白细胞介素—6在突出的腰椎间盘中的表达及其意义

目的对白细胞介素-6(IL-6)在突出的腰椎间盘组织中的含量及产生IL-6的组织细胞类型进行研究,并对其意义进行探讨.方法对12例正常及突出腰的椎间盘组织进行体外培养,用放免方法测定培养液上清中IL-6含量;并在20例突出的腰椎间盘组织中用免疫组化方法对产生IL-6的细胞类型及组织学定位进行研究.结果突出的腰椎间盘组织产生IL-6的量为(987.53±594.44)pg/g,正常对照组IL-6的量为(114.21±63.91)pg/g,两者统计学有显著性差异(P＜0.001),免疫组化结果显示白细胞介素-6阳性细胞在突出椎间盘周围的肉芽组织中表达最强,主要以成纤维细胞、淋巴细胞及软骨细胞为主.结论腰椎间盘组织可自身合成IL-6,IL-6在突出的腰椎间盘组织明显增高,其IL-6主要由突出的腰椎间盘周围的肉芽组织所产生.     

椎间盘退变分子生物学近展

静水压力对金属蛋白酶(MMPs)有明显作用。Handa等报道生理水平静水压力(0.3Mpa)促进蛋白多糖(PG)合成,增加金属蛋白酶-1组织抑制剂(TIMP-1)的活性。静水压力超压力(3Mpa)和低压力时分解作用(降低PG合成)会占优势,导致PG丢失和椎间盘退化。Ishihara等研究发现2.5Mpa静水压力刺激牛椎间盘内环纤维及人椎间盘髓核蛋白多糖的合成,相反10Mpa抑制PG合成。William等报道髓核和环形纤维细胞对1Mpa静水压力表现出不同的反应,髓核细胞被刺激,而环形纤维细胞被抑制。 Liu等研究发现内源性和外源性一氧化氮(NO)均抑制椎间盘PG合成,静水压力影响椎间盘细胞产生NO,NO是静水压力改变PG合成的中间介质。椎间盘NO可能来自肉芽组织细胞,用免疫组化方法证明诱导NO合成酶在突出的腰椎间盘周围肉芽组     

一氧化氮胰腺保护作用与巯基物质和氧自由基的关系

目的　探讨内源性一氧化氮 (NO)对大鼠急性坏死性胰腺炎的作用及其与巯基物质和脂质过氧化之间的关系。　方法　以 5 %牛磺胆酸钠溶液胰胆管注射 (1ml/kg)制成大鼠急性坏死性胰腺炎模型 ,以工具药L 硝基精氨酸 (L NNA)为内源性NO的阻断剂 ,观察内源性NO对胰腺损伤程度、血清淀粉酶浓度、胰腺组织内巯基物质含量和脂质过氧化终产物丙二醛 (MDA)含量的影响。　结果　牛磺胆酸钠胰胆管注射可造成胰腺组织明显的水肿和坏死 ,部分 (2 / 7)发生胰腺实质内出血 ;血清淀粉酶浓度显著升高 ,胰腺组织巯基物质含量降低 ,MDA含量增加 [(1 2 5± 0 2 8)nmol/mg蛋白质vs.(0 5± 0 0 3)nmol/mg蛋白质 ,P <0 0 5 ]。以L NNA(12 5mg/kg)阻断内源性NO ,可明显加重胰腺组织坏死 ,胰腺实质内出血率增加 (10 / 12 ,83 3 % ) ,并血清淀粉酶浓度进一步升高 ,胰腺组织MDA含量进一步增加 [(3 0± 0 40 )nmol/mg蛋白质vs.(1 2 5± 0 2 8)nmol/mg蛋白质 ,P <0 0 5 ]。但对胰腺组织内巯基物质的含量没有影响。　结论　内源性NO具有胰腺保护作用 ,其保护机制可能与抗氧自由基有关。巯基物质可能不参与NO的胰腺保护机制。     

