迟发性运动障碍患者血浆超氧化物歧化酶和一氧化氮及一氧化氮合酶的变化

目的 探讨血浆超氧化物歧化酶(SOD)、一氧化氮(NO)及NO合酶(NOS)的变化与抗精神病药所敛的迟发性运动障碍(TD)的关系。方法 对42例长期使用抗精神病药治疗伴有TD的男性精神分裂症患者的血浆锰SOD(MnSOD)、铜-锌SOD(CuZnSOD)、NO及NOS的活性进行测定,以59例不伴有TD男性精神分裂症患者和50例健康男性作对照组,使用异常不自主运动量表(AIMS)进行临床评估。结果 TD组MnSOD、CuZnSOD和NO分别高于非TD组(P<0.05)或正常对照组(P<0.05),TD组NOS明显低于正常对照组(P<0.05)、略高于非TD组(p<0.05)。TD组MnSOD浓度越高则TD的症状越严重、NOS则相反(P<0.01),且在TD组MnSOD与NO呈显著的负相关(p<0.05)、在非TD组或正常对照组却呈正相关(前者P<0.01)。分层后发现TD组MnSOD浓度在NO较低时显著高于非TD组(P<0.01),而在NO浓度较高时则略低于非TD组(P>0.05)。结论 抗精神病药所致的TD,可能与患者血浆SOD尤其是MnSOD活性增高以及血浆NO浓度升高密切相关,两者可能来源于不同病理过程,但均提示自由基活动异常。     

急性脑梗死后血浆NO、NOS、ET含量的动态变化及尼莫地平对其影响

目的　观察急性脑梗死 (ACI)后血浆一氧化氮 (NO)、一氧化氮合成酶 (NOS)、内皮素 (ET)含量的动态变化 ,以及尼莫地平治疗后对其影响。方法　ACI患者 110例 ,随机分成尼莫地平组 (5 0例 ) (在常规治疗基础上用尼莫地平 )和常规治疗组 (6 0例 )。在发病后不同时点动态观察血浆NO、NOS、ET含量 ,并设 5 0例脑动脉硬化患者为对照组。结果　脑梗死后血浆ET含量显著升高 ,直至恢复期 ;NO、NOS先增高后下降 ;尼莫地平组和常规组比较ET有显著差异 (P <0 .0 1) ,NO、NOS差别不显著 (P >0 .0 5 )。结论　NO、NOS、ET参与并影响了ACI后复杂的病理生理过程 ;尼莫地平部分通过对ET含量的影响发挥其对脑梗死的治疗作用     

帕金森病血抗氧化系统变化及L-多巴的影响

目的　观察帕金森病 (PD)血抗氧化系统变化及 L-多巴的影响。方法　对 3 0例病程 1～ 5年的轻、中度PD采用化学比色法分别测定 L-多巴治疗前后外周静脉血一氧化氮 (NO)、一氧化氮合成酶 (NOS)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH-Px)和脂质过氧化物 (LPO)血浆活性 ,并与同时期 2 0例健康人对照。结果　与对照组比较 ,PD患者 NOS、SOD、GSH-Px降低 ,LPO增高 (P <0 .0 1 ) ;L-多巴治疗后 ,NO、NOS、SOD、GSH-Px进一步降低 ,LPO进一步增高 (P <0 .0 5 )。 结论　PD存在抗氧化酶活性降低 ,过氧化脂质代谢增强现象 ;L-多巴可加强这一异常变化。     

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.     

精神分裂症患者一级亲属的探索性眼球活动障碍研究

目的:探讨精神分裂症患者一级亲属探索性眼球活动(EEM)障碍的发生率及与血清一氧化氮/一氧化氮合成酶(NO/NOS)水平的关系。方法:共收集精神分裂症患者一级亲属193名(研究组),健康对照者150名(对照组)进行EEM检查,同时检测血清NO/NOS水平。结果:精神分裂症一级亲属的EEM异常率(52.3%)显著高于对照组(14.7%)(χ2=52,P<0.01);在精神分裂症一级亲属中,具有EEM障碍者的血清NO和NOS水平显著低于无EEM障碍者(t=2.83,P<0.01;t=2.53,P<0.05)。结论:精神分裂症患者一级亲属EEM障碍的发生率增高,并可能存在血清NO/NOS水平低下。     

