乳化异氟醚预处理对大鼠局灶性脑缺血再灌注的保护作用
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摘要
脑卒中(脑中风)是一组以脑部缺血及出血性损伤症状为主要临床表现的疾病，具有极高的病死率和致残率，近年来，其发病率逐年上升，已经成为全世界第二大死亡原因。脑卒中临床上称为脑梗死，其病理基础是动脉粥样硬化，因此，防止脑梗死形成或缩小梗死体积，恢复脑供血，促进梗死灶周边血液循环就能预防或减少脑卒中的发生。临床上治疗脑卒中的治疗措施很多，如中医、西医等方法，但其疗效都不尽人意。因此，目前脑卒中的治疗更重在预防。近几年来，在脑卒中研究领域兴起的药物预处理方法实质上就是一种预防措施。一些麻醉药预处理的脑保护作用已被研究证实，越来越多的实验证明吸入麻醉药异氟醚(Iso)具有明显的脑保护作用，在围术期预防脑缺血损伤中可能具有重要价值。但是改变剂型的乳化异氟醚是否也有脑缺血耐受作用?为此本实验采用大鼠局灶性脑缺血模型(MCAO)，并通过评估缺血再灌注24h的行为学和脑梗死容积，来探讨：(1)乳化异氟醚预处理是否诱导产生脑缺血耐受作用；(2)乳化异氟醚预处理诱导脑缺血耐受的可能机制。
实验一：SD大鼠局灶性脑缺血模型的建立。方法：采用大脑中动脉阻闭(middle cerebral artery occlusion，MCAO)模型，将40只雄性SD大鼠随机分成5组(n=8)：A．MCAO 60min组；B．MCAO 120min组；C．MCAO150 min组；D．MCAO180min组；E假手术组(仅分离血管，不留置线拴)，观察再灌注后24h动物神经行为学改变及脑梗死容积。结果24h后A-D组神经功能障碍加重，呈递增趋势；24h神经功能损害评分(NDS)E组与A-D组间差异明显(P＜0.05)。再灌注24h脑梗死体积A至D组依次增大，差异明显((P＜0.05)，而E组无梗死灶。A组(132.6±22.1 mm3)梗死容积明显小于B-D组(P＜0.05)，B组(216.9±20.3mm3)和C组(223.8±21.7mm3)显著小于D组(296.8±26.6mm3)B与C缺血组无统计学差异。结论：大鼠MCAO 120min为较佳脑缺血模型，并且能很好的重复大脑中动脉阻闭。
实验二8％乳化异氟醚预处理对SD大鼠局灶性脑缺血耐受的影响。方法：选择60只雄性SD大鼠，体重250～300 g，随机分成6组，假手术组：仅分离血管，不留置线拴；脑缺血模型组(MO组)：缺血前吸入纯氧30min行MCAO，2h后抽出线栓恢复再灌注；吸入异氟醚组(吸入ISO组)：缺血前吸入0.9％(0.9％约相当于大鼠0.7MAC)异氟醚30min；乳化异氟醚组(乳化ISO组)：缺血前给8％乳化异氟醚17ml(kg·h)~(-1)；异丙酚组(PRO组)：缺血前给异丙酚15 mg·kg~(-1)；30％脂肪乳组(30％INT组)：缺血前给30％脂肪乳17ml(kg·h)~(-1)。所有动物均采用右侧颈动脉MCAO2h，观察再灌注后24h动物神经行为学改变及测量脑梗死容积。结果：结果直肠温度，Pa02，PaC02、血压预处理期间三组无明显差异。术后DNS乳化异氟醚组、吸入异氟醚组和异丙酚组明显低于模型组(P＜0.05)；再灌注24h后脑梗死体积模型组为(227.5±18.15)mm~3，乳化异氟醚组，吸入异氟醚组和异丙酚组梗死面积缩小(P＜0.05)，但是乳化异氟醚组和吸入异氟醚组没有显著性差异。结论：缺血前给乳化异氟醚对大鼠局灶性脑缺血再灌注损伤产生一定程度的保护作用。
The cerebral apoplexy (brain stroke) is a group lacks the blood and thehemorrhage damage symptom take the brain as the main clinicalmanifestation disease, Has the extremely high case fatality rate and crippling rate. In recent years, its disease incidence rate year by year rose, alreadybecame the world second big cause of death. The apoplexy on clinical is called the cerebral infarction, itspathology foundation is the atherosclerosis. Therefore, prevented the infarct volume, restores the brain to donate blood, the promotion stemdead stove peripheral blood circulation can prevent or the reducedapoplexy occurrence. Although many protective treatment measures, such as Chinese medical science and western medicine, against brain ischemia damage have been found, few of them show satisfactory curative effect. Therefore, prevention measures are gradually emphasized in the treatment of brain ischernia. Recently, a lot of studies have focused on preconditioning measures of brain ischemia. Numerous studies have demonstrated the neuropretective effects of isoflurane (Iso), which indicates Iso may also play an important role in perioperative neurological management. But emulsified isoflurance whether also does have the function in ischemic tolerance in brain. In this study, weevaluated the effects of emulsified isoflurane preconditioning Of neuroprotection against middle cerebral artery occlusion injury. To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in a rat middle cerebral artery occlusion (MCAO) model.
