一氧化氮与深低温停循环后神经系统缺血再灌注损伤
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资料包括： 论文(4页3228字)
说明：
关键词： 深低温停循环(DHCA) ,一氧化氮(NO) ,神经系统
1967年Hikasa等首次提出体外循环深低温停循环(DHCA)技术并由Okamoto等应用于婴幼儿先天性心脏病，1975年Griepp［1］应用于成人大血管手术以来，大大提高了心脏及大血管手术的成功率，但单纯停循环超过60分钟，术后易出现神经系统的并发症。并发症的发生主要与DHCA脑缺血及再灌注损伤有关，其中谷氨酸的兴奋性神经毒性为造成损伤的重要原因，谷氨酸作用于N-甲基-D-天冬氨酸(NMDA)受体，导致大量Ca2+内流，激活NO合酶，NO的合成增加，因而NO在神经系统缺血再灌注损伤的作用逐渐受到重视。
一、NO的特性
1. NO的生化和生理特性 NO在体内的生理作用非常广泛，对血液循环系统的正常功能起重要的调节作用，包括： (1) 调节血管张力。血管内皮细胞在基础状态下可持续释放NO，以维持一种基础的血管张力；(2) 调节血压。Witte等［2］证实，NO/cGMP系统参与大鼠正常血压节律性波动的调节。高剂量NOS抑制剂L-NAME(30 mg/kg体重)使大鼠呈现相反的血压波动节律；(3) 调节器官血流量。在整体动物，NOS抑制剂体循环给药常可引起冠状血管收缩；(4) 抑制血细胞粘附于内皮。内皮产生的NO可抑制多种血液成分如血小板、淋巴细胞、中性粒细胞和单核细胞粘附于血管内皮细胞；(5) 抑制血管内皮下细胞增殖。内皮释放的NO在体内还有抗血管壁细胞增殖的作用。有研究证实，慢性抑制内源性NO合成会导致冠状动脉及主动脉发生明显的增殖反应，血管壁增厚，血管腔变狭窄［3］；(6) 抑制血小板聚集。Shahbazi等［5］研究了NO供体S-亚硝基-乙酰青霉胺(SNAP)、硝普钠(SNP)、S-亚硝基谷胱甘肽(GSNO)对血小板在覆盖有纤维蛋白原表面的蔓延的影响，发现这些NO供体对血小板的蔓延有抑制作用，且其抑制作用的能力为SNAP＞SNP＞GSNO，这种抑制作用可被氧合血红蛋白所逆转［4］。
目录：
一、NO的特性
二、NO与脑缺血损伤
三、NO与深低温停循环后脑缺血再灌注损伤
参考文献：
1 Griepp RB, Stinson EB, Hollingsworth JF, Buehler. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg, 1995,70:1051-1063.
2 Witte K, Schnecko A, Zuther P, et al. Contribition of the nitric oxide-guanylyl cyclase system to circadian regulation of blood pressure in normotensive Wistar-Wistar-Kyoto rats. Cardiovasc Res, 1995,30:682-688.
3 Nugaguchi K, Egashira K, Takemoto M, et al. Chronic inhibition of nitric oxide synthesis causes coronary microvascular remodeling in Rats. Hypertension, 1995,26:957-962.
4 Shahbazi T, Jones N, Radomski NW, et al. Nitric oxide donors inhibit platelet spreading on surfaces coated with fibrinogen but not with fibronectin. Thromb Res, 1994,75:631-642.
5 Asahi M, Fujii, J, Suzuk K, et al. Inactivation of glutathione peroxidase by nitric oxide: implication for cytotoxicity. J Biol Chem, 1995,270:21035-21039.
6 Castro L, Rodriguez M, Radi R. Aconitase is readily inactivated by peroxynitrite, but not by its precursor, nitric oxide. J Biol Chem, 1994,269:29409-29415.
7 Kroncke KD, Fehseh K, Schmidt T, et al. Nitric oxide destroys zinc-sulfur clusters inducing zine release from metallothionein and inhibition of the zinc finge-type yeast trancription activator LAC9. Biochem Biophys Res Lommun, 1994, 200:1105-1110.
8 Crow JP, Bechman JS. Reactions between nitric oxide superoxide, and peroxynitrite: footprints of peroxynitrite in vivo. Adv Pharmacol, 1995,34:17-43.
9 Liu RH, Hotchkiss JH. Potential genotoxicity of chronically elevated nitric oxide: a reviews. Mutat Res, 1995,339:73-89.
