一氧化氮

Although nitric oxide hyperproduction due to inducible NO synthase is observed in asthma and COPD, nitrotyrosine formation via the reaction between NO and O(2)- in addition to the myeloperoxidase-mediated pathway.

虽然哮喘和COPD患者均存在由诱导型一氧化氮合成酶催化的一氧化氮过度产生，但是，硝基酪氨酸主要通过除髓过氧化物酶介导途径之外的NO和超氧阴离子反应形成。

METHODS: D-galactose (1 000 mg·k-1·d-1 ) was injected into mice hypodermically for 8 weeks to induce aging animal model, and Vit-E (100 mg·kg-1; 250 mg·kg-1) was administered for 6 weeks by ig at the 3rd week of making model. After Vit-E treatment for 8 weeks, water maze test was used to determine the ability of mice's learning and memory. The activities of glutathione peroxidase and succinate dehydrogenase, the content of nitric oxide and activity of nitric oxide synthase in the brain tissue were detected separately.

小鼠连续皮下注射D-半乳糖（1 000 mg·k-1·d-1）8周制备衰老模型，并于第3周开始给予维生素E（100 mg· kg-1；250 mg· kg-1）处理；8周后采用水迷宫测定小鼠学习记忆能力，并取脑组织测定谷胱甘肽过氧化物酶和琥珀酸脱氢酶活性，测定一氧化氮含量和一氧化氮合酶活性。

It is suggested that these nerves may participate in the relaxation and constriction of the nonvascular smooth muscles. Perivascular nerve fibers in the genital organs may play an im-ortant role in the regulation of the uterine vascular tone.

分析雌性大鼠生殖器官内一氧化氮合酶Ⅰ免疫反应阳性神经纤维的分布，提示一氧化氮可能与血管活性或非血管平滑肌运动调节有关。

Whereas, large dose of L-NAME raised the MABP significantly, constricted pial arteriole (90 minutes, 10%), decreased regional spinal cord blood flow (90 minutes, 22%), augmented the dysfunction of neural system.

表明一氧化氮在继发性脊髓损伤中，小剂量的一氧化氮可能起到保护作用，但过量时又可起到破坏作用。

The diastolic function of sphincter of Oddi is impaired by hypercholesterolemia and the sphincter of Oddi is in a spasmic state, which may be caused by the hypercholesterolemia-related abnormal response to nitric oxide or the decreased activity of nitric oxide.

原因可能与高胆固醇改变了细胞膜的生物学特性致胆道口括约肌对一氧化氮的反应异常或者与降低、抑制了一氧化氮的活性有关。

On the normotensive rat, bilateral microinjection of L-arginine (16 n mol/0.1 ul/site), a precursor of nitric oxide into the rVLM, caused a decrease in BP, HR and the pressor response induced by the dPAG stimulation, while microinjection of NG-methyl-Larginine (L-NMMA, 16 n mol/0.1 ul/site), a blockade for NO to form, into the rVLM bilaterally, caused an increase in BP, HR and the pressor response induced by the dPAG stimulation. There was no effect of both drugs mentioned above on the tachycardiac response induced by the dPAG stimulation.

五、在正常血压大鼠，于双侧rVLM微量注射一氧化氮前体(16nmol/0.1μl/site)可引起BP降低、HR减慢、以及电刺激dPAG诱发的防御性升压反应减弱；而于同区微量注射生成一氧化氮的拮抗剂N〓-甲基-L-精氨酸(16nmol/0.1μl/site)则可引起BP升高、HR加快、以及电刺激dPAG诱发的防御性升压反应增强；而上述两药对电刺激dPAG诱发的防御性加快心率反应均无明显作用。

Objective: To investigate the inhibitory effect of a new highly se lective inducible nitric oxide synthase inhibitorNGnitroargininelysine tripeptide on cNOS and iNOS indu ction .

目的：研究硝基精氨酸赖氨酸三肽对组成型一氧化氮合酶和诱导型一氧化氮合酶的抑制程度。

In this study, we examined this point in mice deficient in all 3 NOS isoforms (triply n/i/eNOS-/- mice) that we have recently developed.

本试验中，我们使用最近培育出的缺少三种一氧化氮合酶亚型的小鼠(triply n/i/eNOS-/- mice)以阐明体内一氧化氮的作用。

Methods and Results-: The triply n/i/eNOS-/- mice, but not singly eNOS-/- mice, exhibited markedly reduced survival, possibly due to spontaneous myocardial infarction accompanied by severe coronary arteriosclerotic lesions.

方法和结果--这种一氧化氮合酶亚型三重缺陷而非单一内皮型一氧化氮合酶缺陷的小鼠存活率显著降低，很可能是因为严重的冠状动脉硬化损害并伴发自发性心肌梗死。

Objective To investigate The Changes and effects of nitric oxide and its synthase in the serums and cerebrospinal fluids on Patients with viral encephalitis.

目的 探讨病毒性脑炎患儿血清及脑脊液中一氧化氮、一氧化氮合成酶的变化及临床意义。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。