(1) To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in rats. (2) The Possible mechanism if emulsified isoflurane preconditioning induces ischemic tolerance against brain injury produced by MCAO in rats.
Experiment 1:
OBJECTIVE To provide reasonable and practicable animal models for clinical cerebral ischernia research. METHOD Middle Cerebral Artery Occlusion (MCAO) were carried out on 40 male S-D rats by suture occlusion via infra artery methods. The animals were divided into 5 groups randomly and equally (n=8):group A with 60-min MCAO, group B with 120-min MCAO, group C with 150-min MCAO, group D with 180-min MCAO, group D with sham operation. The neurological outcomes were evaluated at 24 h after the reperfusion. After 24h of reperfusion the brain infarct volumes were measured. RESULTS Neurological dysfuctions and brain infarct volumes gradually increased from A to D, E group and A-D group was significance inThe NDS (P＜0.05). The infarct size A group was lower than B-D group (P＜0.05). B group, C group was lower than E group (P＜0.05). but there was no significance in brain infarct volume between group B and C. CONCLUSION 120-min-MCAO rats were perfect cerebral ischernia models.
Experiment 2:
OBJECTIVE To investigate if Emulsified isoflurane preconditioning induces delayed ischemic tolerance against neuronal damage produced by MCAO in rats. METHOD Sixty male SD rats weighing 250～300 g were anesthetized with intraperitoneal 10%Chloral bydrate 3.5ml/kg. Middle cerebral artery occlusion (MCAO) was performed by surgical exposure of common, internal and external carotid arteries through a longitudinal incision in the neck. A nylon filament (0.20-0.25mm in diameter) with rounded end was inserted into internal carotid carotid artery and threaded cranianlly until resistance was felt. The depth of insertion was about 18-20 mm. The animals were randomly divided intosix equal groups. sham operation group in which caritiod arteries into exposed but no MCAO was performed; ischemia group: the animals inhaled 100% O_2 for 30min before the beginning of MCAO which was maintained for 2h; isoflurane group: 0.9%was inhaled for 30 min before the 2h MCAO. emulsified isoflurance group: 8% emulsified isoflurance 17ml/kg/h was inhaled for 30 min before the 2h MCAO; Propofol group: Propofol 7.5mg/kg was inhaled for 10 min before the 2h MCAO; triglyceride group: 30% triglyceride 17ml/kg/h was inhaled for 30 min before the 2h MCAO;. The neurologic deficit score (NDS) was evaluated 24 h after reperfusion and the infarct volume was calculated at 24 h following reperfusion. RESULTS Rectal temperature, PH, PaO2, PaCO2, blood pressure and blood glucose were controlled and not different among groups during preconditioning. The NDS of isoflurane group, emulsified isoflurance group and Propofol group was lower than ischemia group (P＜0.05). The infarct size, ischemia group was (227.5±18.15)mm~3, isoflurane group, emulsified isoflurance group and Propofol group reduced the infarct size at the end of 24 h reperfusion. (P＜0.05), but there was no significant difference between emulsified isoflurance group and isoflurane group. CONCLUSIONS Inhalation of 8% emulsified isoflurance can protect brain form focal ischemia reperfusion injury to some extent in rats.
实验一：SD大鼠局灶性脑缺血模型的建立。方法：采用大脑中动脉阻闭(middle cerebral artery occlusion，MCAO)模型，将40只雄性SD大鼠随机分成5组(n=8)：A．MCAO 60min组；B．MCAO 120min组；C．MCAO150 min组；D．MCAO180min组；E假手术组(仅分离血管，不留置线拴)，观察再灌注后24h动物神经行为学改变及脑梗死容积。结果24h后A-D组神经功能障碍加重，呈递增趋势；24h神经功能损害评分(NDS)E组与A-D组间差异明显(P＜0.05)。再灌注24h脑梗死体积A至D组依次增大，差异明显((P＜0.05)，而E组无梗死灶。A组(132.6±22.1 mm3)梗死容积明显小于B-D组(P＜0.05)，B组(216.9±20.3mm3)和C组(223.8±21.7mm3)显著小于D组(296.8±26.6mm3)B与C缺血组无统计学差异。结论：大鼠MCAO 120min为较佳脑缺血模型，并且能很好的重复大脑中动脉阻闭。
实验二8％乳化异氟醚预处理对SD大鼠局灶性脑缺血耐受的影响。方法：选择60只雄性SD大鼠，体重250～300 g，随机分成6组，假手术组：仅分离血管，不留置线拴；脑缺血模型组(MO组)：缺血前吸入纯氧30min行MCAO，2h后抽出线栓恢复再灌注；吸入异氟醚组(吸入ISO组)：缺血前吸入0.9％(0.9％约相当于大鼠0.7MAC)异氟醚30min；乳化异氟醚组(乳化ISO组)：缺血前给8％乳化异氟醚17ml(kg·h)~(-1)；异丙酚组(PRO组)：缺血前给异丙酚15 mg·kg~(-1)；30％脂肪乳组(30％INT组)：缺血前给30％脂肪乳17ml(kg·h)~(-1)。所有动物均采用右侧颈动脉MCAO2h，观察再灌注后24h动物神经行为学改变及测量脑梗死容积。结果：结果直肠温度，Pa02，PaC02、血压预处理期间三组无明显差异。术后DNS乳化异氟醚组、吸入异氟醚组和异丙酚组明显低于模型组(P＜0.05)；再灌注24h后脑梗死体积模型组为(227.5±18.15)mm~3，乳化异氟醚组，吸入异氟醚组和异丙酚组梗死面积缩小(P＜0.05)，但是乳化异氟醚组和吸入异氟醚组没有显著性差异。结论：缺血前给乳化异氟醚对大鼠局灶性脑缺血再灌注损伤产生一定程度的保护作用。