10 Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of retina. AMA Arch Ophthalmol, 1957,58:193-201.
11 Olney JW. Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate. Science, 1969,164:719-712.
12 Sato S, Tominage T, Ohnishi T, et al. Electron paramagnetic resonance study on nitric oxide production during brain focal ischemia and reperfusion in the rat. Brain Research, 1994,647:91-96.
13 Anderson RE, Meyer FB. Nitric oxide synthase inhibition by L-NAME during repetitive focal cerebral ischemia in rabbits. Am J Physiol, 1996,271(2pt2):II588-II594.
14 Bolanos JP, Almeida A, Medina JM. Nitric oxide mediates brain mitochondrial damage during perinatal anoxia. Brain Res, 1998, 16:787:117-122.
15 Brock MV, Blue ME, Lowenstein CJ, et al. Induction of Neuronal Nitric Oxide After IIypothermic Circulatory Arrest. Ann Thorac Surg, 1996,62:1313-1320.
16 Steven SL, Tsui MD, Paul M, et al. Nitric Oxide Production Affects Cerebral Perfusion and Metabolism After Deep IIypothermic Circulatory Arrest. Ann Thorac Surg, 1996,61:1699-1707.
17 Hiramatsu T, Jonas RA, Miura T, et al. Cerebral metabolic recovery from deep hypothermic circulation arrest after treatment with arginine and nitro-arginine methyl ester. J Thorac Cardiovasc Surg, 1996, 112:698-707.
18 Remond JM, Zehr KJ, Blue ME, et al. AMPA Glutamate receptor antagonism reduces neurologic injury after hypothermic circulatory arrest. Ann Thorac Surg, 1995,59:579-584.
19 Tseng EE, Brock MV, Lange MS, et al. Neuronal Nitric Oxide Synthase Inhibition Reduces Neuronal Apoptosis After Hypothermic Circulatory Arrest. Ann Thorac Surg, 1997,64:1639-1647.
20 Segawa D, Hatori N, Yoshizu H, et al. The effect of Nitric Oxide Synthase inhibitor on reperfusion injury of the brain under hypothermic circulatory arrest. J Thorac Cardiovasc Surg, 1998,115:925-930.
资料包括： 论文(4页3228字)
说明：
关键词： 深低温停循环(DHCA) ,一氧化氮(NO) ,神经系统
1967年Hikasa等首次提出体外循环深低温停循环(DHCA)技术并由Okamoto等应用于婴幼儿先天性心脏病，1975年Griepp［1］应用于成人大血管手术以来，大大提高了心脏及大血管手术的成功率，但单纯停循环超过60分钟，术后易出现神经系统的并发症。并发症的发生主要与DHCA脑缺血及再灌注损伤有关，其中谷氨酸的兴奋性神经毒性为造成损伤的重要原因，谷氨酸作用于N-甲基-D-天冬氨酸(NMDA)受体，导致大量Ca2+内流，激活NO合酶，NO的合成增加，因而NO在神经系统缺血再灌注损伤的作用逐渐受到重视。
一、NO的特性
1. NO的生化和生理特性 NO在体内的生理作用非常广泛，对血液循环系统的正常功能起重要的调节作用，包括： (1) 调节血管张力。血管内皮细胞在基础状态下可持续释放NO，以维持一种基础的血管张力；(2) 调节血压。Witte等［2］证实，NO/cGMP系统参与大鼠正常血压节律性波动的调节。高剂量NOS抑制剂L-NAME(30 mg/kg体重)使大鼠呈现相反的血压波动节律；(3) 调节器官血流量。在整体动物，NOS抑制剂体循环给药常可引起冠状血管收缩；(4) 抑制血细胞粘附于内皮。内皮产生的NO可抑制多种血液成分如血小板、淋巴细胞、中性粒细胞和单核细胞粘附于血管内皮细胞；(5) 抑制血管内皮下细胞增殖。内皮释放的NO在体内还有抗血管壁细胞增殖的作用。有研究证实，慢性抑制内源性NO合成会导致冠状动脉及主动脉发生明显的增殖反应，血管壁增厚，血管腔变狭窄［3］；(6) 抑制血小板聚集。Shahbazi等［5］研究了NO供体S-亚硝基-乙酰青霉胺(SNAP)、硝普钠(SNP)、S-亚硝基谷胱甘肽(GSNO)对血小板在覆盖有纤维蛋白原表面的蔓延的影响，发现这些NO供体对血小板的蔓延有抑制作用，且其抑制作用的能力为SNAP＞SNP＞GSNO，这种抑制作用可被氧合血红蛋白所逆转［4］。
目录：
一、NO的特性
二、NO与脑缺血损伤
三、NO与深低温停循环后脑缺血再灌注损伤
参考文献：
1 Griepp RB, Stinson EB, Hollingsworth JF, Buehler. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg, 1995,70:1051-1063.
