铈对原代肝细胞内NOS和NO的影响

研究了Ce3+对肝细胞中一氧化氮(NO)和一氧化氮合酶(NOS)的影响.结果表明,Ce3+能使肝细胞中NO含量和NOS活性增加.提示Ce3+有可能影响cGMP信号系统.     

半滑舌鳎组织器官中一氧化氮含量和一氧化氮合酶活性的测定

[目的]研究半滑舌鳎不同组织器官中一氧化氮(NO)含量和不同类型一氧化氮合酶(NOS)活性.[方法]采用Griess试剂法测定NO含量,采用化学比浊法测定NOS的活性.[结果]诱导型一氧化氮合酶(iNOS)在肌肉组织中活性最高,为28.774±4.10U/mgprot,依次为肠、脑、肝脏、头肾、鳃、中肾、脾脏、心脏.肠和脑之间以及肝脏和头肾之间iNOS的活性不存在显著性差异,而其他组织器官之间iNOS的活性都存在显著性差异.结构型一氧化氮合酶(cNOS)在肠组织中活性最高,为55.979±5.048 U/mgprot.所测组织器官中cNOS活性都存在显著性差异.NO含量在脾脏中最高,为38.540±4.535μmol/L.脾脏、头肾、肝脏之间,以及脑、心脏、中肾之间NO含量不存在显著性差异,而其他组织器官之间NO含量都存在显著性差异.[结论]不同组织器官中NO含量和NOS活性不同,这可能与组织器官功能有着密切联系.     

羊体内脏中稀土元素分布特征研究

取自蒙古国境内,自然放牧和喂食添加稀土饲料的羊,宰杀后,立即取出内脏,利用微波消解仪溶解样品,电感耦合等离子体质谱法测定其中的稀土元素。研究了稀土元素在心、肝、脾、胃、肾中的分布特征。结果表明,稀土总量∑REE0.31μg/g~4.59μg/g,平均为1.85μg/g,轻重稀土比值在5.10~19.57之间,平均为11.88,由LREE/HREE值可以看出轻稀土含量明显高于重稀土,这可能与包头地区的稀土分布有关;用稀土饲料喂养的羊的内脏中的稀土含量明显优于自然放牧的,尤其是肝和肾;包头地区的稀土主要以轻稀土为主,只有少量的重稀土,但肝脏中Gd、Tb、Er通过稀土饲料喂养后,相对富集;肾脏中Gd、Tb、Dy、Er、Y通过稀土饲料喂养后,相对富集。     

稀土对Cr25Ni5Mo2Cu3REx双相钢组织和性能的影响

本文以Cr25Ni5Mo2Cu3REx双相不锈钢为对象,采用金相显微镜、万能拉伸试验机、冲击试验机和恒电位仪分析测试手段,研究了1#稀土加入量对Cr25Ni5Mo2Cu3REx双相不锈钢的显微组织、力学性能及腐蚀性能的影响规律。试验结果表明,奥氏体相随着1#稀土加入量的增加先增加后减少,强度随着1#稀土加入量的增加而增加,塑性、韧性和腐蚀性能随1#稀土加入量的增加先增大后下降。当1#稀土加入量在0.10%时,Cr25Ni5Mo2Cu3REx双相不锈钢综合性能最好。     

稀土对HAl62-3-3-0.7合金组织和性能的影响

通过对合金成分的调整分别配制了添加不同量稀土元素的试验用HAl62-3-3-0．7合金。借助金相与扫描电镜观察和分析了各合金的显微组织结构，运用模拟设备测试了各合金的力学性能。文章阐述了稀土元素对该类高强度耐磨黄铜的组织和性能的影响，试验表明适量加入稀土会显著细化晶粒，过量的稀土会导致在合金显微组织中形成线形富稀土相。随着合金中稀土含量的增加，合金的硬度升高，但当稀土含量超过0．1％时，由于线形富稀土相的形成，反而会使合金的力学性能下降。     

稀土对碳素钢在模拟工业性大气腐蚀环境下耐蚀性的影响

 利用浸泡、电化学方法研究了Ce/La混和稀土对碳素钢在腐蚀介质中的缓蚀作用,采用相分析、周浸、锈层分析等方法研究了稀土对碳素钢耐工业性大气腐蚀性能的影响。结果表明：在模拟工业性大气腐蚀环境的酸性NaHSO3溶液中,稀土丝分解后生成的稀土离子是一种混合型缓蚀剂;在对碳素钢的缓蚀过程中,Ce/La离子沉积于同一区域;随钢中稀土含量增加,钢中相界固溶稀土和稀土/铁金属间化合物总量增加,钢的耐蚀性得到大幅度提高。另外,还对稀土减缓钢铁腐蚀过程进行了讨论,提出了稀土对碳素钢的缓蚀机理。     