The cerebral apoplexy (brain stroke) is a group lacks the blood and thehemorrhage damage symptom take the brain as the main clinicalmanifestation disease, Has the extremely high case fatality rate and crippling rate. In recent years, its disease incidence rate year by year rose, alreadybecame the world second big cause of death. The apoplexy on clinical is called the cerebral infarction, itspathology foundation is the atherosclerosis. Therefore, prevented the infarct volume, restores the brain to donate blood, the promotion stemdead stove peripheral blood circulation can prevent or the reducedapoplexy occurrence. Although many protective treatment measures, such as Chinese medical science and western medicine, against brain ischemia damage have been found, few of them show satisfactory curative effect. Therefore, prevention measures are gradually emphasized in the treatment of brain ischernia. Recently, a lot of studies have focused on preconditioning measures of brain ischemia. Numerous studies have demonstrated the neuropretective effects of isoflurane (Iso), which indicates Iso may also play an important role in perioperative neurological management. But emulsified isoflurance whether also does have the function in ischemic tolerance in brain. In this study, weevaluated the effects of emulsified isoflurane preconditioning Of neuroprotection against middle cerebral artery occlusion injury. To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in a rat middle cerebral artery occlusion (MCAO) model.
(1) To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in rats. (2) The Possible mechanism if emulsified isoflurane preconditioning induces ischemic tolerance against brain injury produced by MCAO in rats.
Experiment 1:
OBJECTIVE To provide reasonable and practicable animal models for clinical cerebral ischernia research. METHOD Middle Cerebral Artery Occlusion (MCAO) were carried out on 40 male S-D rats by suture occlusion via infra artery methods. The animals were divided into 5 groups randomly and equally (n=8):group A with 60-min MCAO, group B with 120-min MCAO, group C with 150-min MCAO, group D with 180-min MCAO, group D with sham operation. The neurological outcomes were evaluated at 24 h after the reperfusion. After 24h of reperfusion the brain infarct volumes were measured. RESULTS Neurological dysfuctions and brain infarct volumes gradually increased from A to D, E group and A-D group was significance inThe NDS (P＜0.05). The infarct size A group was lower than B-D group (P＜0.05). B group, C group was lower than E group (P＜0.05). but there was no significance in brain infarct volume between group B and C. CONCLUSION 120-min-MCAO rats were perfect cerebral ischernia models.
Experiment 2:
OBJECTIVE To investigate if Emulsified isoflurane preconditioning induces delayed ischemic tolerance against neuronal damage produced by MCAO in rats. METHOD Sixty male SD rats weighing 250～300 g were anesthetized with intraperitoneal 10%Chloral bydrate 3.5ml/kg. Middle cerebral artery occlusion (MCAO) was performed by surgical exposure of common, internal and external carotid arteries through a longitudinal incision in the neck. A nylon filament (0.20-0.25mm in diameter) with rounded end was inserted into internal carotid carotid artery and threaded cranianlly until resistance was felt. The depth of insertion was about 18-20 mm. The animals were randomly divided intosix equal groups. sham operation group in which caritiod arteries into exposed but no MCAO was performed; ischemia group: the animals inhaled 100% O_2 for 30min before the beginning of MCAO which was maintained for 2h; isoflurane group: 0.9%was inhaled for 30 min before the 2h MCAO. emulsified isoflurance group: 8% emulsified isoflurance 17ml/kg/h was inhaled for 30 min before the 2h MCAO; Propofol group: Propofol 7.5mg/kg was inhaled for 10 min before the 2h MCAO; triglyceride group: 30% triglyceride 17ml/kg/h was inhaled for 30 min before the 2h MCAO;. The neurologic deficit score (NDS) was evaluated 24 h after reperfusion and the infarct volume was calculated at 24 h following reperfusion. RESULTS Rectal temperature, PH, PaO2, PaCO2, blood pressure and blood glucose were controlled and not different among groups during preconditioning. The NDS of isoflurane group, emulsified isoflurance group and Propofol group was lower than ischemia group (P＜0.05). The infarct size, ischemia group was (227.5±18.15)mm~3, isoflurane group, emulsified isoflurance group and Propofol group reduced the infarct size at the end of 24 h reperfusion. (P＜0.05), but there was no significant difference between emulsified isoflurance group and isoflurane group. CONCLUSIONS Inhalation of 8% emulsified isoflurance can protect brain form focal ischemia reperfusion injury to some extent in rats.
引文
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30. Schlack W, Preckel B, Stunneck D, et al. Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart. Br J Anaesth. 1998;81:913-9.
31. Kokita N, Hara A, Abiko Y, et al. Propofol improves functional and metabolic recovery in ischemic reperfused isolated rat hearts. Anesth Analg. 1998;86:252-58.