一氧化氮合酶抑制剂对延缓腰椎间盘退变的影响

目的　探讨一氧化氮合酶(NOS)抑制剂L N6 亚氨乙基 赖氨酸(L NIL)和S 甲基异硫脲(SMT)对退变腰椎间盘组织代谢的影响。方法　无菌条件下,取2 0例腰椎间盘突出症患者的椎间盘组织体外培养,分别加入1mmol/L浓度的SMT和L NIL ,培养72h后,通过检测硝酸盐和亚硝酸盐的含量来观察椎间盘NO的释放量及NOS的活性;原位杂交法检测椎间盘组织iNOSmRNA和MMP3mRNA的表达。培养10d后,化学比色法观察椎间盘蛋白多糖含量和羟脯氨酸释放量的变化。结果　L NIL组髓核和纤维环NO释放量(65 .6±4.5 ,68.8±5 .7) μmol/L和SMT组髓核和纤维环NO释放量(69.5±6.5 ,69.1±6.1) μmol/L较对照组NO释放量(10 7.9±4.4,93 .1±5 .9) μmol/L明显减少(P <0 .0 1)。L NIL组和SMT组髓核组织中蛋白多糖含量(5 1.3±9.6,48.2±8.5 )kg/L ,比对照组(3 2 .1±6.4)kg/L明显增加(P <0 .0 1) ,羟脯氨酸释放量(1.1±0 .4,1.2±0 .5 )kg/L比对照组(3 .4±0 .8)kg/L显著减少(P <0 .0 1) ;同时,原位杂交法未检测到iNOSmRNA和MMP3mRNA的表达。结论　NOS抑制剂L NIL和SMT能抑制过量NO的释放,对延缓椎间盘退变具有积极的作用     

胆囊癌血管生成关系与一氧化氮及碱性成纤维生长因子的研究

我们检测胆囊癌组织及正常胆囊组织中诱导型一氧化氮合成酶 (iNOS)及碱性成纤维生长因子 (bFGF)的表达及测定胆囊癌组织中微血管密度 (MVD) ,探讨一氧化氮 (NO)及bFGF与胆囊癌血管生成的关系。一、材料和方法1.临床材料 :收集本院 1997年 6月～ 2 0 0 1年 2月间经手术切除的胆囊癌标本 40例。标本经福马林固定 ,石蜡包埋 ,所有标本均经苏木素 伊红 (HE)染色病理证实。男 11例 ,女 2 9例 ,年龄(5 8.6± 12 .6)岁。另取正常胆囊组织 8例标本作为对照。2 .实验试剂 :兔抗人F Ⅷ相关抗原多克隆抗体购自美国Sigma公司 ,兔抗人iNOS多克…     

诱生型一氧化氮合酶选择性抑制剂对急性胰腺炎大鼠胰腺组织的影响

目的　探讨急性胰腺炎大鼠胰腺组织中诱生型一氧化氮合酶 (iNOS)选择性抑制剂(氨基胍 )对胰腺组织的影响。方法　分别测定各组胰腺组织中原生型一氧化氮合酶 (cNOS)和iN OS活性、一氧化氮 (NO)含量 ;观察各组胰腺组织病理变化 ,并对胰腺组织损伤进行评分。结果　与胰腺炎组比较 ,单用氨基胍可明显降低NO含量 [( 2 2 .4± 0 .3) μmol/g ,P <0 .0 5 ] ,而胰腺病理评分无降低 ( 8.8± 0 .6 ,P >0 .0 5 ) ,联合应用L 精氨酸不但可明显降低NO含量 [( 2 5 .6± 0 .4) μmol/g ,P <0 .0 5 ] ,并且胰腺病理评分明显降低 ( 6 .3± 1.4,P <0 .0 5 )。 结论　联合应用选择性iNOS抑制剂和NO供体 ,可降低胰腺组织中NO含量 ,并能改善胰腺组织病理损伤。     

