一氧化氮及其合成酶与脑创伤性损害

一氧化氮(NO)是一种具有生物活性作用的小分子,它分布于人体多种组织中。NO内源合成的关键酶是一氧化氮合成酶(NOS)。脑损伤能诱导局部神经元和传入到损伤区域的神经元表达NOS,伤口内反应性的星形细胞和相关的胶质细胞聚集并有较高的NOS活性。NO发挥神经毒性作用的中心环节是损伤DNA,使细胞内能量储备耗竭而引起细胞死亡。     

癫癎患者血清一氧化氮和一氧化氮合酶活性水平的研究

目的　探讨一氧化氮 (NK)和一氧化氮合酶 (NOS)在癫患者中血清活性水平及意义。方法　采用化学比色法对 10 0例癫患者血清中NO和NOS活性水平进行检测。结果　癫患者间歇期血清中NO和NOS活性水平显著高于对照组 (P <0 0 1)。结论　NO和NOS在癫病理过程中起重要作用。     

儿童癫癎患者血清一氧化氮及一氧化氮合酶活性水平的研究

目的　探讨一氧化氮 (NO)及一氧化氮合酶 (NOS)在儿童癫患者中血清活性水平及意义。方法　采用化学比色法对12 4例儿童癫患者血清中NO及NOS活性水平进行检测。结果　儿童癫患者发作期及间歇期血清中NO及NOS活性水平均显著高于对照组 (P <0 0 1) ,发作期血清中NO及NOS活性水平均高于间歇期 (P <0 0 5 )。结论　NO及NOS在儿童癫病理过程中起重要作用     

一氧化氮及合成酶与脑梗塞

自 Furchgott和 Zawadzki[1 ] 首次提出内皮舒张因子(EDRF)这一概念 ,且后来证实 EDRF是 L -精氨酸 (L - Arg)在一氧化氮合成酶 (NOS)作用下产生的 NO后[2 ] ,其早期研究认为其作用较简单 :扩张脑血管 ,增加脑血流 ,抑制血小板及白细胞在血管内皮的粘附聚集 ,似乎 NO对脑梗塞起保护作用。然而 ,随着对 NO及 NOS同分异构体的研究 ,NO的毒性作用也渐已证实。NOS不恰当的激活及 NO过度产生可介导兴奋性氨基酸的毒性作用。本文就 NO及 NOS在脑梗塞中近年的研究进展作一综述。一、NOS同分异构体NO是由底物 L- Arg在 NOS催化作…     

一氧化氮与脑外伤研究进展

一氧化氮(NO)是体内一种重要的小分子介质,参与全身多种病理生理过程,是近来研究的热点之一,近年来发现其在脑外伤的病理生理过程中起作重要作用。1 NO和NOS的一般生物学特征 NO是左旋精氨酸(L-arginine,L-Arg)与氧分子在一氧化氮合成酶(Nitric Oxide Synthase,NOS)催化作用下的产物,带有不成对电子,易溶于水及脂肪,易在细胞内外自由弥散,半衰期很短仅20～30s。 NOS是体内合成NO的关键酶,按其基因序列和     

一氧化氮可能是导致抑郁症的主要因素

一直以来认为一氧化氮(NO)在机体各种疾病的生理病理机制中发挥着重要作用.它参与调节体内各种神经递质系统,因此推断NO在神经系统疾病的发病机制中也发挥着重要作用.在脑内NO与许多生理活动有关,如:神经信号传递、神经发生、突触可塑性、基因表达调控、调节性行为和侵略性行为、学习、疼痛和抑郁等.许多证据都表明NO参与抑郁症发病机制,NO调节新一代抗抑郁药的活性已得到证明.现主要讨论抑郁状态机体NO水平改变及NO在抑郁症发病机制中的作用.NOS抑制剂有可能成为未来首选的抗抑郁药物.     

