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1.
内源性一氧化氮合酶抑制物与心血管疾病   总被引:3,自引:0,他引:3  
机体存在一种调节一氧化氮合成的内源性机制,内源性一氧化氮合酶抑制物单甲基精氨酸与二甲基精氨酸能抑制一氧化氮合酶,阻止一氧化氮的合成。患动脉粥样硬化、高血压等心血管疾病时内源性一氧化氮合酶抑制物显著升高,可能是促进心血管疾病发展的重要原因之一。  相似文献   

2.
目的 探讨血清一氧化氮水平、总一氧化氮合酶和诱导型一氧化氮合酶活力与病毒性肝炎的关系.方法 用生化方法 检测对照组、中度慢性乙型肝炎、肝硬化、慢性重症肝炎及乙戊肝重叠感染患者血清一氧化氮、总一氧化氮合酶和诱导型一氧化氮合酶水平.结果 中度慢性乙型肝炎、肝硬化及乙戊肝重叠感染患者血清一氧化氮水平、总一氧化氮合酶和诱导型一氧化氮合酶活力与对照组比较明显升高,慢性重症肝炎患者血清一氧化氮水平、总一氧化氮合酶和诱导型一氧化氮合酶活力与对照组比较明显降低(P<0.05).结论 一氧化氮、总一氧化氮合酶和诱导型一氧化氮合酶在病毒性肝炎发病中具有重要作用,并在一定程度上与肝损害程度相关.  相似文献   

3.
一氧化氮及内源性一氧化氮合酶抑制剂与心血管疾病   总被引:1,自引:0,他引:1  
一氧化氮(NO)是内皮细胞释放的一种舒血管因子,具有许多心血管生理效应,NO不足以及过多对心血管系统都有显著不良作用.非对称型左旋二甲基精氨酸(ADMA)是机体自身产生的一种能与NO合成底物左旋精氨酸竞争NO合酶,使NO合成减少的物质,被称为内源性NO合酶(NOS)抑制剂,与心血管疾病的发生发展有关.  相似文献   

4.
一氧化氮及内源性一氧化氮合酶抑制剂与心血管疾病   总被引:1,自引:0,他引:1  
一氧化氮(NO)及内皮细胞释放的一种舒血管因子,具有许多心血管生理效应,NO不足以及过多对心血管系统都有显著不良作用,非对称型左旋二甲基精氨酸(ADMA)是机体自身产生的一种能与NO合成底物左旋精氨酸竞争NO合酶,使NO合成减少的物质,被称为内源性NO合酶(NOS)抑制剂,与心血管疾病的发生发展有关。  相似文献   

5.
血管内皮细胞损伤及其功能紊乱在心血管疾病(如冠心痛)发生发展过程中起重要作用.某些内皮特异性基因的表达直接影响病变的发生和发展进程,如内皮型一氧化氮合酶.后者介导体内左旋精氨酸降解产生一氧化氮.内皮型一氧化氮合酶的基因表达调控有转录水平的调控、转录后调控和翻译后调控,而转录因子在内皮型一氧化氮合酶基因的表达调控过程中起关键性作用.  相似文献   

6.
一氧化氮可调节肺血管张力,维持肺血管正常结构和肺循环的低阻力状态,在低氧性肺动脉高压的发生机制中起重要作用.由于一氧化氮具有独特的理化性质和生物学活性,因此目前研究主要集中在对其合成的关键酶一氧化氮合酶.下面就一氧化氮、一氧化氮合酶在低氧性肺动脉高压发病中的作用机制及临床应用的研究作一简单综述.  相似文献   

7.
一氧化氮一氧化氮合酶与心功能   总被引:6,自引:2,他引:4  
一氧化氮是一个细胞-细胞间信息传递因子,作为第二信使和神经递质在体内起着重要而广泛的作用,它还可介导细胞免疫和细胞毒性;一氧化氮合酶作为内源性一氧化氮生成的限速酶,有三种同工酶,其在体内的分布与表达调控机制不同;生理、病理条件下,一氧化氮与心功能变化密切相关  相似文献   

8.
内源性一氧化氮合酶竞争抑制剂与冠心病   总被引:1,自引:0,他引:1  
近年研究表明,体内存在的内源性一氧化氮合酶竞争抑制剂--不对称二甲基精氨酸影响一氧化氮的合成,并认为是预测内皮功能障碍和心血管疾病独立的危险因素.  相似文献   