首发偏执型精神分裂症血清NO/NOS水平的研究

目的探讨首发偏执型精神分裂症血清一氧化氮/一氧化氮合成酶（NO/NOS）水平及与精神症状的关系。方法共收集首发偏执型精神分裂症患者26例（研究组）,健康对照者30例（对照组）,采用阳性与阴性症状量表（PANSS）评定患者的精神症状,同时检测血清NO/NOS水平。结果首发偏执型精神分裂症血清NO/NOS水平均显著高于健康对照组（t=2.08,P〈0.05;t=2.72,P〈0.05）,血清NO/NOS水平与精神症状无显著相关性（P〉0.05）;血清NO水平与血清NOS水平两者存在显著正相关（r=0.41,P〈0.05）。结论首发偏执型精神分裂症患者存在血清NO/NOS水平病理性增高。     

卡托普利上调缺血性脑卒中患者血小板一氧化氮合酶的实验和临床研究

目的　研究卡托普利对缺血性脑卒中患者血小板一氧化氮合酶 (NOS)的上调及临床应用。方法　测定急性缺血性脑卒中患者及健康体检者的血小板NOS及在体外加氧化低密度脂蛋白 (oxLDL)、卡托普利后血小板NOS的活性 ;检测患者服卡托普利前、服后 1个月及 3个月的血浆oxLDL、NOS、一氧化氮 (NO) ,血小板NOS、NO ,同时检查神经功能。结果　 (1)卒中组和对照组血小板加oxLDL后 ,NOS值均明显下降 (P <0 .0 1) ,卒中组下降更明显 ;(2 )两组血小板同时加卡托普利、oxLDL后 ,NOS值均明显升高 (P <0 .0 1) ,卒中组升高更明显 ;(3)两组血小板单纯加卡托普利后 ,其NOS值均明显升高 (P <0 .0 1) ,同样亦是卒中组升高更明显 ;(4 ) 4 0例缺血性脑卒中患者服用卡托普利后血浆oxLDL明显下降 ,血小板NOS、NO ,血浆NOS、NO明显增高 ,神经功能明显改善。结论　卡托普利有直接上调血小板NOS的作用 ,卡托普利通过提高血小板NOS活性的作用 ,可以改善内皮功能 ,防治脑卒中     

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。     

西比灵对鼠脑缺血再灌注损伤模型的血清及脑组织中SOD、MDA、N0、NOS含量及病理学的影响

目的 研究西比灵对鼠脑缺血再灌注损伤模型的血清及脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、一氧化氮合酶(NOS)的含量及病理学改变的影响。方法 选用21只沙土鼠并随机分为3组,脑缺血再灌注组(再灌注组)、西比灵预防组(预防组)及对照组,每组7只,分别测定血清、脑组织中SOD、MDA、NO、NOS的含量,并用电镜检测其病理学的变化。结果 与对照组比较,再灌注组显示严重的病理损害,其血清、脑组织中MDA、N0、NOS含量明显上升、SOD含量明显下降,两组比较有显著性差异(均P<0.01);与再灌注组比,预防组病理改变较轻,其血清、脑组织中MDA、NO、NOS明显下降,SOD明显上升,两组比较均有显著性差异(分别P<0.01和P<0.05)。结论 西比灵可减少自由基,诱导SOD生成,具有保护脑细胞的作用。     

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     

The indices of endogenous oxidative and antioxidative processes in plasma from schizophrenic patients. The possible role of oxidant/antioxidant imbalance

There is great evidence in recent years that oxygen free radicals play an important role in the pathophysiology of schizophrenia. The present study was performed to assess the changes in plasma nitric oxide (NO) and thiobarbituric acid-reactive substances (TBARS) levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) activities in schizophrenic patients compared to age- and sex-matched normal controls. A hundred patients with schizophrenia and 51 healthy volunteers were included in the study. XO, SOD, and GSH-Px activities as well as NO and TBARS levels were estimated by standard biochemical techniques in the plasma of normal healthy controls and schizophrenia patients. In schizophrenia, increased plasma XO activity (P < .0001) and NO levels (P < .0001), decreased SOD activity (P < .0001), and unchanged GSH-Px activity were detected compared to control group. Plasma TBARS levels were increased in schizophrenic patients (P < .01), especially in the residual subtype. TBARS levels in nonsmoker schizophrenic patients were found to be higher than nonsmoker controls. Although TBARS levels in both patients and controls were found to be higher in smokers as compared to nonsmokers, it was not statistically significant. No effects of duration of the illness, gender, and low and high dose of daily neuroleptic treatment equivalent to chlorpromazine on oxidant and antioxidant parameters were observed. Because the dose and the duration of treatment with drugs have no influence on the results, it can be interpreted that the findings are more likely to be related mainly to the underlying disease. These findings indicated a possible role of increased oxidative stress and diminished enzymatic antioxidants, both of which may be relevant to the pathophysiology of schizophrenia. On the other hand, increased NO production by nitric oxide synthetases (NOSs) suggests a possible role of NO in the pathophysiological process of schizophrenia. These findings may also suggest some clues for the new treatment strategies with antioxidants and NO synthase (NOS) inhibitors in schizophrenia.     