32. Kokita N, Hara A. Propofol attenuates hydrogen peroixide-induced mechanical and metabolic derangements in the isolated rat heart. Anesthesiology. 1996;84:117-27.
33. Ko SH, Yu CW, Lee SK, et al. Propofol attenuates ischemic-reperfusion injury in the isolated rat heart. Anesth Analg. 1997;85:719-24.
34．顾尔伟，赵庆．异氟醚与咪唑安定或丙泊酚联合应用对心肌缺血．再灌注期心肌肌钙蛋白Ⅰ的影响．临床麻醉学杂志，2002；18(11)：588-90．
35. White PF, Stanley TH, Apfelbaum JL, Grasela TH, Hug CC Jr, McLeskey CH, Nahrwold ML, Roizen MF, Thisted RA, Walawander CA. Effects on recovery when isoflurane is used to supplement propofol-nitrous oxide anesthesia. Anesth Analg. 1993 Oct;77(4 Suppl):S15-20.
36. Chang Y, Lin SY, Susetio L, Hu JW, Hsu HW, Liu CC. Propofol modifies recovery from isoflurane-nitrous oxide anesthesia. Acta Anaesthesiol Sin. 1994 Jun;32(2):89-94.
37. Jellish WS, Leonetti JP, Fahey K, Fury P. Comparison of 3 different anesthetic techniques on 24-hour recovery after otologic surgical procedures. Otolaryngol Head Neck Surg. 1999 Mar;120(3):406-11.
38. Myles PS, Hunt JO, Fletcher H, Smart J, Jackson T. Part Ⅰ: propofol, thiopental, sevoflurane, and isoflurane-A randomized, controlled trial of effectiveness. Anesth Analg. 2000 Nov;91(5):1163-9.
39. Godet G, Watremez C, El Kettani C, Soriano C, Coriat P. A comparison of sevoflurane, target-controlled infusion propofol, and propofol/isoflurane anesthesia in patients undergoing carotid surgery: a quality of anesthesia and recovery profile. Anesth Analg. 2001 Sep;93(3):560-5.
40. Matta BF, Mayberg TS, Lam AM. Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans. Anesthesiology. 1995 Nov;83(5):980-5.
41 Shin YS, Lee KY, Lee KJ, Kim MH, Kim JR, Park KW. Effects of propofol and thiopental sodium on the intracranial pressure under halothane or isoflurane anesthesia in the rabbit. Yonsei Med J. 1993 Jun;34(2): 152-7.
1. Cope DK, Impastato WK, Cohen MV, et al. Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology 1997; 86: 699-709
2. Preckel B, Schlack W, Thamer V. Enflurane and isoflurane, but not halothane, protect against myocardial reperfusion injure after cardioplegic arrest with HTK solution in the isolated rat heart. Anesth Analg 1998; 87; 1221-7
3. Patel PM, Drummond JC, Cole DJ, et al. Isoflurane and pentobarbital reduce the frequency of transient ischemic depolarizations during focal ischemia in rats. Anesth Analg 1998; 86:773-80
4. Kon S, Imai M, Inaba H. Isoflurane attenuates early neutrophil-independent hypoxia-reoxygenation injuries in the reperfused liver in fasted rats. Anesthesiology 1997; 86:128-36
5. Liu R, Ishibe Y, Ueda M. Isoflurane-sevoflurane administration before ischemia attenuates ischemia-reperfusion-induced injury in isolated rat lungs. Anesthesiology 2000; 92:833-40
6. Liu R, Ishibe Y, Ueda M, et al. Isoflurane administration before ischemia and during reperfusion attenuates ischemia/reperfusion-induced injury of isolatedrabbit lung. Anesth Analg 1999; 89: 561-5
7. Bast A, Haenen GR, Doelman CJ. Oxidants and antioxidants: State of the art. Am J Med. 1991;91:2S-13S.
8. Nakagawara M, Takeshige K, Takamatsu J, et al. Inhibition of superoxide production and Ca~(2+) mobilization in human neutrophils by halothane, enflurane, and isoflurane.Anesthesiology. 1986 ;64(1):4-12.
9. Tanguay M, Blaise G, Dumont L, et al. Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts. Journal of Cardiovascular Pharmacology 1991; 18: 863-70.
10. Araki M, Inaba H, Mizuguchi T. Isoflurane modulates phorbol myristate acetate-, prostaglandin D2-, and prostaglandin E2-induced alterations in hepatic flow and metabolism in the perfused liver in fasted rats. Anesth Analg. 1994 ;79(2):267-73.
11. Frohlich D, Rothe G, Schwall B, et al. Effects of volatile anaesthetics on human neutrophil oxidative response to the bacterial peptide FMLP. Br J Anaesth. 1997 78(6):718-23.
12. Glantz L, Ginosar Y, Chevion M, et al. Halothane prevents postischemic production of hydroxyl radicals in the canine heart. Anesthesiology. 1997 ; 86(2): 440 -7.
13. Kevin LG, Novalija E, Riess ML, et al. Sevoflurane exposure generates superoxide but leads to decreased superoxide during ischemia and reperfusion in isolated hearts. Anesth Analg. 2003 ;96(4):949-55
14. Hu G, Vasiliauskas T, Salem MR, et al. Neutrophils pretreated with volatile anesthetics lose ability to cause cardiac dysfunction. Anesthesiology. 2003 ; 98(3): 712-8.