9.
为研究高密度脂蛋白和氧化型高密度脂蛋白对ECV-304分泌一氧化氮,一氧化氮合酶和内皮素1的影响,探讨高密度脂蛋白对内皮细胞保护作用的可能机理,分别用不同浓度的高密度脂蛋白和氧化型高密度脂蛋白处理培养的人脐-静脉内皮细胞系ECV-304,用比色法和放射免疫法测定一氧化氮,一氧化氮合酶和内皮素1。结果 发现随着高密度脂蛋白浓度的升高,上清液中一氧化氮,一氧化氮合酶含量上升,内皮素1含量下降。随着培养液中氧化型高密度脂蛋白浓度的升高,上清液中一氧化氮,一氧化氮合酶含量下降,内皮素1含量上升。结果提示高密度脂蛋白促使一氧化氮,一氧化氮合酶合成和分泌增加及内皮素1生成减少,可能是其细胞保护作用和抗动脉粥样硬化作用的重要机制之一。而氧化型高密度脂蛋白促使一氧化氮,一氧化氮合酶合成和分泌减少及内皮素1生成增加,可能是其细胞损伤作用和促动脉粥样硬化作用的重要机制之一。  相似文献   

10.
非对称型左旋二甲基精氨酸是机体自身产生的一氧化氮合成底物左旋精氨酸的类似物,能够竞争性抑制一氧化氮合酶的活性,使一氧化氮合成减少,被称为内源性一氧化氮合酶抑制剂。非对称型左旋二甲基精氨酸与高血压、冠心病等心血管疾病的发生和发展有关。  相似文献   

11.
采用溶栓疗法、动脉搭桥术、冠状动脉血管成形术等技术,使缺血组织和器官重新恢复血流,挽救了众多危急重病人的生命,然而,缺血器官及组织在恢复血流的同时,均伴随着缺血/再灌注损伤,是目前临床上亟待解决的问题。在对心血管疾病的研究过程中,随着心肌保护研究的不断深入,如何减轻心肌缺血/再灌注损伤成为心肌保护问题的关键。越来越多的研究表明,心肌缺血/再灌注损伤与诱导型一氧化氮合酶表达过量一氧化氮紧密相关。研究表明,诱导型一氧化氮合酶既有心肌保护作用,也有促心肌损伤作用,而通过对诱导型一氧化氮合酶抑制剂的应用,有望减轻心肌损伤的进展,保护损伤心肌。  相似文献   

12.
内源性一氧化氮(NO)和一氧化碳(CO)是先后发现的2种气体信号分子,NO合酶(NOS)和血红素加氧酶(HO)分别是生成NO和CO的氧合酶。研究表明,NOS/NO系统和HO/CO系统均与缺血性脑损伤的发生发展密切相关,而且两者之间还存在着错综复杂的相互作用,对其作用机制的深入了解有助于探索缺血性脑损伤的临床治疗途径。  相似文献   

13.
Cardiogenic shock (CS) in acute myocardial infarction, after successful coronary angioplasty, still carries a case fatality rate of 50%. These patients succumb to a systemic metabolic storm, superimposed on extensive myocardial necrosis and stunning. Nitric oxide (NO) overproduction contributes to the pathophysiology of this morbid state. Current data regarding the physiologic effects of NO and nitric oxide synthase (NOS) inhibitors on the cardiovascular system are reviewed. Clinical trials assessing the safety and efficacy of NOS inhibitors in CS are summarized.  相似文献   

14.
To evaluate the effect of esophageal acid exposure on epithelial function, transmucosal potential, histopathological markers of acute tissue damage, and local nitric oxide production were examined in healthy volunteers treated with proton pump inhibitors (group I), patients with treated reflux disease (group II), and patients with untreated erosive reflux disease (group III). The participants were randomized to esophageal perfusion with either saline or HCl. Denominators of acute acid exposure were balloon cells in superficial layers and superficial densification. The nitric oxide concentrations in groups I to III increased from < 1, 10.0± 10.0, and 20.6± 19.9 ppb, respectively, to 300± 80, 1360± 1080, and 920± 700 ppb after HCl infusion (P < 0.001). Inducible nitric oxide synthase was consistently expressed in the epithelium. Blood flow was lower among reflux patients but did not correlate with acid exposure or nitric oxide. Nitric oxide is formed following acid perfusion and predominantly in gastroesophageal reflux disease.  相似文献   

15.
Dabrowski A, Gabryelewicz A. Nitric oxide contributes to multiorgan oxidative stress in acute experimental pancreatitis. Scand J Gasteroenterol 1994;29:943-948.