局灶脑缺血后早,晚期一氧化氮合成酶的活性变化

一氧化氮(NO)在脑缺血中起重要作用,一氧化氮合成酶(NOS)作为NO合成的关键酶,其活性变化直接调节NO的生成量及生物学效应。本文在建立兔MCAO局灶脑缺血模型基础上,测定缺血后不同时间缺血区和正常脑组织的NOS活性。结果显示,脑缺血早期(1h内)NOS活性突然升高,随之下降;脑缺血后24h NOS活性又升高,至48h、96h明显升高。     

一氧化氮和一氧化氮合酶在鼠脑内形成吗啡依赖的作用研究

目的：研究一氧化氮（NO）和一氧化氮合酶（NOS）在吗啡依赖形成中的作用。方法;对吗啡依赖和戒断大鼠脑内NO含量和NOS活力进行测定。结果：未发现吗啡依赖和戒断大鼠脑内NO含量和NOS活力有改变。结论：对NO／NOS与吗啡依赖的关系还有待进一步研究。     

惊恐障碍与心绞痛患者血清一氧化氮水平对照研究

目的:探讨惊恐障碍与心绞痛之间的关系.方法:检测并比较17例惊恐障碍(惊恐障碍组)与27例心绞痛(心绞痛组)及39名健康者(对照组)血清一氧化氮(NO)和一氧化氮合酶(NOS).结果:两患者组血清NO水平均显著低于对照组,惊恐障碍组与心绞痛组比较血清NO水平无显著差异;惊恐障碍组血清NOS水平与对照组比较无显著差异,心绞痛组血清NOS水平显著低于对照组,两患者组血清NOS水平无显著差异.结论:惊恐障碍与心绞痛症状相似可能与NO的下降有关.惊恐障碍成为心绞痛的危险因素由NO下降得到解释.     

一氧化氮的神经毒性与保护作用

在脑缺血、兴奋毒性、创伤和退行性疾病等中枢神经损伤后一氧化氮(NO)及其合酶明显增加 NO具有神经毒性与保护的双向作用,ncNOS和iNOS均与神经损伤机制有关,而ecNOS可能有助于防护神经损伤。     

Nitric oxide and nitric oxide synthase in Huntington's disease

Nitric oxide (NO) is a biologically active inorganic molecule produced when the semiessential amino acid l-arginine is converted to l-citrulline and NO via the enzyme nitric oxide synthase (NOS). NO is known to be involved in the regulation of many physiological processes, such as control of blood flow, platelet adhesion, endocrine function, neurotransmission, neuromodulation, and inflammation, to name only a few. During neuropathological conditions, the production of NO can be either protective or toxic, dependent on the stage of the disease, the isoforms of NOS involved, and the initial pathological event. This paper reviews the properties of NO and NOS and the pathophysiology of Huntington's disease (HD). It discusses ways in which NO and NOS may interact with the protein product of HD and reviews data implicating NOS in the neuropathology of HD. This is followed by a synthesis of current information regarding how NO/NOS may contribute to HD-related pathology and identification of areas for potential future research.     

一氧化氮／一氧化氮合酶与神经创伤

一氧化氮是一种简单的气体分子，可在哺乳类神经细胞内经一氧化氮合酶作用产生。ＮＯ在神经创伤修复中的多重作用近年来已受到越来越多的重视。本文对ＮＯ／ＮＯＳ与神经创伤和再生之间的关系作一综述。     

Inducible nitric oxide synthase and nitric oxide production by oligodendrocytes

It has been previously demonstrated that microglia and astrocytes produce micromolar amounts of nitric oxide in vitro. In this study, we demonstrate that primary rat oligodendrocytes can be stimulated to produce iNOS mRNA as detected by Northern blot and in situ hybridization analysis and a 131-kDa iNOS protein by Western blot analysis; protein was also detected in cells by single- and double-label immunohistochemistry for iNOS and the oligodendrocyte-specific marker CNPase. NO/NOS are produced as a consequence of activation of the gene encoding the inducible nitric oxide synthase as determined by inhibition with actinomycin D and cyclohexamide. The iNOS is functional, leading to calcium/calmodulin-independent NO production in these in vitro cultures. J. Neurosci. Res. 48:372–384, 1997. © 1997 Wiley-Liss, Inc.     