Reduced plasma nitric oxide metabolites before and after antipsychotic treatment in patients with schizophrenia compared to controls

BACKGROUND: Nitric oxide (NO) is believed to have a role in the pathophysiology of schizophrenia. We examined plasma levels of NO metabolites in patients with schizophrenia and normal controls. We also determined the impact of 6-week risperidone treatment on circulating NO metabolites in patients with schizophrenia. METHOD: Plasma NO metabolite (NO(x)) levels were measured in 55 schizophrenia patients before and after 6-week treatment with risperidone and in 55 normal controls. Severity of schizophrenia and response to treatment were assessed with the positive and negative syndrome scale (PANSS) for schizophrenia. NO(x) levels were estimated by the Griess method. RESULTS: Pre-treatment plasma NO(x) levels in schizophrenia patients (8.97+/-6.74 micromol/L) were lower than those of normal controls (14.51+/-6.30 micromol/L) (p<0.01). Schizophrenia patients had lower post-treatment NO(x) levels (10.99+/-8.31 micromol/L) than those of normal controls (p<0.01). There was marginal significant change between plasma NO(x) levels before and after 6-week treatment (p=0.056). Moreover, in 37 treatment responders (>/=30% improvement in PANSS score), post-treatment plasma NO(x) significantly increased in comparison to pre-treatment NO(x) (p=0.028). CONCLUSIONS: Plasma levels of NO(x) in patients with schizophrenia were significantly lower than normal controls both before and after the treatment. Our findings suggest that the improvement of psychiatric symptoms can lead to partially normalize a deficiency of NO after treatment in schizophrenia patients. Our findings support the hypothesis that the NO system is dampened in schizophrenia.     

Is the arginine-nitric oxide pathway involved in the pathogenesis of schizophrenia?

The reciprocal regulation of arginase and nitric oxide synthase (NOS) in L-arginine-metabolizing pathways has been demonstrated. There are various evidences of the role of the nitric oxide (NO) in several neuropsychiatric disorders including schizophrenia. However, there is no study which has investigated the role of arginase as an important part of the arginine regulatory system affecting NOS activity in schizophrenia. This study aims to investigate arginase, manganese (Mn) and total nitrite levels (a metabolite of NO) and their relationship to the arginine-NO pathway in patients with schizophrenia. Arginase activities, Mn and total nitrite levels were measured in plasma from 46 patients with schizophrenia and 32 healthy control subjects. Plasma arginase activities and Mn were found to be significantly lower and total nitrite level higher in patients with schizophrenia compared with controls. Our results suggest that the arginine-NO pathway is involved in the pathogenesis of schizophrenia.     

自由基代谢与精神分裂症临床症状和药物治疗的关系

目的：探讨自由基代谢与精神分裂症临床症状和药物治疗的关系。方法：是否治疗的慢性精神分裂症患者各４０例分别评定定阳性和阴性症状量表（ＰＡＮＳＳ）,并测定膜脂质过氧化物丙二醛（ＭＤＡ）含量、铜／锌超氧化物歧化酶（Ｇｕ－ＺｎＳＯＤ）和谷胱苷肽过氧化物酶（ＧＳＨ－Ｐｘ）活性。结果：与健康对照组相比,未治疗组患者ＭＤＡ含量和ＧＳＨ－Ｐｘ活性显著增加,治疗组患者无显著改变;而两组患者ＳＯＤ活性显著降低;未治疗     

Allelic association of the neuronal nitric oxide synthase (NOS1) gene with schizophrenia

