高压氧对脑梗死后血清一氧化氮和一氧化氮合酶含量的影响

目的 研究高压氧对脑梗死后血清一氧化氮、一氧化氮合酶含量的影响。方法 将脑梗死患者分为高压氧治疗组和非高压氧治疗组,观察不同病期血清一氧化氮、一氧化氮合酶含量的变化,并与正常对照组进行比较。结果 高压氧治疗组一氧化氮含量较非高压氧治疗组上升快,在治疗后15天恢复正常,但在一疗程高压氧治疗结束后,却又有所下降;一氧化氮合酶含量在治疗后均有上升,未能恢复到正常水平,两组之间无差异。结论 高压氧通过提高NO的含量,减轻缺血区脑组织的损伤,改善脑血循环;高压氧对NOS有一定影响,但作用不大;应适当延长高压氧疗程,尽可能缓解因NOS含量下降所造成的NO释放量不足。     

不同病原体中枢神经系统感染患者血清和脑脊液中一氧化氮 总一氧化氮合酶的动态变化

目的观察不同病原体所致中枢神经系统（CNS）感染患者脑脊液（CSF）及血清中一氧化氮（NO）浓度、总一氧化氮合酶（NOS）活力的动态变化，为临床鉴别不同病原体所致中枢神经系统感染提供实验室依据。方法硝酸还原酶法和化学比色法检测30例中枢神经系统感染患者治疗前、治疗2周后CSF中及入院时、住院第3、5、9、14天血清中NO浓度、总NOS活力的动态变化。结果中枢神经系统感染患者不同病原体所致病毒性脑膜炎、化脓性脑膜炎、结核性脑膜炎组不同时点血清NO浓度、总NOS活力组间比较，差异均无统计学意义（P〉0.05）；病毒性脑膜炎、化脓性脑膜炎、结核性脑膜炎患者治疗前、治疗2周后脑脊液中NO浓度、总NOS活力之间差异均无统计学意义（P〉0．05）。结论血清中NO浓度、总NOS活力尚不能作为化脓性脑膜炎、病毒性脑膜炎、结核性脑膜炎临床鉴别诊断的实验室依据之一。     

依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶的影响

目的探讨人工合成的植物雌激素依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶合酶的影响。方法6个月龄雌性SD大鼠60只分为假手术组（10只SD大鼠）和去卵巢组（50只）;再将去卵巢大鼠分为阴性对照组,依普拉芬高、中、低剂量组和雌激素对照组（各10只）,分别给予基础饲料和不同剂量的依普拉芬,12周后测定血清NO及NOS。结果与假手术组相比,去卵巢大鼠阴性对照组血清NO及NOS明显降低,依普拉芬组高于阴性对照组,与假手术组比较差异无统计学意义。同时低于雌激素组。结论NO及NOS参与了骨质疏松的病理生理过程;依普拉芬可以通过提高去卵巢大鼠血清NO及NOS浓度达到防治绝经后骨质疏松症的作用。     

一氧化氮合酶抑制研究进展

一氧化氮具有广泛的生理功能，但过量产生或释放时能介导多种疾病的发生，一氧化氮合酶抑制剂可阻止一氧化氮过量合成，因此具有治疗价值，本文拟对近年来一氧化氮合酶抑制剂的研究进展作了一概述。     

依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶的影响

目的 探讨人工合成的植物雌激素依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶合酶的影响.方法 6个月龄雌性SD大鼠60只分为假手术组(10只SD大鼠)和去卵巢组(50只);再将去卵巢大鼠分为阴性对照组,依普拉芬高、中、低剂量组和雌激素对照组(各10只),分别给予基础饲料和不同剂量的依普拉芬,12周后测定血清NO及NOS.结果 与假手术组相比,去卵巢大鼠阴性对照组血清NO及NOS明显降低,依普拉芬组高于阴性对照组,与假手术组比较差异无统计学意义.同时低于雌激素组.结论 NO及NOS参与了骨质疏松的病理生理过程;依普拉芬可以通过提高去卵巢大鼠血清NO及NOS浓度达到防治绝经后骨质疏松症的作用.     

老年糖尿病合并高血压患者血清内脂素与一氧化氮、一氧化氮合酶的关系

目的：研究老年糖尿病（DM）合并高血压（HT）患者血清内脂素（visfatin）水平的变化及与一氧化氮（NO）、一氧化氮合酶（NOS）的关系.方法：选择合并HT和血压正常老年DM患者各60例、正常老年人30例,测定其血清visfatin、NO、NOS水平.结果：与血压正常组比较合并HT老年DM患者血清visfatin明显升高（P＜0.01）,血清NO、NOS水平明显降低.（P＜0.01）.合并HT老年DM患者血清visfatin与平均动脉压（MAP）呈明显正相关（P＜0.01）,血清NO、NOS水平与MAP呈明显负相关（r=-0.587,r=-0.641,均P＜0.01）.血清visfatin与NO、NOS水平呈明显负相关（r=-0.628,r=-0.663,均P＜ 0.01）.结论：老年DM合并HT患者血清visfatin明显升高,血清NO、NOS水平明显降低,血清visfatin与NO、NOS相互作用在老年DM合并HT的发生发展中发挥重要作用.     

