EE, Brock MV, Kwon CC, et al. Quantitative analyses of intracerebral excitatory amino acids and citrulline following hypothermic circulatory arrest [J] . Surg Forum 1997,48:297-99.
35. Brock MV, Blue ME, Lowenstein CJ, et al. Induction of neuronal nitric oxide following hypothermic circulatory arrest[J]. Ann Thorac Surg 1996;62:1313-20.
36. Kenneth M Taylor. Brain damage during cardiopulmonary bypass[J]. Ann Thorac Surg 1998,65(1):20-26
37. Ulrich Missler, Nicola Orlowski, Axel Notzold, et al. Early elevation of S-100b protein in blood after cardiac surgery is not a predictor of ischemic cerebral injury[J]. Clinical Chimica Acta 2002, 321(1-2):29-33
38. Evgenij V. Potapov, Matthias Loebe, Hashim Abdul-Khaliq, et al. Postoperative course of S-100b protein and neuron-specific enolase in patients after implantation of continuous and pulsatile flow lvads[J]. The Journal of Heart and Lung Transplantation, 2001,20(12):1310-1316
39. Selawi Dogan, Kai Graubitz, Tayfun Aybek, Mohammad Fawad Khan, et al. How safe is the port access technique in minimally invasive coronary artery bypass grafting?[J]. The Annals of Thoracic Surgery, 2002,74(5),1537-1543
40. Scholz, Martin Wimmen Greninecker, Gerhard Kleine, Peter Dzemali. Cariporide(HOE642) Limits S-100b release during cardiac surgery[J]. Journal of Cardiovascular Pharmacology, 2003, 41(3): 468-473
41. Schmidt, Reinelt. Differences in the release of S-100b protein during cardiopulmonary bypass[J]. Anaesthesia, 2002, 57(1): 91-92