一氧化氮在获得性肾囊肿癌变过程中的作用

目的　探讨一氧化氮 (NO)过多产生在获得性肾囊肿 (ACDK)发生肾癌过程中的作用。　方法　用高压液相自动分析方法测定 1 6例 1 8份ACDK和 1 2份单纯性肾囊肿囊内液体中NO的代谢产物亚硝酸盐 /硝酸盐 (NO-2 /NO-3 )的含量 ,同时测定 5份ACDK患者血浆NO-2 /NO-3 的含量。采用免疫组织化学方法 (LSAB法 )检测 1 7份ACDK和 2 0例非ACDK肾组织一氧化氮合酶 (iNOS)的表达。　结果　ACDK囊内液NO-2 /NO-3 的含量 (1 5 1 .6± 6 4.2 μmol/L)明显高于单纯性肾囊肿组(5 0 .1± 33.6 μmol/L) ,差异有极显著性 (P <0 .0 0 1 )。其中在相同的 5例ACDK患者中囊内液NO-2 /NO-3 的浓度明显的高于血浆中的浓度。在免疫组织化学染色 (LSAB法 )检测肾组织iNOS的表达中 ,1 7份ACDK中 1 4例 (82 % )为阳性。 1 3例正常肾组织和 7例非ACDK慢性肾衰的肾组织均无i NOS的表达。　结论　NO在ACDK囊内液中过多产生有可能是其囊上皮发生肾癌的原因之一。     

NOSTRIN在无精子症患者睾丸组织中的表达

目的:通过测定无精子症患者睾丸组织中内皮型一氧化氮合酶运输介导物(NOSTRIN)和内皮型一氧化氮合酶(eNOS)的表达,探讨其与无精子症发病的相关性。方法:采用免疫组化法检测17例特发性无精子症患者(病例组)和10例正常男性(正常组)睾丸组织中NOSTRIN的定位和定量表达;RT-PCR检测睾丸组织中NOSTRINmRNA的表达;分光光度法测定睾丸组织中eNOS的活性;应用硝酸还原酶法测定睾丸组织上清液中NO代谢产物亚硝酸基/亚硝基(NO2-/NO3-)水平。结果:NOSTRIN在睾丸组织中表达于生精细胞、支持细胞以及血管内皮细胞,NOSTRIN在特发性无精子症患者睾丸中的表达水平显著低于正常男性;病例组患者睾丸组织中NOSTRINmRNA呈弱表达(0.312±0.076),明显低于正常组(0.793±0.082,P<0.01);病例组患者睾丸组织eNOS活性[(33.727±3.58)U/mg]与正常组[(17.69±3.84)U/mg]比较显著增高(P<0.01);病例组患者睾丸中NO2-/NO3-水平为[(48.56±8.49)μmol/L],与正常组[(25.37±9.61)μmol/L]比较显著升高(P<0.01);病例组睾丸组织中NOSTRIN表达水平与eNOS活性呈负相关(r=-0.57,P<0.01),与NO代谢产物NO2-/NO3-同样呈负相关(r=-0.61,P<0.01)。结论:无精子症患者睾丸组织中NOSTRIN表达水平降低,eNOS活性增强,NO-/NO-水平升高,这可能与无精子症的发生有着相关性。     