P_(507)-盐酸体系中氯化铵对RE~(3+)萃取分离的影响研究

针对稀土溶剂萃取分离过程中的氨氮问题,进行了氯化铵对稀土萃取分离过程的影响研究,结果表明,在实验采用的PrCl_3、TmCl_3、NdCl_3、YbCl_3、GdCl_3、SmCl_3溶液中,氯化铵的溶解度随稀土离子浓度的增大而减小,除SmCl_3溶液外,几乎呈线性关系;氯化铵浓度在饱和状态下,稀土溶液的粘度随着稀土浓度的增加而增大,除YbCl_3、SmCl_3溶液外,几乎呈线性关系;氯化铵的加入,几乎不影响稀土饱和萃取容量、稀土萃取分离系数、反萃率。     

不同运动负荷对大鼠海马组织NGF和nNOS表达的影响及其意义

目的:探讨不同运动负荷对大鼠海马组织神经生长因子(NGF)和神经型一氧化氮合酶(nNOS)表达的影响及机制,为运动干预脑健康及预防脑老化研究奠定基础.方法:40只Wistar雄性大鼠随机分为不进行运动干预的对照组和每天进行15、30和60 min的小、中、大游泳运动负荷的实验组,实验8周后取大鼠脑组织,免疫组织化学S-P法检测大鼠海马组织NGF和nNOS表达水平及形态学表现.结果:与对照组比较,小、中、大运动负荷组大鼠海马组织NGF阳性表达水平均明显升高(P<0.05,P<0.01);与小运动负荷组比较,中、大运动负荷组大鼠海马组织NGF阳性表达水平升高(P<0.01),但中等运动负荷组大鼠与大运动负荷组比较差异无统计学意义(P>0.05).与对照组比较,中、大运动负荷组大鼠海马组织nNOS阳性表达水平升高(P<0.01);与小运动负荷组比较,中、大运动负荷组大鼠海马组织nNOS阳性表达水平升高(P<0.05,P<0.01),大运动负荷组大鼠海马组织nNOS阳性表达水平高于中运动负荷组(P<0.01).免疫组织化学染色:大鼠海马组织NGF阳性神经元主要表达在神经细胞胞浆,呈棕色;nNDS阳性神经元呈棕褐色,着色主要位于胞浆.结论:大脑海马组织NGF和nNOS的表达水平在一定范围内随着运动负荷的增加而升高,提示在不同的运动负荷阶段NGF和nNOS对海马神经的生长和损伤的修复具有重要作用.     

稀土对Al-4.5%Cu合金作用的研究

本文介绍了富铈及富镧混合稀土对Al-4.5%Cu合金的充型能力、抗热裂性、晶粒度以及力学性能的影响。稀土含量为0.3%时,流动性试样长度增加37～120%,充型面积增加了37%,抗热裂性能也提高。加入0.3%富La混合稀土的Al-4.5%Cu合金%提高33MPa,相对值提高20%;δ提高了1.7%,相对值提高55%。由于稀土的加入,晶粒也大为细化,加入0.3%稀土后,单位长虞上的晶粒数增加了1.5倍。文章还介绍了稀土对合金润湿角的影响。     

稀土硬质合金及注射成形技术

北京有色金属研究总院近日向社会推出稀土硬质合金及注射成形技术。据介绍 ,在现有硬质合金牌号的成分中加入稀土元素后 ,大大改善了合金的强度、硬度及韧性 ,并提高合金的抗氧化性等 ,在国内外具有特色。采用注射成形工艺开发的硬质合金螺旋铣刀产品 (2～4 8mm) ,具有广阔的应用前景。稀土硬质合金可用于制作机加工行业的各种刀具 ,石油钻井行业的各种喷嘴、钻头齿柱以及模具和各种矿业工具等。根据不同的用途 ,选择不同牌号的合金 ,从而制定相应的技术指标。本稀土合金注射成形技术已获得美国专利。稀土硬质合金及注射成形技术@耀星…     

Effects of nitric oxide synthase inhibition and endothelin ETA receptor blockade on haemodynamics in hypertensive rats

