人参总皂甙对不完全性脑缺血后海马CA1区NOS阳性神经元表达的影响

目的探讨人参总皂甙(GS)对不完全性脑缺血及再灌注不同时间后海马CA1区一氧化氮合酶(NOS)的影响及对神经元的保护作用.方法用双侧颈总动脉夹闭加放血的方法制成大鼠不完性脑缺血及再灌注模型,以还原烟酰胺腺嘌呤二核苷酸脱氢酶(NADPH-d)组织化学方法观察缺血及再灌注后海马CA1区NOS阳性神经元变化及GS对其的影响.结果单纯缺血组海马CA1区在缺血30min时NOS阳性细胞数最高(44.5±7.42),为假手术组2倍,再灌注2h、12h、24h、3d后逐渐下降,5d时恢复正常水平(21.12±3.50),缺血再灌注3d、5d时出现神经细胞损伤.GS能抑制缺血30min及再灌注各时程中NOS阳性神经元数量变化,并能预防缺血再灌注后迟发的神经元损害.结论GS对大鼠不完全性脑缺血及再灌注不同时程后海马CA1区NOS的异常表达有抑制作用,对神经元的保护作用.     

Sideropenic Dysphagia综合征膜性蹼26例分析

目的 :研究SideropenicDysphagla (S -D)综合征膜性蹼产生的机制。方法 :回顾分析S -D综合征2 6例的临床资料。结果 :影像学检查显示膜性蹼在颈段食道前壁呈 2mm深的模样陷凹。血液学检查为缺铁性低血红蛋白性贫血改变。结论 :缺铁性贫血是S -D综合征的原因 ,铁剂治疗有效     

NO在体外循环中脑损伤作用机制的研究进展

一氧化氮及一氧化氮合酶在体外循环导致的脑损伤中具有重要作用,它可以通过扩张血管/抑制血小板聚集与黏附/减少细胞凋亡等对脑组织产生保护作用。一氧化氮的临床应用仍需对其作用机制作进一步深入研究。     

异丙酚对慢性神经痛大鼠脊髓诱导型一氧化氮合酶表达的影响

目的 研究不同剂量异丙酚对慢性神经痛大鼠触诱发痛痛阈及其脊髓组织诱导型一氧化氮合酶(iNOS)mRNA的影响。方法 Wistar大鼠40只,随机分为四组,Ⅰ组为空白对照;Ⅱ、Ⅲ、Ⅳ组结扎左侧坐骨神经。术后第7天,Ⅰ、Ⅱ组腹腔注射生理盐水50 ml·kg-1,Ⅲ、Ⅳ组腹腔注射异丙酚50 ml·kg-1或75ml·kg-1,每天一次共6 d。在术后第6、10和12天,使用Von Frey法分别测定各组大鼠触诱发痛痛阈,比较不同剂量的异丙酚对大鼠痛阈的影响。术后第12天取L4-5和L5-6节段脊神经节和脊髓组织,采用半定量RT-PCR法,对各组大鼠脊髓组织iNOS mRNA表达进行检测。结果 术后第10和12天,Ⅲ、Ⅳ组大鼠双侧的痛阈值高于Ⅱ组(P<0.05);术后第12天,Ⅲ、Ⅳ组大鼠脊髓组织iNOS mRNA表达低于Ⅱ组(P<0.05)。结论 异丙酚通过抑制脊髓组织iNOS mRNA转录,降低其表达,而起到一定的抗伤害作用。     

实验性糖尿病早期大鼠背根神经节一氧化氮合酶基因表达的变化

目的：观察糖尿病早期(2周)大鼠背根神经节(DRG)中一氧化氮合酶(nNOS、iNOS、eNOS)的表达变化以及胰岛素对其的影响。方法：按60mg／kg一次性腹腔注射链脲佐菌素(STZ)制备胰岛素依赖性糖尿病大鼠模型(16只)，造模成功后随机分成2组(模型组和治疗组)，治疗组于造模成功后第2天开始给予胰岛素治疗，正常对照组(8只)与模型组予皮下注射同样体积的生理盐水。2周后取各组大鼠背根神经节，Trizol法提取总RNA，应用RT—PCR法测定3种NOS mRNA的表达。结果：在糖尿病早期大鼠DRG中，iNOS表达明显上调，胰岛素能有效逆转此变化。而nNOS和eNOS的表达无明显变化。结论：在早期糖尿病DRG中iNOS基因表达异常，可能与糖尿病外周神经病变的发生发展有关。     

猪心脏移植缺血再灌注损伤中NO和NOS的表达

①目的　了解猪同种原位心脏移植术后早期一氧化氮 (NO)、一氧化氮合酶 (NOS)含量的变化 ,及其与早期缺血再灌注损伤的关系。②方法　建立猪同种原位心脏移植模型。供心在移植前低温保存 (Thomas液 ,4℃ ) 4h ,移植成功心脏复搏后 2h取材。应用组织化学方法测定心肌组织中NO、NOS的含量 ,应用核酸原位末端标记法 (TUNEL)测定心肌细胞凋亡指数 ,作为评价心肌缺血再灌注损伤的指标。以正常心肌及单纯缺血心肌组织作为对照。③结果　移植后心肌组织NO、NOS的含量较缺血组与正常组低 ,差异有显著意义 (F =2 7.2 2 9、16 .2 0 3,q =5 .716～ 6 .4 12 ,P <0 .0 1)。移植组心肌细胞凋亡指数与正常组及缺血组比较明显升高 ,差异有显著性(F =16 3.884 ,q =7.4 82、6 .975 ,P <0 .0 1)。心肌组织NO、NOS含量与心肌细胞凋亡指数呈负相关关系 (r =- 0 .886、- 0 .795 ,P <0 .0 1)。④结论　猪心脏移植后早期心肌缺血再灌注损伤所致的细胞死亡主要表现为心肌细胞凋亡 ;再灌注期间内源性NO、NOS的减少参与了心脏移植后早期缺血再灌注损伤的发生     