2 Witte K, Schnecko A, Zuther P, et al. Contribition of the nitric oxide-guanylyl cyclase system to circadian regulation of blood pressure in normotensive Wistar-Wistar-Kyoto rats. Cardiovasc Res, 1995,30:682-688.
3 Nugaguchi K, Egashira K, Takemoto M, et al. Chronic inhibition of nitric oxide synthesis causes coronary microvascular remodeling in Rats. Hypertension, 1995,26:957-962.
4 Shahbazi T, Jones N, Radomski NW, et al. Nitric oxide donors inhibit platelet spreading on surfaces coated with fibrinogen but not with fibronectin. Thromb Res, 1994,75:631-642.
5 Asahi M, Fujii, J, Suzuk K, et al. Inactivation of glutathione peroxidase by nitric oxide: implication for cytotoxicity. J Biol Chem, 1995,270:21035-21039.
6 Castro L, Rodriguez M, Radi R. Aconitase is readily inactivated by peroxynitrite, but not by its precursor, nitric oxide. J Biol Chem, 1994,269:29409-29415.
7 Kroncke KD, Fehseh K, Schmidt T, et al. Nitric oxide destroys zinc-sulfur clusters inducing zine release from metallothionein and inhibition of the zinc finge-type yeast trancription activator LAC9. Biochem Biophys Res Lommun, 1994, 200:1105-1110.
8 Crow JP, Bechman JS. Reactions between nitric oxide superoxide, and peroxynitrite: footprints of peroxynitrite in vivo. Adv Pharmacol, 1995,34:17-43.
9 Liu RH, Hotchkiss JH. Potential genotoxicity of chronically elevated nitric oxide: a reviews. Mutat Res, 1995,339:73-89.
10 Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of retina. AMA Arch Ophthalmol, 1957,58:193-201.
11 Olney JW. Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate. Science, 1969,164:719-712.
12 Sato S, Tominage T, Ohnishi T, et al. Electron paramagnetic resonance study on nitric oxide production during brain focal ischemia and reperfusion in the rat. Brain Research, 1994,647:91-96.
13 Anderson RE, Meyer FB. Nitric oxide synthase inhibition by L-NAME during repetitive focal cerebral ischemia in rabbits. Am J Physiol, 1996,271(2pt2):II588-II594.
14 Bolanos JP, Almeida A, Medina JM. Nitric oxide mediates brain mitochondrial damage during perinatal anoxia. Brain Res, 1998, 16:787:117-122.
15 Brock MV, Blue ME, Lowenstein CJ, et al. Induction of Neuronal Nitric Oxide After IIypothermic Circulatory Arrest. Ann Thorac Surg, 1996,62:1313-1320.
16 Steven SL, Tsui MD, Paul M, et al. Nitric Oxide Production Affects Cerebral Perfusion and Metabolism After Deep IIypothermic Circulatory Arrest. Ann Thorac Surg, 1996,61:1699-1707.
17 Hiramatsu T, Jonas RA, Miura T, et al. Cerebral metabolic recovery from deep hypothermic circulation arrest after treatment with arginine and nitro-arginine methyl ester. J Thorac Cardiovasc Surg, 1996, 112:698-707.
18 Remond JM, Zehr KJ, Blue ME, et al. AMPA Glutamate receptor antagonism reduces neurologic injury after hypothermic circulatory arrest. Ann Thorac Surg, 1995,59:579-584.
19 Tseng EE, Brock MV, Lange MS, et al. Neuronal Nitric Oxide Synthase Inhibition Reduces Neuronal Apoptosis After Hypothermic Circulatory Arrest. Ann Thorac Surg, 1997,64:1639-1647.
20 Segawa D, Hatori N, Yoshizu H, et al. The effect of Nitric Oxide Synthase inhibitor on reperfusion injury of the brain under hypothermic circulatory arrest. J Thorac Cardiovasc Surg, 1998,115:925-930.