环氧化酶2与血管内皮生长因子在突出腰椎间盘中的表达及意义

目的：探讨环氧化酶2（COX-2）、血管内皮生长因子（VEGF）在突出腰椎间盘中的表达及其意义。方法：62个突出椎间盘标本取自58例腰椎间盘突出症手术患者,包括突起型22个,破裂型20个,游离型20个。取材部位分别为突出组织或游离组织（A部位）和椎间隙残余髓核组织（B部位）。对照组取自4例新鲜年轻尸体的L3/4、L4/5及L5/S1椎间盘组织共12个标本,取材部位为椎间盘边缘（A部位）和中央髓核（B部位）;应用免疫组化法对各组标本中COX-2和VEGF的表达进行检测;应用图像分析系统测量标本中COX-2和VEGF表达量的平均光密度值。结果：在腰椎间盘突出组,特别是破裂型和游离型组的突出组织中存在富含新生血管的肉芽组织,COX-2和VEGF染色阳性细胞主要表达于肉芽组织中及突出组织的椎间盘细胞中,对照组未见阳性染色细胞。在突出组的A部位从突起型、破裂型到游离型COX-2和VEGF的表达均逐渐增高,差异有显著性（P〈0.01）。突出组的A部位COX-2和VEGF的表达明显高于B部位（P〈0.01）。腰椎间盘组织中COX-2和VEGF的表达存在明显相关性（r=0.855,P〈0.01）。结论：COX-2、VEGF参与腰椎间盘退变、突出的发病过程;随着腰椎间盘退变突出的进展,COX-2、VEGF的表达均逐渐增高;COX-2与VEGF表达密切相关。     

腰椎间盘中转化生长因子β1的合成和基因表达

目的　观察腰椎间盘中内源性转化生长因子 β1(TFG - β1)表达分布规律及其细胞来源。 方法　采用免疫组化及原位杂交技术检测 16例胎儿期、8例生长期、12例成熟退变期和 2 7例突出椎间盘中TGF - β1蛋白合成和基因表达。结果胎儿椎间盘脊索细胞和类软骨细胞出现阳性免疫染色 ,并对TGF - β1mRNA呈强表达 ,阳性率为94 .3% (15 / 16 ) ;生长期椎间盘中软骨样细胞和成纤维细胞呈阳性表达 ,阳性率为 87.5 % (7/ 8) ,与胎儿期相比差别不显著 (P >0 .0 5 ) ,表达量低于胎儿期 (P <0 .0 5 ) ;成熟退变期阳性细胞明显减少 ;破裂型椎间盘突出组织中软骨样细胞、巨噬细胞呈阳性表达 ,阳性率为 37.4 % (10 / 2 7) ,低于胎儿期阳性率 (P <0 .0 5 )。结论　胎儿期、生长期和破裂型突出椎间盘组织可产生内源性TGF - β1,提示TGF - β1可能是腰椎间盘发育、生长和退变过程中重要调节因子。     

Herniation of cervical intervertebral disc: immunohistochemical examination and measurement of nitric oxide production.

STUDY DESIGN: Surgically obtained cervical herniated intervertebral discs were examined histologically and immunohistochemically. The production of nitric oxide (NO) in the local tissue was examined using the electron spin resonance (ESR) method. OBJECTIVES: To investigate the local histologic and immunohistochemical changes in cervical disc herniation, including NO production, and to compare such changes with those in autopsy cases. SUMMARY OF BACKGROUND DATA: Very little is known about the histopathologic processes of cervical disc herniation. In addition, no information is available on the level of in vivo NO production in cervical disc herniation. METHODS: Thirty-six herniated cervical discs obtained from 31 patients were immunohistochemically examined for localization of blood vessels, matrix metalloproteinase (MMP)-3, and inducible NO synthetase (iNOS). We also compared the production of NO, measured by the ESR method, in eight specimens with that of five control discs obtained from fresh cadavers. RESULTS: The presence of herniated discs correlated with the degeneration of cartilaginous endplate and torn anulus fibrosus. Formation of new blood vessels around the herniated discs was detected, using von Willebrand factor antibody, in seven uncontained hernias and 20 contained hernias. Immunohistochemical studies showed the presence of cells positive for MMP-3 (chondrocytes), iNOS (chondrocytes and granulation tissue) in cervical disc hernias. ESR analysis showed a significantly higher NO production in herniated cervical discs than in disc samples of fresh cadavers. CONCLUSIONS: Herniated cervical intervertebral disc is characterized by the presence of an inflammatory process associated with neovascularization and increased expression of MMP-3. Production of NO was markedly high in both contained- and uncontained-type hernias.     