Nitric oxide (NO) has been identified as a widespread and multifunctional biological messenger molecule in the central nervous system (CNS), with possible roles in neurotransmission, neurosecretion, synaptic plasticity, and tissue injury in many neurological disorders, including schizophrenia. Neuronal NO is widely produced in the brain from L-arginine catalyzed by neuronal NO synthase (NOS1). We therefore hypothesized that the NOS1 gene may play a role in the pathophysiology of schizophrenia. In the present study, we examined the genetic association between a novel single nucleotide polymorphism (SNP: a C-->T transition located 276 base pairs downstream from the translation termination site) of the human NOS1 gene, which is located in chromosome 12q24, and schizophrenia (215 Japanese patients with schizophrenia and 182 healthy controls). The allele frequencies of the polymorphism in exon 29 of the NOS1 gene differed significantly between patients with schizophrenia and controls (chi(2) = 20.10, df = 1, P = 0.000007; relative risk = 1.92; 95% confidence interval = 1.44-2.55). Our results suggest that the NOS1 gene polymorphism may confer increased susceptibility to schizophrenia.     

Elevated homocysteine level in siblings of patients with schizophrenia

Increased homocysteine plasma levels were reported in patients with schizophrenia and Levine et al. (2002) suggested that such increase characterizes mainly males. In the following study we examined whether such increased levels also characterize male siblings of schizophrenia patients. Forty-four pairs of schizophrenia patients and their corresponding healthy male siblings were recruited and sampled for homocysteine. We also had age-matched controls for each of the sibling. The median homocysteine plasma level for patients was 13.0 µMol/L and 11.7 µMol/L for their male siblings compared with a median of 10.9 µMol/L for the siblings' controls. There was no significant difference between homocysteine plasma level in patients and their siblings. Significant difference was found for homocysteine plasma level between the siblings' group and their matched controls. A partial correlation of Ln plasma homocysteine level between patients and their siblings was found to be close to a zero correlation of −0.089, p=0.57 for the whole study group and −0.15, p=0.38 in the male–male patient-sibling pairs. Our results show that elevated homocysteine plasma level may characterize schizophrenia patients' male siblings, a finding that seems to agree with previous studies suggesting elevated homocysteine level as a risk factor for developing schizophrenia.     

急性一氧化碳中毒后迟发性脑病患者血清NO与NOS水平及其临床意义

目的 探讨血清一氧化氮(nitric oxide,NO)、一氧化氮合酶(nitric oxide synthsae,NOS)的水平及其动态变化与急性一氧化碳中毒后迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)患者病情变化的关系.方法 应用比色法(colorimetric method)动态测定31例DEACMP患者血清NO及NOS水平,并与30例急性一氧化碳中毒(acute carbon monoxide poisoning,ACMP)后未发生迟发脑病患者和30 例正常对照进行比较.结果 DEACMP患者急性期血清NO及NOS水平[(62.67 ± 14.39)μmol/L,(27.68 ± 6.14)U/mL]明显高于正常对照组[(50.18 ± 9.95) μmol/L,(20.88 ± 6.32)U/mL] (均P ＜ 0.05),与ACMP组急性期[(62.00 ± 16.46)μmol/L,(28.13 ± 5.23)U/mL]比较无统计学差异(均P ＞ 0.05);DEACMP患者恢复期血清NO及NOS水平[(54.66 ± 11.73)μmol/L,(21.74 ± 5.88)U/mL]明显低于急性期(均P ＜ 0.05),与ACMP组随访期[(52.79 ± 11.22)μmol/L,(20.64 ± 5.92)U/mL]比较无统计学差异(均P ＞ 0.05).结论 NO-NOS系统参与了DEACMP的发病机制,NO-NOS水平变化与病情变化基本一致.     

缺血性脑卒中患者血浆NO浓度变化的研究

目的 研究不同类型的缺血性脑卒中患者的血浆一氧化氮（NO）浓度变化及其临床意义。方法 采用硝酸还原酶法测定230例脑梗死患者、103例腔隙性脑梗死患者以及169名正常对照者的血浆NO浓度。结果 脑梗死组血浆NO浓度与另两组相比显著增高（均P＜0．01）,而腔隙性脑梗死患者的血浆NO浓度低于对照组（P＜0．05）。结论 脑梗患者急性期血浆NO浓度可作为缺血损害的一个参考指标;而腔隙性脑梗死组NO浓度下降反映患者的高血压等基础病变的存在。