糖尿病合并高血压患者血清脂联素与一氧化氮、一氧化氮合酶的关系

目的：观察糖尿病合并高血压患者血清脂联素与一氧化氮、一氧化氮合酶水平变化,探讨患者血清脂联素与一氧化氮、一氧化氮合成酶的关系。方法：应用酶联免疫吸附法及硝酸还原酶比色法测定50例合并高血压糖尿病患者及30例血压正常糖尿病患者血清脂联素与一氧化、氮一氧化氮合成酶水平。结果：合并高血压糖尿病患者血清脂联素,一氧化氮、一氧化氮合成酶水平较血压正常糖尿病患者明显那降低（均P＜0.01）。合并高血压糖尿病患者血清脂联素与一氧化氮、一氧化氮合酶呈明显正相关（r=0.651,r=0.536,均P＜0.01）。结论：血清脂联素,一氧化氮、一氧化氮合酶水平降低,脂联素与一氧化氮、一氧化氮合酶相互作用相互影响,在糖尿病合并高血压的发病中发挥重要作用。     

清脑镇痛液对偏头痛动物模型血清中一氧化氮、一氧化氮合酶含量的影响

目的研究清脑镇痛液对偏头痛模型NO、NOS含量的影响。方法 wistar大鼠随机分为6组:高、中、低剂量组、阳性对照组、偏头痛模型组、空白对照组。皮下注射NTG复制偏头痛模型,造模4h后测定各组NO、NOS的含量。结果模型组NO、NOS含量与空白对照组比较均有显著性升高(P<0.01)。高剂量组及阳性对照组NO、NOS含量与模型组比较均有显著性降低(P<0.01)。结论清脑镇痛液可抑制由NTG诱导的NO和NOS异常升高水平,从而发挥治疗偏头痛的作用。     

糖皮质激素对双氯氛酸钠肝损伤大鼠一氧化氮合酶及一氧化氮的影响

目的探讨糖皮质激素地塞米松(Dex)对双氯氛酸钠(Dcf)肝损伤大鼠一氧化氮合酶(NOS)表达及一氧化氮(NO)的影响。方法大鼠随机分为正常组、Dcf组及Dex组。Dcf组给予Dcf 100 mg/kg腹腔注射,Dex组在Dcf注射前1 h予10 mg/kg腹腔注射,24 h后测血清ALT、AST、TBil水平观察肝组织病理学变化,化学法检测血清及肝组织NO含量,免疫组化法检测肝组织内皮型NOS(eNOS)和诱导型NOS(iNOS)的表达。结果 Dcf组血清ALT、AST、TBil水平明显升高(P<0.05),病理积分大幅度增高,血清和肝组织NO含量明显高于正常组(P<0.01),肝组织iNOS表达显著增强(P<0.01),eNOS表达减弱。Dex可明显改善升高的转氨酶及病理积分(P<0.05),并降低肝组织iNOS表达及NO含量(P<0.05)。结论 iNOS和NO在Dcf肝损伤中起促进作用,糖皮质激素可能通过抑制体内iNOS表达,减少NO合成起到肝保护作用。     

香菇多糖对巨噬细胞一氧化氮和一氧化氮合酶活性的影响

目的研究香菇多糖(LTN)诱导巨噬细胞的一氧化氮(NO)生成和一氧化氮合酶(iNOS)的活性,探讨LTN的免疫调节作用机理.方法采用Griess反应和荧光法测定不同剂量的LTN作用小鼠腹腔巨噬细胞后NO的生成量和iNOS活性.观察mRNA转录抑制剂、蛋白质合成抑制剂和iNOS抑制剂对巨噬细胞NO的生成和iNOS活性的影响.结果LTN能使小鼠腹腔巨噬细胞NO生成增加,iNOS活性增高,并呈作用剂量依赖关系.3种抑制剂均能抑制LTN诱导的小鼠腹腔巨噬细胞N0的生成和iNOS活性.结论LTN能刺激小鼠腹腔巨噬细胞提高iNOS活性和NO的生成.提示LTN的免疫调节作用机制可能与LTN刺激巨噬细胞NO生成有关.     