Herniated and spondylotic intervertebral discs of the human cervical spine: histological and immunohistological findings in 500 en bloc surgical samples. Laboratory investigation

OBJECT: In this paper the authors' goal was to identify histological and immunohistochemical differences between cervical disc hemrniation and spondylosis. METHODS: A total of 500 cervical intervertebral discs were excised from 364 patients: 198 patients with disc herniation and 166 patients with spondylosis. We examined en bloc samples of endplate-ligament-disc complexes. Types of herniation and graded degrees of disc degeneration on MR images were examined histologically and immunohistochemically. RESULTS: The herniated discs showed granulation tissue, newly developed blood vessels, and massive infiltration of CD68-positive macrophages, which surrounded the herniated tissue mainly in the ruptured outer layer of the anulus fibrosus. The vascular invasion was most significant in uncontained (extruded)-type herniated discs. Chondrocytes positive for matrix metalloproteinase (MMP)-3, tumor necrosis factor (TNF)-alpha, basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) were abundant in both herniated and spondylotic discs. Free nerve fibers, positive for nerve growth factor (NGF), neurofilament 68, growth-associated protein (GAP)-43, and substance P, were strongly apparent in and around the outer layer of uncontained (extruded)-type herniated discs, with enhanced expression of NGF. The authors observed that herniated discs showed more advanced degeneration in the outer layer of the anulus fibrosus around the granulation tissue than spondylotic discs. On the other hand, spondylotic discs showed more advanced degeneration in the cartilaginous endplate and inner layer of the anulus fibrosus than herniated discs. Spondylotic discs also had thicker bony endplates and expressed TNFalpha and MMP-3 more diffusely than herniated discs, especially in the inner layer of the anulus fibrosus. CONCLUSIONS: The authors' results indicate that herniated and spondylotic intervertebral discs undergo different degenerative processes. It is likely that TNFa, MMP-3, bFGF, and VEGF expression is upregulated via the herniated mass in the herniated intervertebral discs, but by nutritional impairment in the spondylotic discs. Macrophage accumulation around newly formed blood vessels in the herniated disc tissues seemed to be regulated by MMP-3 and TNFalpha expression, and both herniated and spondylotic discs exhibited marked neoangiogenesis associated with increased bFGF and VEGF expression. Nerve fibers were associated with NGF overexpression in the outer layer of the anulus fibrosus as well as in endothelial cells of the small blood vessels.     

Nitric oxide mediates the change of proteoglycan synthesis in the human lumbar intervertebral disc in response to hydrostatic pressure