15. Samuta T, Becker GL, Pohorecki R, et al. Effects of isoflurane dose, duration of anoxia, and reoxygenation on isoflurane's preservation of energy balance in anoxic isolated hepatocytes. Anesth Analg. 1993 ;77(1):38-43.
16. Pathak BL, Becker GL, Reilly PJ, et al. Isoflurane partially preserves energy balance in isolated hepatocytes during in vitro anoxia. Anesth Analg. 1991 ; 72(5): 571-7.
17. Matsushita M, Ohashi I, Becker GL, et al. Isoflurane preserves adenosine triphosphate levels in anoxic isolated rat hepatocytes by stimulating glycolytic adenosine triphosphate formation. Anesth Analg. 1996 ;82(6):1261-7.
18. Oguchi T, Kashimoto S, Yamaguchi T, et al. Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart. Br J Anaesth. 1995 ;74(5):569-75.
19. Kanaya N, Kobayashi I, Nakayama M, et al. ATP sparing effect of isoflurane during ischaemia and reperfusion of the canine heart. Br J Anaesth. 1995 ;74(5):563-8.
20. Eppinger MJ, Jones ML, Deeb GM, et al. Pattern of injury and the role of neutrophils in reperfusion injury of rat lung. J Surg Res 1995 ;58(6):713-8
21. Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res. 1999 ;43(4):860-78.
22. Cavanagh SP, Gough MJ, Homer-Vanniasinkam S. The role of the neutrophil in ischaemia-reperfusion injury: potential therapeutic interventions. Cardiovasc Surg. 1998 ;6(2):112-8.
23. Serracino-Inglott F, Habib NA, Mathie RT. Hepatic ischemia-reperfusion injury. Am J Surg. 2001; 181 (2): 160-6.
24. Doerschuk CM. The role of CD18-mediated adhesion in neutrophil sequestration induced by infusion of activated plasma in rabbits.Am J Respir Cell Mol Biol. 1992;7(2):140-8
25. Moore TM, Khimenko P, Adkins WK, et al. Adhesion molecules contribute to ischemia and reperfusion-induced injury in the isolated rat lung. J Appl Physiol 1995;78(6):2245-52
26. Wegner CD. Adhesion molecules. London: Academic Press Limited 1994:163
27. Lu YT, Chen PQ Liu SF. Time course of lung ischemia-reperfusion-induced ICAM-1 expression and its role in ischemia-reperfusion lung injury. J Appl Physiol. 2002 ;93(2):620-8.
28. Arnaout MA. Structure and function of the leukocyte adhesion molecules CD11/CD18. Blood. 1990 ;75(5): 1037-50.
29. Kowalski C, Zahler S, Becker BF, et al. Halothane, isoflurane, and sevoflurane reduce postischemic adhesion of neutrophils in the coronary system. Anesthesiology. 1997 ;86(1):188-95.
30. Mobert J, Zahler S, Becker BF, et al. Inhibition of neutrophil activation by volatile anesthetics decreases adhesion to cultured human endothelial cells. Anesthesiology. 1999 ;90(5): 1372-81.
31. Nishimaki H, Fukuda S, Ishimoto M, et al. Isoflurane ameliorates the posthypoxic deoxygenation of the rat brain-the role of cell adhesion molecules of polymorphonuclear leukocytes. Resuscitation 2002 ;54(2):207-14
32. de Rossi LW, Horn NA, Buhre W, et al. The effect of isoflurane on neutrophil selectin and beta(2)-integrin activation in vitro. Anesth Analg 2002 ;95(3):583-7.
33. Krishnadasan B, Naidu BV, Byrne K, et al. The role of proinflammatory cytokines in lung ischemia-reperfusion injury. J Thorac Cardiovasc Surg. 2003 ;125(2):261-72.
34. Squadrito F, Altavilla D, Zingarelli B, et al. Tumor necrosis factor involvement in myocardial ischemia reperfusion injury. Eur J Pharmacol. 1993; 237:223-30
35. Lentsch AB, Kato A, Yoshidome H, et al. Inflammatory mechanisms and therapeutic strategies for warm hepatic ischemia/reperfusion injury. Hepatology. 2000; 32(2): 169-73.
36. Seekamp A, Warren JS, Remiock DG, et al. Requirements for tumor necrosis factor alpha and interleukin 1 in limb ischemia reperfusion injury. Am J Pathol. 1993; 143:453-63.
37. De Perrot M, Sekine Y, Fischer S, et al. Interleukin-8 release during early reperfusion predicts graft function in human lung transplantation. Am J Respir Crit Care Med. 2002 ;165(2):211-5.
38. Sekido N, Mukaida N, Harada A, et al. Prevention of lung reperfusion injury in rabbits by a monoclonal antibody against interleukin-8. Nature. 1993; 365(6447): 654 -7.
39. Giraud O, Molliex S, Rolland C, et al. Halogenated anesthetics reduce interleukin-1 beta-induced cytokine secretion by rat alveolar type II cells in primary culture. Anesthesiology. 2003; 98(1):3-4.