The effect of nitric oxide synthase blockers,nitric oxide donors,and anti-ovarian antibodies on murine oocytes

The effects of NO synthase (NOS) blockers, NO donors, and anti-ovarian antibodies (AOABs) on the amount of oocytes isolated from murine ovary and their meiotic maturation were studied. It was established that the NOS blockers inhibit the their meiotic maturation of oocytes, while NO donors influenced neither the number of oocytes nor their ability to meiotic maturation in diaestrus or oestrous cycle. The AOAB effect on the gametogenesis was dose-dependent: inhibition for large doses and activation for small doses. The NO/NOS ovarian system is involved into mechanism of the AOAB action on murine oocytes. It is suggested that a decrease in the ovarian NO production, as well as the AOAB-induced inhibition of the murine oogenesis, are factors influencing female infertility.     

The effect of divalent cations on neuronal nitric oxide synthase activity.

Neuronal nitric oxide synthase (NOS I) is a Ca(2+)/calmodulin-binding enzyme that generates nitric oxide (NO*) and L-citrulline from the oxidation of L-arginine, and superoxide (O(2)*(-)) from the one-electron reduction of oxygen (O(2)). Nitric oxide in particular has been implicated in many physiological processes, including vasodilator tone, hypertension, and the development and properties of neuronal function. Unlike Ca(2+), which is tightly regulated in the cell, many other divalent cations are unfettered and can compete for the four Ca(2+) binding sites on calmodulin. The results presented in this article survey the effects of various divalent metal ions on NOS I-mediated catalysis. As in the case of Ca(2+), we demonstrate that Ni(2+), Ba(2+), and Mn(2+) can activate NOS I to metabolize L-arginine to L-citrulline and NO*, and afford O(2)*(-) in the absence of L-arginine. In contrast, Cd(2+) did not activate NOS I to produce either NO* or O(2)*(-), and the combination of Ca(2+) and either Cd(2+), Ni(2+), or Mn(2+) inhibited enzyme activity. These interactions may initiate cellular toxicity by negatively affecting NOS I activity through production of NO*, O(2)*(-) and products derived from these free radicals.     

慢性阻塞性肺疾病患者外周血脂肪炎症因子一氧化氮一氧化氮合成酶水平及其意义

目的分析慢性阻塞性肺疾病(COPD)患者外周血脂肪炎症因子、一氧化氮(NO)、一氧化氮合成酶(NOS)水平及其意义。方法选取我科2013年1月至2015年1月COPD稳定期患者共49例。根据是否存在肺动脉高压,分为COPD伴肺动脉高压组和COPD不伴肺动脉高压组。选取同期行体检健康志愿者22名作为对照组。对比3组外周血脂肪炎症因子、NO和NOS水平。结果 COPD伴肺动脉高压组的外周血脂肪炎症因子、NO、NOS水平显著低于COPD组不伴肺动脉高压组和对照组(P<0.05);COPD组不伴肺动脉高压组的外周血脂肪炎症因子、NO、NOS显著低于对照组(P<0.05)。COPD伴肺动脉高压组、COPD组不伴肺动脉高压组和对照组的脂肪炎症因子和NO、脂肪炎症因子和NOS、NO和NOS之间均具有相关性(P<0.05)。结论在COPD患者,特别是合并肺动脉高压的患者中,脂肪炎症因子、NO、NOS显著下降,说明三者代谢异常可能和肺循环稳态失衡密切相关。     

血清一氧化氮及一氧化氮合酶体系与轻度胃肠炎合并婴幼儿良性惊厥的相关性研究

目的探讨一氧化氮(NO)及一氧化氮合酶(NOS)体系在轻度胃肠炎合并婴幼儿良性惊厥(BICE)发病机制中的作用。方法收集2010年1月至2012年7月于山西省儿童医院诊治的BICE患儿40例、热性惊厥患儿26例、轮状病毒肠炎患儿14例及同期门诊体检的健康儿童30名,分别采用硝酸还原酶法、酶测定法检测血清中NO水平,总一氧化氮合酶(TNOS)水平及诱导型一氧化氮合酶(iNOS)水平。结果 BICE组患儿血清NO及iNOS水平明显高于健康儿童、热性惊厥组及轮状病毒肠炎组患儿(P<0.05),但TNOS水平各组间差异无统计学意义(P>0.05)。BICE严重组及普通组患儿血清NO水平差异无统计学意义(t=1.25,P>0.05),BICE轮状病毒阳性组与阴性组患儿血清中NO水平差异无统计学意义(t=1.12,P>0.05)。结论 iNOS增加而导致的NO水平升高,可能与BICE患者的发病有关。     

Mitochondrial nitric oxide synthase

Mitochondria produce nitric oxide (NO) through a Ca(2+)-sensitive mitochondrial NO synthase (mtNOS). The NO produced by mtNOS regulates mitochondrial oxygen consumption and transmembrane potential via a reversible reaction with cytochrome c oxidase. The reaction of this NO with superoxide anion yields peroxynitrite, which irreversibly modifies susceptible targets within mitochondria and induces oxidative and/or nitrative stress. In this article, we review the current understanding of the roles of mtNOS as a crucial biochemical regulator of mitochondrial functions and attempt to reconcile apparent discrepancies in the literature on mtNOS.     