1. The objectives of the present study were to study regional differences in haemodynamics between spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats induced by the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) and the endothelin ETA receptor antagonist BQ 123 in vivo in tissues known to be important for blood pressure (BP) regulation (heart, kidney and skeletal muscle). Furthermore, the effect of acetylcholine (ACh) infusion (2 micrograms/kg per min) was examined after L-NMMA or BQ 123. The microsphere method was used for determinations of cardiac index (CI) and regional haemodynamics. 2. NG-Monomethyl-L-arginine (20 mg/kg) increased BP (26-48%; P < 0.01) and reduced CI in both rat strains. BQ 123 (1 mg/kg) reduced BP slightly (-4 to 11%; P < 0.05). 3. NG-Monomethyl-L-arginine significantly increased myocardial and skeletal muscle vascular resistance in SHR only; however, in the kidney, L-NMMA reduced blood flow and increased vascular resistance in both rat strains. 4. BQ 123 induced minor changes in regional haemodynamics that were not significantly different between the two strains. 5. Acetylcholine following BQ 123 induced an increase in myocardial blood flow in WKY rats, but decreased blood flow in SHR. Acetylcholine following L-NMMA reduced myocardial blood flow in both strains. 6. Acetylcholine following BQ 123 induced renal vasodilation in WKY rats but, following L-NMMA, ACh did not induce renal vasodilation in either rat strain. In contrast, L-NMMA did not abolish the vasodilation of acetylcholine in skeletal muscle in WKY rats. 7. In conclusion, the contribution of nitric oxide to basal vessel tone was not impaired in the heart, skeletal muscle and kidney in SHR. Antagonism of ETA receptors caused similar haemodynamic responses in both rat strains in these organs. Furthermore, NOS inhibition, but not ETA blockade, blunted the expected ACh-induced vasodilation in the heart and kidney in WKY rats, but not in skeletal muscle in both strains.     

Variability of plasma HDL subclass concentrations in men and women over time

1. Nitric oxide (NO) has been suggested as a gastrointestinal neurotransmitter, mediating the gastric receptive relaxation and the relaxation in the peristaltic reflex. The aim of the present study was to measure nerve-induced NO formation in vivo in the gastrointestinal tract. 2. Formation of the nitric oxide oxidation products nitrite and nitrate during vagal nerve stimulation were measured in the anaesthetized rabbit. Microdialysis probes were inserted into the wall of the stomach and proximal colon, and nitrite and nitrate in dialysate measured by capillary electrophoresis. 3. During bilateral vagal nerve stimulation there was an increase in nitrite and nitrate formation at the level of the stomach and in nitrite formation at the level of the colon. This increase was inhibited by intravenous administration of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME 30 mg kg-1). Furthermore, L-NAME significantly increased nerve-induced gastric and colonic contractions, as well as spontaneous colonic contractions. 4. In summary, we present a new methodological procedure for quantification of small changes in nitric oxide formation in vivo. This study provides evidence that nitric oxide is released in the stomach and colonic wall during vagal nerve activity, at concentrations able to cause inhibition of smooth muscle contractions in vivo.     

Role of nitric oxide in regulation of gastric acid secretion in rats: effects of NO donors and NO synthase inhibitor

1. The role of nitric oxide (NO) in the regulation of acid secretion was examined in the anaesthetized rat. 2. A rat stomach was mounted in an ex vivo chamber, instilled with 2 ml of saline every 15 min, and the recovered sample was titrated at pH 7.0 against 0.1 N NaOH by use of an automatic titrator for acid secretion. Gastric mucosal blood flow (GMBF) was measured simultaneously by laser Doppler flowmeter. 3. Intragastric application of NO donors such as FK409 (3 and 6 mg ml[-1]) and sodium nitroprusside (SNP; 6 and 12 mg ml[-1]) as well as i.p. administration of cimetidine (60 mg kg[-1]), a histamine H2-receptor antagonist, significantly inhibited the increase in acid secretion in response to pentagastrin (60 microg kg(-1) h(-1), i.v.), in doses that increased gastric mucosal blood flow (GMBF). 4. Intragastric application of FK409 (6 mg ml[-1]) increased both basal and stimulated acid secretion induced by YM-14673 (0.3 mg kg(-1), i.v.), an analogue of thyrotropin-releasing hormone (TRH), but had no effect on the acid secretory response induced by histamine (4 mg kg(-1) h(-1), i.v.). 5. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1), i.v.) did not affect basal acid secretion, but significantly potentiated the increase in acid secretion induced by YM-14673 and slightly augmented the acid secretory response to pentagastrin. 6. Both pentagastrin and YM-14673 increased the release of nitrite plus nitrate (NOx), stable NO metabolites, into the gastric lumen, and these changes were completely inhibited by prior administration of L-NAME (10 mg kg(-1), i.v.). 7. Pentagastrin caused an increase in luminal release of histamine and this response was significantly suppressed by intragastric application of FK409 (6 mg ml[-1]). 8. These results suggest that either exogenous or endogenous NO has an inhibitory action on gastric acid secretion through suppression of histamine release from enterochromaffin-like (ECL) cells.     