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3 Kitagawa K, Matsumota M, Tagaya M, et al.'Ischemic tolerance'phenomenon found in the brain. Brain Res, 1990, 528(1):21-24
4 Kapinya KJ, Prass K, Dimagl U. Isoflurane induced prolonged protection against cerebral ischemia in mice:a redox sensitive mechanism J. Neuroreport, 2002, 13:1431-1435
5 Payne RS, Ozan A, Norbert R, et al. Sevoflurane-induced preconditioning protects against cerebra ischemic neuronal damage in rats. J.Brain Research,2005,1034 (1-2):147-152.
6 Kersten JR,Schmeling JI,Pagel PS,et al .Isoflurane mimics ischemic preconditioning via activation of K_(ATP) channels .Anesthesiology, 1997,87:361-370 .
7 Ismaeil MS,Tkachenko I Kurt Gamperl A,et al .Mechanisms of isofiurane-induced my ocardial preconditioning in rabbits .Anesthesiology, 1999,90:812-821
8 Eger RP,Macleod BA .Anaesthesia by intravenous emulsified isoflurane in mice[J] Can J Anaesth,1995;42:173-176
9 Loner R,Miura T,Milk T et al .Preconditioning stimuli and inadvertent preconditioning.[J]. Mol Cell Cardiol,1995,27:743-747
10 chugh NA,Cook SM,Schairer JL et al .Ischemia and reperfusion induced ventricular arrhythmias in dogs: effect of estrogen. J Physiol,1995,268(6ptz):H2569-2573
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15 Chelly E, acques E, Doursootet al, Cardiac and Regional Hemodynamic Interactions between Halothane and Nitric Oxide Synthase Activity in Dogs Anesthesiology, 1996:85;3A141～149
16 Stratford N, Murphy P. Effect of lipid and propofol on oxidation of haemoglobin by reactive oxygen species Br. J. Anaesth, 1997; 78:320 - 322.
17 刘俊杰，赵俊，主编．现代麻醉学，第二版．北京：人民卫生出版社，1996；274—276
18 朱波．中枢神经系统缺血缺氧损伤模型．国外医学麻醉学与复苏分册，2002；23(1)：17}-201
19 Murry CE, Jennings RB, Reimer KA. P reconditioning with ischemia: A delay of lethal cell injury in ischemic myocardium [J]. Circulation, 1986; 74 (5): 1124—1136.
20 Xiong LZ, Zhu ZH, Dong HL, Hu WN, Hou LC. Isoflurane preconditioning induces neuroprotection against middle cerebral artery occlusion damage in rat [J]. Zhong hua Mazuixue Zazhi (Chin J Anesthesiol), 2000; (12): 730—732.
21 Zonga EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery :occlusion without craniotomy in rats. Stroke ,[J].1989,20:84—91
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3．孙海峰，王泉云，梁小民，张贞雄，刘进．乳化异氟醚腹腔注射对大鼠的麻醉作用与安全性．中华麻醉学杂志，2004；24(1)：51-3．
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7. JB Glen, SC Hunter. Pharmacology of an emulsion formulation of ICI 35 868. Br J Anaesth. 1984;56:617-26.
8．庄心良，曾因明，陈伯銮主编．现代麻醉学．第三版．北京：人民卫生出版社，2003．481-7．
9. Jellish WS, Leonetti JP, Fahey K, Fury E Comparison of 3 different anesthetic techniques on 24-hour recovery after otologic surgical procedures. Otolaryngol Head Neck Surg. 1999 Mar;120(3):406-11.
10. Talke P, Caldwell JE, Brown R, Dodson B, Howley J, Richardson CA. A comparison of three anesthetic techniques in patients undergoing craniotomy for supratentorial intracranial surgery. Anesth Analg. 2002;95(2):430-5.
11. Song D, Joshi GP, White PT, et al. Fast-track eligibility after ambulatory anesthesia: a comparison of desflurane, sevoflurane and propofol. Anaesth Analg. 1998;86:267-73:
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13. Kitagawa K, Matsumoto M, Tagaya M, et all "Ischemic tolerance" phenonmenon found in the brain[J]. Brain Res, 1990,528:21—24
14．蒲小平，李长岭．脑缺血的细胞应答对研制新药的启示[J]．中国药学杂志，1999，34(9)：579—581．
15. Murry CE, Jennings RB, Reimer KA. P reconditioning with ischemia: A delay of lethal cell injury in ischemic myocardium [J]. Circulation, 1986; 74 (5): 1124—1136.
16. Xiong LZ, Zhu ZH, Dong HL, Hu WN, Hou LC. Isoflurane preconditioning induces neuroprotection against middle cerebral artery occlusion damage in rat [J]. Zhong hua Mazuixue Zazhi (Chin J Anesthesiol), 2000; (12) : 730—732.
17. longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery: occlusion without craniotomy in rats. Stroke,[J]. 1989,20:84—91
18. Chelly E, acques E, Doursoot et al, Cardiac and Regional Hemodynamic Interactions between Halothane and Nitric Oxide Synthase Activity in Dogs Anesthesiology[J].1996:85;3A141—149
19. Stratford N, Murphy P. Effect of lipid and propofol on oxidation of haemoglobin by reactive oxygen species [J]. Br. J. Anaesth, 1997; 78:320—322
20. Tsai YC, Huang SJ, Lai YY, et all Propofol does not reduce infarct volume in rats undergoing permanent middle cerebral artery occlusion[J]. Acta Anaesthesiol Sin ,1994,32:99—104.