Background: Nitric oxide is a highly reactive free radical gas. The study was undertaken to determine the nitric oxide contribution to oxidative stress in acute experimental pancreatitis induced in Wistar rats. Methods: Acute haemorrhagic pancreatitis was induced in male Wistar rats by means of a retrograde intraductal injection of 5% Na-taurocholate. The rats were treated with the nitric oxide donor, sodium nitroprusside (SNP) (0.25mg/kg), or with JVtu-nitro-L-arginine methyl ester (l-NAME) (10mg/kg), which is an inhibitor of nitric oxide synthase. We measured malondialdehyde and sulphhydryl group concentrations in pancreatic, lung, and liver tissue. Results: In rats with acute pancreatitis treated with SNP, oxidative stress, expressed by malondialdehyde increase and sulphhydryl group depletion, was much more pronounced than in the other groups. In contrast, intensity of the oxidative stress was significantly reduced in rats treated with l-NAME. Conclusion: The data suggest that nitric oxide is partly responsible for oxidative stress in acute haemorrhagic pancreatitis.  相似文献   

16.
目的观察芪红合剂含药血清对人外周血内皮祖细胞(EPCs)一氧化氮(NO)、一氧化氮合酶(NOS)的影响,探讨其对人外周血内皮祖细胞的保护机制。方法12只雄性Wistar大鼠随机分为芪红合剂组(低剂量组、中剂量组、高剂量组)和对照组,制备含药血清和空白血清。采集健康成人外周血,分离单核细胞,体外培养7d后,收集贴壁细胞,激光共聚焦显微镜及流式细胞仪鉴定正在分化的EPCs,加入含不同浓度芪红合剂药物血清及空白血清的M199培养基孵育24h,将其在倒置荧光显微镜下计数,硝酸还原酶法测定NO,化学比色法测定NOS。结果芪红合剂药物组的血清NO水平和NOS活性明显高于空白血清对照组(P0.05),并且呈剂量依赖性。结论芪红合剂可能通过增加EPCsNOS活性,促进NO分泌,防止血管内皮损伤及动员血管内皮祖细胞修复损伤血管来发挥血管内皮保护作用。  相似文献   

17.
肝硬化大鼠胃壁一氧化氮合酶的组化研究   总被引:3,自引:0,他引:3  
目的:门脉高压性胃病在组织学上以胃臂粘膜及粘膜下血管扩张为特征,一氧化氮作为扩血管物质可能参与了此异常的发生。方法:使用NADPH黄递酶组化法显示肝硬化大鼠胃臂一氧化氮合酶(NOS)活性。结果:肝硬化大鼠胃粘膜上皮、胃壁内小动脉及小静脉NOS染色均增强,胃粘膜上皮脱落、变性、不规整,胃壁内小动脉、小静脉扭曲变形。结论:肝硬化大鼠胃壁一氧化氮合酶产生增加,可能参与了肝硬化门脉高压性胃病的发生。  相似文献   

18.
Cardiac myocytes express two types of nitric oxide (NO) synthase, eNOS and iNOS. eNOS activity is regulated by the contractile state of the heart, while iNOS expression is induced by cytokines. Nitric oxide induced by cytokines causes negative inotropic and lethal effects on cardiac myocytes. Expression of iNOS in the myocardium is increased in patients with dilated cardiomyopathy with clinical evidence of heart failure. Several neurohumoral factors activated in chronic heart failure augment cardiac iNOS expression and could cause cardiac dysfunction and cell damage.  相似文献   

19.
Endothelial nitric oxide synthase (eNOS) is an enzyme that plays a critical role in normal cardiovascular function. Caveolae are structures within the surface membrane of cells in which many signaling and second messenger pathways, including nitric oxide, are regulated. Many interventions in cardiovascular disease act, in part, either by changing factors that directly influence eNOS, or by changing a complex set of proteins that act indirectly on caveolae, to alter eNOS activity. In this review, we will focus on the regulation of eNOS activity by circulating factors which are altered in cardiovascular disease and the effects of pharmacological interventions that act partially through effects on eNOS.  相似文献   

20.
Swallowing induces esophageal shortening due to contraction of the longitudinal muscle (LM) layer. Experiments in the opossum have shown an excitatory effect of nitric oxide (NO) on esophageal LM strips. We evaluated the role of NO in swallow-induced esophageal shortening and assessed the effect of NO in vitro on feline LM strips. Swallow-induced esophageal shortening was studied before and after NO synthase blockade with l-NAME. In five cats esophageal shortening was measured using two endoscopically affixed mucosal clips. In another five cats LM contraction was measured by a strain gauge sutured on the serosal side at 2 cm above the LES; muscle strips from that region were obtained for in vitro studies. Swallowing induced esophageal shortening of 48.3 ± 8.3% and LM contraction of 4.4 ± 0.8 g in the control period and 32.1 ± 8% and 3.0 ± 0.4 g after l-NAME (P < 0.05). Nitric oxide and SNP did not change the basal tone of esophageal LM strips but provoked inhibition of metacholine-induced tonic and phasic activity. Electrical field stimulation induced frequency-dependent contractions that were reduced by atropine without further reduction after l-NAME. In conclusion, the reduction of esophageal shortening after l-NAME during the in vivo experiments suggested an excitatory effect of NO on the feline esophagus. The in vitro experiments, however, showed no contractile effect of NO or SNP on LM strips, but an inhibitory effect on the precontracted tissue. The influence of NO synthase blockade on in vivo esophageal LM shortening might be secondary to its effect on circular muscle contractility.  相似文献   

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