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1. 目的：研究辣椒素對大鼠面部皮膚一氧化氮合酶陽性神經(jīng)的影響一氧化氮，探討CAP治療三叉神經(jīng)的鎮(zhèn)痛機(jī)制。

Objective:To research the effect of capsicin on the NOS in rat facial skin, and to explore the analgesic mechanism of CAP in treating prosopalgia thereby.

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2. 目的 研究電針對抑郁癥模型大鼠陰莖組織一氧化氮和環(huán)磷酸鳥苷的影響。

Objective To investigate the effect of electroacupuncture on nitric oxide and cyclic guanosine monophosphate levels in penile tissues of rats with depression.

3. 目的 觀察麥芽醇對大鼠局灶性腦缺血再灌注損傷后誘導(dǎo)型一氧化氮合酶的影響。

ABSTRACT:Objective To investigate the effects of maltol on the expression of iNOS after focal cerebral ischemia reperfusion injury in rats.

4. 探討神經(jīng)型一氧化氮合酶抑制劑7-硝基吲唑(7-NI)在煙霧吸入性肺損傷中的作用。40只SD雄性大鼠被隨機(jī)分為正常對照組(n=8)、煙霧吸入性肺損傷模型組(n=16)和7-NI治療組(n=16)，建立煙霧吸入性肺損傷模型。7-NI治療組在致傷后立即腹腔注射7-NI 20 mg/kg(溶于2 ml花生油中)；正常對照組及模型組腹腔注射2 ml花生油。

M{rX*o0 OBJECTIVE: To investigate the effects of neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) on smoke inhalation pulmonary injury in rats. METHODS: Forty healthy male SD rats were randomly divided into three groups: control group (n=8), smoke inhalation model group (n=16) and 7-NI treatment group (n=16). After reproducing the smoke inhalation model, to the 7-NI treatment group rats 7-NI (20 mg/kg in 2 ml arachis oil) was administered by intraperitoneal injection, while in the control group and the model group, 2 ml arachis oil was administered by intraperitoneal injection.

5. 探討神經(jīng)型一氧化氮合酶抑制劑7-硝基吲唑(7-NI)在煙霧吸入性肺損傷中的作用。40只SD雄性大鼠被隨機(jī)分為正常對照組(n=8)、煙霧吸入性肺損傷模型組(n=16)和7-NI治療組(n=16)一氧化氮，建立煙霧吸入性肺損傷模型。7-NI治療組在致傷后立即腹腔注射7-NI 20 mg/kg(溶于2 ml花生油中)；正常對照組及模型組腹腔注射2 ml花生油。

After reproducing the smoke inhalation model, to the 7-NI treatment group rats 7-NI (20 mg/kg in 2 ml arachis oil) was administered by intraperitoneal injection, while in the control group and the model group, 2 ml arachis oil was administered by intraperitoneal injection.

6. 目的 觀察急性應(yīng)激對大鼠血小板一氧化氮釋放的影響及其機(jī)制。

Objective To investigate the effect of water-immersion restraint stress on nitric oxide production and its mechanism in rat platelets.

7. 目的：探討一氧化氮及內(nèi)皮素在支氣管哮喘發(fā)病中的作用。

Objective:To investigate the role of serum nitric oxide and endothelin in bronchial asthmatic attack.

8. 一氧化氮

8. 這些現(xiàn)象被認(rèn)為與血紅蛋白和一氧化氮之間的氧化還原與和結(jié)合過程相關(guān)。

These phenomena are proposed to be related with the electron transfer and binding process between hemoglobin and NO.

9. 一氧化氮

9. 黃芪對鯉頭腎中巨噬細(xì)胞的增殖和一氧化氮產(chǎn)量的影響：離體研究。

Effect of Astragalus radix on proliferation and nitric oxide production of head kidney macrophages in Cyprinus carpio:an in vitro study.

10. 因此 ，本文旨在觀察茶色素對內(nèi)皮細(xì)胞一氧化氮合酶生成的影響。1 材料與方

The results suggest that the effect of tea pigments on eNOS expression is one of the mechanisms of its antiatheroselerosis.

11. 靈芝孢子；腹根切斷：運動神經(jīng)元；神經(jīng)營養(yǎng)素-3；一氧化氮合酶；神經(jīng)元存活；免疫組織化學(xué)；原位雜交；大鼠

Ganoderma spore; Ventral root cut; Motor neuron; Neurotrophin_3（NT_3）; Nitric oxide synthase; Neuronal survival; Immunohistochemistry; In situ hybridization; Rat

12. 一氧化氮

12. 目的：探討一氧化氮的前體物質(zhì)精氨酸對急性胰腺炎大鼠止凝血指標(biāo)的影響。

Objective:To evaluate the effect of the arginine on thehematologic disorders of rat acute pancreatitis.