21. Weir DL, Goodchild CS, Graham DI. Propofol: Effects of indices of cerebral ischemia [J]. J Neurosurg Agesthesiol, 1989,1:284—289.
22. Li CR, Cheng JT, Lin FC, et al. Effect of thjipental, prorofol, and tomidate on vincristine toxicity in PC12 cells [J]. Cell Biol Toxicol, 2002,18: 63—70.
23. Verborgh C, Verbessem D, Camu F. Haemodynamic effects of isoflurane during propofol anaesthesia. Br J Anaesth. 1992 Jul;69(1):36-9.
24. Nakayama M, Kanaya N, Tsuchida H, Namiki A. The effect of propofol and thiamylal on hypertensive responses to a rapid increase in isofiurane concentration. J Clin Anesth. 1999 Feb;11(1):8-10.
25．翁两全．异丙酚用于稳定高血压脑出血病人围麻醉期血流动力学的临床研究．福建医药杂志，2002；24(2)：17-8．
26. Pagel PS, Hettrick DA, Kersten JR, Lowe D, Warltier DC. Propofol, but not thiopentone or etomidate, enhances isoflurane-induced coronary vasodilatation in dogs. Can J Anaesth. 1998 Aug;45(8):809-17.
27．王金波，徐赞，王培民，王可富．异丙酚和异氟醚对大鼠心室肌细胞L-型钙离子通道的影响．肿瘤防治杂志，2001；8(3)：263-5．
28. Cope DK, Impastato WK, Cohen Mv, et al. Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology. 1997;86:699-709.
29. Ross S, Foex P. Protective effects of anaesthetics in reversible and irreversible ischemic reperfusion injury. Br J Anaesth. 1999;82:622-32.
30. Schlack W, Preckel B, Stunneck D, et al. Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart. Br J Anaesth. 1998;81:913-9.
31. Kokita N, Hara A, Abiko Y, et al. Propofol improves functional and metabolic recovery in ischemic reperfused isolated rat hearts. Anesth Analg. 1998;86:252-58.
32. Kokita N, Hara A. Propofol attenuates hydrogen peroixide-induced mechanical and metabolic derangements in the isolated rat heart. Anesthesiology. 1996;84:117-27.
33. Ko SH, Yu CW, Lee SK, et al. Propofol attenuates ischemic-reperfusion injury in the isolated rat heart. Anesth Analg. 1997;85:719-24.
34．顾尔伟，赵庆．异氟醚与咪唑安定或丙泊酚联合应用对心肌缺血．再灌注期心肌肌钙蛋白Ⅰ的影响．临床麻醉学杂志，2002；18(11)：588-90．
35. White PF, Stanley TH, Apfelbaum JL, Grasela TH, Hug CC Jr, McLeskey CH, Nahrwold ML, Roizen MF, Thisted RA, Walawander CA. Effects on recovery when isoflurane is used to supplement propofol-nitrous oxide anesthesia. Anesth Analg. 1993 Oct;77(4 Suppl):S15-20.
36. Chang Y, Lin SY, Susetio L, Hu JW, Hsu HW, Liu CC. Propofol modifies recovery from isoflurane-nitrous oxide anesthesia. Acta Anaesthesiol Sin. 1994 Jun;32(2):89-94.
37. Jellish WS, Leonetti JP, Fahey K, Fury P. Comparison of 3 different anesthetic techniques on 24-hour recovery after otologic surgical procedures. Otolaryngol Head Neck Surg. 1999 Mar;120(3):406-11.
38. Myles PS, Hunt JO, Fletcher H, Smart J, Jackson T. Part Ⅰ: propofol, thiopental, sevoflurane, and isoflurane-A randomized, controlled trial of effectiveness. Anesth Analg. 2000 Nov;91(5):1163-9.
39. Godet G, Watremez C, El Kettani C, Soriano C, Coriat P. A comparison of sevoflurane, target-controlled infusion propofol, and propofol/isoflurane anesthesia in patients undergoing carotid surgery: a quality of anesthesia and recovery profile. Anesth Analg. 2001 Sep;93(3):560-5.
40. Matta BF, Mayberg TS, Lam AM. Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans. Anesthesiology. 1995 Nov;83(5):980-5.
41 Shin YS, Lee KY, Lee KJ, Kim MH, Kim JR, Park KW. Effects of propofol and thiopental sodium on the intracranial pressure under halothane or isoflurane anesthesia in the rabbit. Yonsei Med J. 1993 Jun;34(2): 152-7.