Chronic morphine increases biosynthesis of nitric oxide synthase in the rat spinal cord

The present study was undertaken to determine the influence of chronic morphine treatment on the biosynthesis of nitric oxide synthase (NOS) in the rat spinal cord using in situ hybridization and immunohistochemical methods. Repeated administration of morphine (20-100 mg/kg/day; 10 days) increased the NOS mRNA level in laminae I-IV and X 3 h after the last injection. That effect was accompanied by an increase in both the number of NOS-positive cells (24 h) and the optical density of NOS-immunoreactivity (3 and 24 h). The results indicate that repeated morphine administration increases NOS biosynthesis in the rat spinal cord, which may reflect adaptive changes accounting for development of opiate tolerance and dependence.     

Effect of acetylsalicylic acid on nitric oxide production in infarcted heart in situ

The effect of Acetylsalicylic Acid (ASA, Aspirin) on the myocardial production of the inducible form of nitric oxide synthase (iNOS) and the oxidation products of nitric oxide (nitrite, NO-2 and nitrate, NO-3: NOx) were studied in the rabbit heart two days after ligation of a branch of the left circumflex coronary artery. ASA was administered intravenously as AspisolR, DL-Lysinmono(acetylsalicylate) which is soluble in water. Animals received a total dose of 250, 375, or 500 mg/kg of ASA in five divided doses intravenously. Significant inhibition of iNOS was noted in the infarcted portion of the myocardium at 375 and 500 mg/kg of ASA. The reduction in myocardial nitric oxide (NO) production was paralleled by a diminution in coronary arterial-venous difference of NOx, demonstrating that ASA inhibition extended also to the oxidation products of NO. ASA is an inhibitor of cyclooxygenase (COX). The inhibition of iNOS by ASA demonstrates the close relationship between COX and iNOS activity in the heart in situ. Whether activity of the infarcted heart is influenced by the diminution in the production of NO by ASA is not known.     

Regulation of the endogenous NO pathway by prolonged inhaled NO in rats

Nitric oxide (NO) modulates the endogenous NO-cGMP pathway. We determined whether prolonged inhaled NO downregulates the NO-cGMP pathway, which may explain clinically observed rebound pulmonary hypertension. Rats were placed in a normoxic (N; 21% O2) or hypoxic (H; 10% O2) environment with and without inhaled NO (20 parts/million) for 1 or 3 wk. Subsequently, nitric oxide synthase (NOS) and soluble guanylate cyclase (GC) activity and endothelial NOS (eNOS) protein levels were measured. Perfusate cGMP levels and endothelium-dependent and -independent vasodilation were determined in isolated lungs. eNOS protein levels and NOS activity were not altered by inhaled NO in N or H rats. GC activity was decreased by 60 +/- 10 and 55 +/- 11% in N and H rats, respectively, after 1 wk of inhaled NO but was not affected after 3 wk. Inhaled NO had no effect on perfusate cGMP in N lungs. Inhaled NO attenuated the increase in cGMP levels caused by 3 wk of H by 57 +/- 11%, but there was no rebound in cGMP after 24 h of recovery. Endothelium-dependent vasodilation was not altered, and endothelium-independent vasodilation was not altered (N) or slightly increased (H, 10 +/- 3%) by prolonged inhaled NO. In conclusion, inhaled NO did not alter the endogenous NO-cGMP pathway as determined by eNOS protein levels, NOS activity, or endothelium-dependent vasodilation under N and H conditions. GC activity was decreased after 1 wk; however, GC activity was not altered by 3 wk of inhaled NO and endothelium-independent vasodilation was not decreased.     