13. 呼出的一氧化氮和PEF變化無顯著關(guān)系。

No significant relationship was evidenced between exhaled NO and PEF variations.

14. 一氧化氮的近義詞

14. 結(jié)果：急性胰腺炎期間會損害肺的氧合能力、代謝情況，以及引起乳酸酸中毒和呼出氣一氧化氮水平升高一氧化氮，而這些情況在假手術(shù)組中顯示可被 TEA 所改善。

RESULTS: Deteriorated oxygenation, metabolic and lactate acidosis, as well as exhaled nitric oxide levels occurring during acutepancreatitis, were reduced by TEA to levels observed in sham-operatedanimals.

15. 本實驗通過建立重癥急性胰腺炎大鼠動物模型，動態(tài)觀察血漿和肺組織內(nèi)一氧化氮(Nitric oxide，NO)產(chǎn)生的變化，及誘導(dǎo)型一氧化氮合酶的表達(dá)，探討一氧化氮與重癥急性胰腺炎肺損傷的關(guān)系，觀察生長抑素類似物奧曲肽對肺損傷的治療作用。

To investigate the possible beneficial effects andthe mechanism of octreotide on the lung injury severe acutepancreatitis rats. The experimental rat model of severe acutepancreatitis was induced by retrograde cholangiopancreatic ductinjection of 5% sodium taurocholate.

16. 一氧化氮

16. 4一氧化氮(Nitric Oxide，NO)供體——釩酸鈉(Sodium Metavanadate，vanadate)和硝普鈉(Sodium Nitroprusside，SNP)都能夠抑制DFO誘導(dǎo)的白血病細(xì)胞凋亡，但對CoCl2誘導(dǎo)的細(xì)胞凋亡沒有抑制作用。

In no alteration of HIF-1αprotein, nitric oxide donors, metavanadate and sodium nitroprusside, significantly abrogated DFO-induced apoptosis.

17.

17. 綜合本研究的結(jié)果，不只顯示了PTPs 半胱胺酸亞硝基化作用重要的基本分子機(jī)制，并且證實了一氧化氮藉由亞硝基化作用影響PTPs活性而扮演重要細(xì)胞生理調(diào)控的角色。

Our results not only reveal the fundamental basis for the mechanistic detail of Cys nitrosylation of PTPs, but offer insights into a novel biological role of NO that may govern tyrosine phosphorylation-dependent signaling through regulation of cellular PTPs.

18. 所有納入病例均排除以下患有引起繼發(fā)性骨質(zhì)疏松癥的各種內(nèi)分泌疾病者（如柯興氏病、甲狀腺功能亢進(jìn)、甲狀旁腺功能亢進(jìn)、甲狀腺囊腫或機(jī)能低下、糖尿病等）；其他嚴(yán)重疾病干擾骨代謝者；測試前3個月內(nèi)未使用過雌激素、降鈣素、一氧化氮、糖皮質(zhì)激素等干擾骨代謝或?qū)?nèi)皮素有影響作用的藥品；測試前1年內(nèi)無骨折；患有嚴(yán)重心腦血管等與內(nèi)皮素水平相關(guān)密切之疾病及肝腎功能異常者。

All patients with secondary osteoporosis caused by all endocrine diseases including Cushing's disease, hyperthyrosis, hyperparathyroidism, capsula glandulae thyroideae or thyroid hypofunction and diabetes, and patients whose bone metabolism was interfered by grave diseases were excluded. Three months before the trial, the patients did not receive any drug that could interfere the bone metabolism or affect endothelin, such as estrogenic hormone, calcitionin, nitrogen monoxidum, glucocorticoid. In addition, the patients suffering from bone fracture within 1 year or grave cardio-cerebrovascular disease, which had intimate correlation with endothelin, liver and kidney disfunction were eliminated.

19. 放療副作用自由基損傷會影響相矢基因的產(chǎn)物表達(dá)，如：一氧化氮合成必需酶NOS，抗凋亡基因h－2，抑癌基因P53 ％D腫瘤血管生成密切相矢的VEGF氧氣報警器，抗氧化劑則有一定的抑制作用。

We also find that the local radiation can cause the more expression of some genes such as p53 and NOS, at the same time reduce the expression of bcl-2 and VEGF. But the antioxidants have the reverse effect.

20. 目前僅有少量文獻(xiàn)報道一氧化氮（nitric oxide甲烷報警器，NO）在腎臟血管反應(yīng)性的調(diào)控中起一定作用［23］，過氧亞硝基陰離子（peroxynitrite，ONOO-）對腎血管反應(yīng)性的影響尚未見報道。

Methods IPK was used to examine the effects of renal IR on renal vascular response, the effects of iNOS inhibition on the renal vascular response changes caused by renal IR, and the effects of administration of ONOO- on above parameters.

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