The effect of nitric oxide synthase blockade on responses to morphine in rat aortic rings

1 It has been suggested that opioids may play an indirect role in the regulation of the peripheral circulation through the control of nitric oxide (NO) release in vascular tissue. The current study was undertaken to investigate the effect of nitric oxide synthase (NOS) blockade on responses to morphine in phenylephrine (PE)- or KCl-precontracted rat aortic rings. 2 Morphine (3 x 10(-8) - 3 x 10(-5) M) administration did not cause any significant effect on basal tonus of endothelium-intact or endothelium-denuded preparations. Morphine produced concentration-dependent relaxation responses in endothelium-intact as well as in endothelium-denuded rat aortic rings precontracted by PE or KCl. Removal of endothelium did not significantly alter the relaxation responses to morphine. 3 The relaxant responses to morphine were significantly and partially inhibited by pretreatment of tissues with naloxone (NAL, 3 x 10(-5) M) for 5 min. The inhibitory effect of NAL on relaxant responses to morphine in PE- or KCl-precontracted rings did not differ significantly between endothelium-intact and endothelium-denuded preparations. 4 Incubation of endothelium-intact or endothelium-denuded rat aortic rings with NOS inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) for 20 min did not cause a significant inhibition on relaxation responses to morphine. 5 These findings confirmed the presence of opiate receptors in rat thoracic aorta, but suggested that mechanisms other than NO release play a role in the relaxant effect of morphine on rat aortic rings.     

氯沙坦对肝硬化大鼠血清内毒素及一氧化氮的影响

目的:探讨氯沙坦对肝硬化大鼠血清一氧化氮(NO)、内毒素水平的影响.方法:成年雄性Wistar大鼠肝硬化形成后,随机分为两组,即模型组、氯沙坦治疗组,另取6只正常大鼠作为正常组.治疗21 d,采取硝酸还原酶法测量血清NO水平、鲎试剂偶氮显色法测量内毒素水平.结果:与正常组大鼠相比,模型组大鼠血清NO与内毒素水平显著增高.治疗组与模型组相比,上述指标降低具有显著性.结论:氯沙坦可降低肝硬化大鼠血清NO、内毒素水平.     

小剂量阿司匹林对LDL所致内皮损伤的保护作用与内源性一氧化氮合酶抑制物的关系

目的研究阿司匹林对低密度脂蛋白(LDL)诱导的血管内皮损伤的保护作用与内源性一氧化氮合酶抑制物的关系.方法 SD大鼠在乙醚麻醉下,舌下静脉注射人血清LDL(4 mg·kg-1)诱发血管内皮功能损伤.检测血中非对称性二甲基精氨酸(ADMA)、丙二醛(MDA)和肿瘤坏死因子α(TNF-α)的含量,以及二甲精氨酸二甲胺水解酶(DDAH)活性,并观察离体胸主动脉环的内皮依赖性舒张反应.结果单次静脉注射LDL(4 mg·kg-1)显著抑制乙酰胆碱(ACh)诱导的内皮依赖性舒张,增加血液中ADMA、MDA和TNF-α水平,降低DDAH活性.两个剂量阿司匹林(30或100 mg·kg-1)均能显著减轻LDL所致ACh诱导内皮依赖性舒张的损伤,但较大剂量阿司匹林作用较小剂量阿司匹林组作用为弱;两个剂量阿司匹林也能抑制LDL所致MDA和TNF-a浓度升高;小剂量阿司匹林能显著抑制ADMA浓度升高和增加DDAH活性,但较高剂量的阿司匹林对ADMA浓度和DDAH活性无影响.结论小剂量阿司匹林对LDL诱导的血管内皮细胞损伤有保护作用,其保护作用与增加DDAH活性和降低ADMA浓度有关.     

Inducible nitric oxide synthase and inflammation

Nitric oxide (NO), derived from L-arginine (L-Arg) by the enzyme nitric oxide synthase (NOS), is involved in acute and chronic inflammatory events. In view of the complexity associated with the inflammatory response, the dissection of possible mechanisms by which NO modulates this response will be profitable in designing novel and more efficacious NOS inhibitors. In this review we describe the consequences associated with the induction of inducible nitric oxide synthase (iNOS) and its therapeutic implications.