Inhibition of Expression of Hypoxia-inducible Factor-1α mRNA by Nitric Oxide in Hypoxic Pulmonary Hypertension Rats

Hypoxiaisadirectfactorcausinghypoxicpul monaryhypertension (HPH) .hypoxiainduciblefac tor 1α (HIF 1α)isfoundtobethemostcrucialfactorsofarwhichmediatesthecellularresponsetohypoxi a[1] .OurpreviousstudyrevealedthatoverexpressionofHIF 1andendothelin 1(ET 1…     

An overview of new pharmacological treatments for cerebrovascular dysfunction after experimental subarachnoid hemorrhage

Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysms. Mechanisms contributing to the development of vasospasm, abnormal reactivity of cerebral arteries and cerebral ischemia after SAH have been intensively investigated in recent years. It has been suggested that the pathogenesis of vasospasm is related to a number of pathological processes, including endothelial damage, smooth muscle cell contraction resulting from spasmogenic substances generated during lyses of subarachnoid blood clots, changes in vascular responsiveness and inflammatory or immunological reactions of the vascular wall.A great deal of experimental and clinical research has been conducted in an effort to find ways to prevent these complications. However, to date, the main therapeutic interventions remain elusive and are limited to the manipulation of systemic blood pressure, alteration of blood volume or viscosity, and control of arterial dioxide tension.Even though no single pharmacological agent or treatment protocol has been identified which could prevent or reverse these deadly complications, a number of promising drugs have been investigated. Among these is the hormone erythropoietin (EPO), the main regulator of erythropoiesis. It has recently been found that EPO produces a neuroprotective action during experimental SAH when its recombinant form (rHuEPO) is systemically administered.This topic review collects the relevant literature on the main investigative therapies for cerebrovascular dysfunction after aneurysmal SAH. In addition, it points out rHuEPO, which may hold promise in future clinical trials to prevent the occurrence of vasospasm and cerebral ischemia after SAH.     

Down-regulation of inducible nitric oxide synthase (iNOS) in rat with congenital hydronephrosis

BACKGROUND: Most of our knowledge concerning obstructive uropathy has been derived mainly from surgically manipulated animal models, and the pathogenesis of congenital obstructive hydronephrosis is not fully elucidated. Nitric oxide (NO) acts as an important biological modulator with diverse physiological functions, which can be either toxic or protective depending on the situation. NO is synthesized from l-arginine by nitric oxide synthase, and in the kidney iNOS is expressed spontaneously. The aim of our study is to investigate the expression of iNOS protein and its relationship with tubulointerstitial fibrosis and tubular cell apoptosis in congenital hydronephrosis. METHODS: We conducted histological studies on 18 kidneys of six-week-old-rats from an inbred colony of congenital hydronephrosis with reference to the histological grading of the affected kidney, tubulointerstitial fibrosis, renal tubular atrophy, and tubular cell apoptosis. Renal transforming growth factor-beta1 (TGF-beta1) level was determined by a sandwich ELISA assay and the expression of iNOS was analyzed by western blotting. RESULTS: Most of the hydronephrotic kidneys were markedly enlarged with dilatation of the collecting system, parenchymal thinning, tubular atrophy, interstitial infiltration and fibrosis. Renal TGF-beta1 level was higher in hydronephrotic kidneys than normal control kidneys (364.81 +/- 52.60 vs. 221.19 +/- 22.53 pg/mg protein, P < 0.05). Tubular apoptotic score in hydronephrotic kidneys was also significantly higher than in the normal control kidneys (1.97 +/- 0.42 vs. 0.14 +/- 0.02/HPF, P < 0.01). The expression of iNOS protein was lower in the affected kidneys compared with the normal control kidneys (8.79 +/- 0.78 vs. 14.00 +/- 0.83 arbitrary unit, P < 0.01). There was a negative correlation between iNOS expression and histological grading in congenital hydronephrosis. The iNOS expression also correlated negatively with renal interstitial fibrosis, TGF-beta1 level and tubular cell apoptosis. CONCLUSION: Our study confirmed the down-regulation of iNOS expression in affected kidneys from rats with congenital hydronephrosis, in which the cytoprotective effect of NO may be lost or weakened.     

妊娠肝内胆汁淤积症患者血清一氧化氮和内皮素的变化及意义

目的：探讨妊娠肝内胆汁淤积症（ICP）患者外周静脉血清、新生儿脐静脉血清中一氧化氮（NO）、内皮素（ET）、丙二醛（MDA）和超氧化物歧化酶（SOD）含量的变化及在ICP发病中的作用。方法：以ICP组28例为研究组，测定其外周静脉血清及新生儿脐静脉血清中的NO、ET、MDA和SOD，以年龄相近的24例正常孕妇作为对照组。结果：ICP患者的MDA和ET含量较正常晚期妊娠显著增高（P＜0．01），ICP患者的NO和SOD含量与对照组相比无显著性差异（P＞0．05）。母血清中NO、ET、MDA含量均较新生儿脐静脉血清中的含量高，差异有显著性（P＜0．01）。结论：妊娠期体内氧化和抗氧化失衡及ET水平的增高可能与ICP的发生、发展有关。