Ethylene oxide polyneuropathy

Sensorimotor polyneuropathy developed in two workers who had been exposed to ethylene oxide gas repeatedly for several months. Sural nerve biopsies revealed axonal degeneration with mild changes of the myelin sheath. Unmyelinated fibers were also involved. Muscle biopsies showed typical denervation atrophy. Symptoms improved after exposure to ethylene oxide terminated.     

Involvement of nitric oxide and nitric oxide synthase activity in anticonvulsive action

The anticonvulsant drug Diazepam (DIA-2 mg/kg b. wt), the nitric oxide (NO) donor L-Arginine (L-Arg-2000 mg/kg b. wt) and the putative nitric oxide synthase (NOS) inhibitor N(G)-Nitro-L-Arginine methyl ester (L-NAME-50 mg/kg b. wt) were used to determine the role of endogenous NO on convulsions induced by picrotoxin (PCT-5 mg/kg b. wt) in rats. Rats given a convulsant dose of PCT (5 mg/kg b. wt) had convulsion and it suppresses the NOS activity and NO concentration in brain regions. The anticonvulsant L-Arg alone significantly increases the NO concentration and NOS activity in brain regions, but not diazepam. Whereas DIA, along with L-Arg, enhances the NO and NOS activity when compared to L-Arg alone. The combination of both OIA and L-Arg completely suppressed the convulsions. L-NAME alone had no effect to produce convulsions but it completely decreased NO concentration and NOS activity and potentiated the PCT convulsions. This was reverted by pre- and post treatment of DIA plus L-Arg indicating, the increased NO concentration and NOS activity in brain regions suppresses convulsions.     

Nitrous oxide anesthesia-associated myelopathy

BACKGROUND: The role of nitrous oxide exposure in neurologic complications of subclinical cobalamin deficiency has been reported, but few cases are well documented. OBSERVATION: Two weeks after surgery for prosthetic adenoma, a 69-year-old man developed ascending paresthesia of the limbs, severe ataxia of gait, tactile sensory loss on the 4 limbs and trunk, and absent tendon reflexes. After a second surgical intervention, the patient became confused. Four months after onset, the patient had paraplegia, severe weakness of the upper limbs, cutaneous anesthesia sparing the head, and confusion. Moderate macrocytosis, low serum B12 levels, and a positive Schilling test result led to the diagnosis of pernicious anemia. Results of electrophysiologic examinations showed a diffuse demyelinating neuropathy. Magnetic resonance imaging of the spinal cord disclosed hyperintensities of the dorsal columns on T2-weighted images. CONCLUSIONS: Pernicious anemia can result in severe neurologic symptoms with only mild hematologic changes. The role of nitrous oxide anesthesia in revealing subclinical B12 deficiency must be emphazised. Magnetic resonance imaging of the spinal cord might be helpful in making the diagnosis.     

Nitric oxide and sleep

Nitric oxide (NO) is a biological messenger synthesized by three main isoforms of NO synthase (NOS): neuronal (nNOS, constitutive calcium dependent), endothelial (eNOS, constitutive, calcium dependent) and inducible (iNOS, calcium independent). NOS is distributed in the brain either in circumscribed neuronal sets or in sparse interneurons. Within the laterodorsal tegmentum (LDT), pedunculopontine tegmentum and dorsal raphe nucleus, NOS-containing neurons overlap neurons grouped according to their contribution to sleep mechanisms. The main target for NO is the soluble guanylate cyclase that triggers an overproduction of cyclic guanosine monophosphate. NO in neurons of the pontine tegmentum facilitates sleep (particularly rapid-eye-movement sleep), and NO contained within the LDT intervenes in modulating the discharge of the neurons through an auto-inhibitory process involving the co-synthesized neurotransmitters. Moreover, NO synthesized within cholinergic neurons of the basal forebrain, while under control of the LDT, may modulate the spectral components of the EEG instead of the amounts of different sleep states. Finally, impairment of NO production (e.g. neurodegeneration, iNOS induction) has identifiable effects, including ageing, neuropathologies and parasitaemia.