Modulation of quinolinic acid-induced depletion of striatal NADPH diaphorase and enkephalinergic neurons by inhibition of nitric oxide synthase

The present study was designed to examine the role of nitric oxide (NO) in quinolinic acid (QUIN)-induced depletion of rat striatal nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase and enkephalinergic neurons. Intrastriatal injection of QUIN produced a dose-dependent decrease in NADPH diaphorase and enkephalin positive cells, with cell loss being evident following the injection of 6 and 18 nmol QUIN, respectively. To evaluate the role of NO in QUIN-induced toxicity, animals were pretreated with the non-specific nitric oxide synthase (NOS) inhibitor, Nomega-nitro-l-arginine (l-NAME) or the selective neuronal NOS inhibitor, 7-nitro indazole (7-NI). l-NAME (2x250 mg/kg, i.p. 8 h apart) maximally inhibited striatal NOS activity by 85%, while 7-NI (50 mg/kg, i.p.) maximally inhibited striatal NOS activity by 60%. Pretreatment with l-NAME or 7-NI potentiated the loss of NADPH diaphorase neurons resulting from intrastriatal injection of low doses of QUIN (18 nmol). Neither NOS inhibitor had any effect on the loss of striatal NADPH diaphorase neurons induced by a higher dose of QUIN (24 nmol). In contrast, 7-NI partially prevented the QUIN (18 and 24 nmol)-induced loss of enkephalinergic neurons, while l-NAME had no effect. These results indicate that NO formation may play a role in QUIN-induced loss of enkephalinergic neurons, but not in the loss of NADPH diaphorase neurons.     

Central Nitric Oxide Synthase Inhibition Disrupts Maternal Behavior in the Rat.

Blocking nitric oxide (NO) production, by 3rd ventricle administration of a nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 250 μg/5 μl, postpartum [pp]) decreased milk ejections in Day 10 pp rats. On Day 4 pp, L-NAME treatment eliminated pup retrieval and at both stages of lactation suppressed maternal aggression. Fewer rats treated with L-NAME on Day 10 pp retrieved 4-day-old pups than controls, although all nursed older litters. Following exposure to a mobile intruder, Fos expression was lower in the medial preoptic area and the bed nucleus of the stria terminalis in L-NAME-treated rats than in controls but was lower in the medial amygdala only following exposure to an anaesthetized intruder. Thus, the elevated levels of NO observed in lactation may contribute to the mechanism(s) that mediate maternal behavior and aggression. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Nitric oxide plays an important role in the diurnal change of tuberoinfundibular dopaminergic neuronal activity and prolactin secretion in ovariectomized, estrogen/progesterone-treated rats

A significant diurnal change of tuberoinfundibular dopaminergic (TIDA) neuronal activity coincident with the estrogen (E2)-induced afternoon PRL surge has been reported in ovariectomized, E2-primed (OVX+E2) rats. Systemic injection of a nitric oxide (NO) synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NA, 50 mg/kg, i.p. at 1000 and 1200 h), significantly blocked the diurnal changes of TIDA neuronal activity and PRL secretion at 1500 and 1700 h in OVX+E2 rats. Coadministration of L-arginine (300 mg/kg, i.p.) with L-NA completely prevented the effects of L-NA. Total nitrite/nitrate levels in the serum of L-NA- and L-NA+L-arginine-treated rats substantiated the effects of L-NA and L-arginine on NO production. Pretreatment of antisense oligodeoxynucleotide (ODN; 1 microg/3 microl; intracerebroventricularly at 48, 24, and 7 h before sacrifice) against the messenger RNA (mRNA) of constitutive NOS, i.e. neuronal NOS or endothelial NOS, was also effective in preventing the diurnal changes of TIDA neuronal activity and PRL surge at 1500 h. The same treatment of antisense ODN against the mRNA of inducible NOS, i.e. macrophage NOS, had no effect. Progesterone (P4) has been reported to advance and augment the diurnal changes of TIDA neuronal activity and the afternoon PRL surge, by 1 h, in both proestrous and OVX+E2 rats. We further showed that L-NA dose dependently (50 but not 5 mg/kg, i.p. at 1000 and 1200 h) blocked the effect of P4 on TIDA neurons and serum PRL at 1300 h, which effect could be negated by simultaneous administration of L-arginine (300 mg/kg, i.p.). Pretreatment with antisense ODNs against the mRNA of neuronal NOS or endothelial NOS, but not macrophage NOS, was also effective in preventing the P4's effect on TIDA neuronal activity and PRL secretion at 1300 h. In summary, NO may play a physiological role in the E2- and P4-regulated diurnal changes of TIDA neuronal activity and PRL secretion.