1. Cope DK, Impastato WK, Cohen MV, et al. Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology 1997; 86: 699-709
2. Preckel B, Schlack W, Thamer V. Enflurane and isoflurane, but not halothane, protect against myocardial reperfusion injure after cardioplegic arrest with HTK solution in the isolated rat heart. Anesth Analg 1998; 87; 1221-7
3. Patel PM, Drummond JC, Cole DJ, et al. Isoflurane and pentobarbital reduce the frequency of transient ischemic depolarizations during focal ischemia in rats. Anesth Analg 1998; 86:773-80
4. Kon S, Imai M, Inaba H. Isoflurane attenuates early neutrophil-independent hypoxia-reoxygenation injuries in the reperfused liver in fasted rats. Anesthesiology 1997; 86:128-36
5. Liu R, Ishibe Y, Ueda M. Isoflurane-sevoflurane administration before ischemia attenuates ischemia-reperfusion-induced injury in isolated rat lungs. Anesthesiology 2000; 92:833-40
6. Liu R, Ishibe Y, Ueda M, et al. Isoflurane administration before ischemia and during reperfusion attenuates ischemia/reperfusion-induced injury of isolatedrabbit lung. Anesth Analg 1999; 89: 561-5
7. Bast A, Haenen GR, Doelman CJ. Oxidants and antioxidants: State of the art. Am J Med. 1991;91:2S-13S.
8. Nakagawara M, Takeshige K, Takamatsu J, et al. Inhibition of superoxide production and Ca~(2+) mobilization in human neutrophils by halothane, enflurane, and isoflurane.Anesthesiology. 1986 ;64(1):4-12.
9. Tanguay M, Blaise G, Dumont L, et al. Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts. Journal of Cardiovascular Pharmacology 1991; 18: 863-70.
10. Araki M, Inaba H, Mizuguchi T. Isoflurane modulates phorbol myristate acetate-, prostaglandin D2-, and prostaglandin E2-induced alterations in hepatic flow and metabolism in the perfused liver in fasted rats. Anesth Analg. 1994 ;79(2):267-73.
11. Frohlich D, Rothe G, Schwall B, et al. Effects of volatile anaesthetics on human neutrophil oxidative response to the bacterial peptide FMLP. Br J Anaesth. 1997 78(6):718-23.
12. Glantz L, Ginosar Y, Chevion M, et al. Halothane prevents postischemic production of hydroxyl radicals in the canine heart. Anesthesiology. 1997 ; 86(2): 440 -7.
13. Kevin LG, Novalija E, Riess ML, et al. Sevoflurane exposure generates superoxide but leads to decreased superoxide during ischemia and reperfusion in isolated hearts. Anesth Analg. 2003 ;96(4):949-55
14. Hu G, Vasiliauskas T, Salem MR, et al. Neutrophils pretreated with volatile anesthetics lose ability to cause cardiac dysfunction. Anesthesiology. 2003 ; 98(3): 712-8.
15. Samuta T, Becker GL, Pohorecki R, et al. Effects of isoflurane dose, duration of anoxia, and reoxygenation on isoflurane's preservation of energy balance in anoxic isolated hepatocytes. Anesth Analg. 1993 ;77(1):38-43.
16. Pathak BL, Becker GL, Reilly PJ, et al. Isoflurane partially preserves energy balance in isolated hepatocytes during in vitro anoxia. Anesth Analg. 1991 ; 72(5): 571-7.
17. Matsushita M, Ohashi I, Becker GL, et al. Isoflurane preserves adenosine triphosphate levels in anoxic isolated rat hepatocytes by stimulating glycolytic adenosine triphosphate formation. Anesth Analg. 1996 ;82(6):1261-7.
18. Oguchi T, Kashimoto S, Yamaguchi T, et al. Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart. Br J Anaesth. 1995 ;74(5):569-75.
19. Kanaya N, Kobayashi I, Nakayama M, et al. ATP sparing effect of isoflurane during ischaemia and reperfusion of the canine heart. Br J Anaesth. 1995 ;74(5):563-8.
20. Eppinger MJ, Jones ML, Deeb GM, et al. Pattern of injury and the role of neutrophils in reperfusion injury of rat lung. J Surg Res 1995 ;58(6):713-8
21. Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res. 1999 ;43(4):860-78.
22. Cavanagh SP, Gough MJ, Homer-Vanniasinkam S. The role of the neutrophil in ischaemia-reperfusion injury: potential therapeutic interventions. Cardiovasc Surg. 1998 ;6(2):112-8.
23. Serracino-Inglott F, Habib NA, Mathie RT. Hepatic ischemia-reperfusion injury. Am J Surg. 2001; 181 (2): 160-6.
24. Doerschuk CM. The role of CD18-mediated adhesion in neutrophil sequestration induced by infusion of activated plasma in rabbits.Am J Respir Cell Mol Biol. 1992;7(2):140-8
25. Moore TM, Khimenko P, Adkins WK, et al. Adhesion molecules contribute to ischemia and reperfusion-induced injury in the isolated rat lung. J Appl Physiol 1995;78(6):2245-52
26. Wegner CD. Adhesion molecules. London: Academic Press Limited 1994:163
27. Lu YT, Chen PQ Liu SF. Time course of lung ischemia-reperfusion-induced ICAM-1 expression and its role in ischemia-reperfusion lung injury. J Appl Physiol. 2002 ;93(2):620-8.
28. Arnaout MA. Structure and function of the leukocyte adhesion molecules CD11/CD18. Blood. 1990 ;75(5): 1037-50.
29. Kowalski C, Zahler S, Becker BF, et al. Halothane, isoflurane, and sevoflurane reduce postischemic adhesion of neutrophils in the coronary system. Anesthesiology. 1997 ;86(1):188-95.
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