STUDY DESIGN: This in vitro study clarifies the role of nitric oxide (NO) in human lumbar intervertebral disc metabolism. OBJECTIVE: To investigate the effects of NO on proteoglycan synthesis in human lumbar discs and to test the hypothesis that NO is a mediator of the changes in proteoglycan synthesis in response to hydrostatic pressure. SUMMARY OF BACKGROUND DATA: The authors have clarified that hydrostatic pressure has an apparent effect on proteoglycan synthesis as well as matrix metalloproteinase production in the intervertebral disc. The cellular mechanisms underlying the response of disc cells to hydrostatic pressure remain to be clarified. Herniated lumbar discs produce NO in response to interleukin (IL)-1 beta. In articular cartilage, NO mediates the change of proteoglycan synthesis by IL-1 or shear stress. METHODS: Fifty-eight lumbar intervertebral disc specimens were obtained from patients who had undergone posterior discectomy. The specimens were chopped into 1-2-mm cubes and were incubated in a plastic syringe with 1 mL Dulbecco's modified Eagle's medium (DMEM). The syringes were placed in a water-filled pressure vessel kept at 37 C. Hydrostatic pressures of 1 (control), 3, and 30 atmospheres (atm) were applied. Proteoglycan synthesis was determined from (35)S-sulfate incorporation rates. Nitrite (the stable oxidation product of NO) concentration in DMEM was determined by a spectrophotometric method based on the Griess reaction. As a competitive inhibitor of NO synthases, N(G)-methyl-l-arginine (l-NMA, 10-1000 micromol) and as an organic donor of NO, S-nitroso-N-acetylpenicillamine (SNAP, 1-200 micromol) were used. RESULTS: Addition of l-NMA suppressed NO production and increased proteoglycan synthesis rates in the intervertebral disc specimens in a dose-dependent fashion. Addition of SNAP increased exogenous NO content in the medium significantly and suppressed proteoglycan synthesis rates in a dose-dependent fashion. Three-atmosphere hydrostatic pressure stimulated the proteoglycan synthesis rates. Rates were approximately 1.3-fold greater than at 1 atm, whereas 30-atm pressure inhibited proteoglycan synthesis rates. However, the hydrostaticpressure had inverse effect on NO production. At 3 atm, NO production decreased slightly relative to 1 atm, whereas at a pressure of 30 atm, NO production was increased and was approximately 1.32-fold greater than at 1 atm. L-NMA enhanced the 3-atm pressure-induced increase in proteoglycan synthesis and also relieved the suppression of proteoglycan synthesis at a pressure of 30 atm. CONCLUSION: The current study confirmed the previous finding that human herniated lumbar disc cultures spontaneously produce NO. Endogenously generated and exogenously supplied NO inhibited proteoglycan synthesis in the intervertebral disc. Hydrostatic pressure influenced NO production by disc cells, and NO is one of the mediators that changes proteoglycan synthesis in response to hydrostatic pressure. These results may show that autocrine and paracrine mechanisms of NO play an important role in the regulation of disc cell metabolism under mechanical stress and in the pathophysiology of intervertebral disc degeneration.     

一氧化氮在神经根性疼痛中的作用

目的：探索一氧化氮(NO)在髓核突出所致的神经根性疼痛中的作用。方法：取大鼠自体尾椎髓核无压迫下放置在L4和L5神经根表面，分别在术后3d及1、2、3、4周时观察大鼠后足机械刺激和热刺激敏感性的变化，并用免疫组化方法对移植髓核中的一氧化氮合酶(NOS)进行检测．探索NO在疼痛中的作用：结果：在无明显机械压迫情况下，大鼠腰神经根上放置自体髓核可产生痛觉过敏，移植髓核组织中NOS染色阳性一结论：髓核自身是引起腰腿痛的重要原因，NO可能参与疼痛的产生.     

Role of nitric oxide in wound repair

After injury, wound healing is essential for recovery of the integrity of the body. It is a complex, sequential cascade of events. Nitric oxide (NO) is a small radical, formed from the amino acid L-arginine by three distinct isoforms of nitric oxide synthase. The inducible isoform (iNOS) is synthesized in the early phase of wound healing by inflammatory cells, mainly macrophages. However many cells participate in NO synthesis during the proliferative phase after wounding. NO released through iNOS regulates collagen formation, cell proliferation and wound contraction in distinct ways in animal models of wound healing. Although iNOS gene deletion delays, and arginine and NO administration improve healing, the exact mechanisms of action of NO on wound healing parameters are still unknown. The current review summarizes what is known about the role of NO in wound healing and points out path for further research.     

The role of mast cells in disc herniation inflammation.

STUDY DESIGN: A study of herniated lumbar disc tissue samples and control disc material to determine the presence of mast cells in disc herniations. OBJECTIVES: To analyze whether mast cells have any involvement in disc herniation pathophysiology and lumbar pain, because mast cells may have an important role in acute and chronic inflammatory responses. SUMMARY OF BACKGROUND DATA: Studies of inflammatory cells, biochemical mediators of inflammation, and tissue degrading enzymes have suggested that these factors may be involved--and perhaps play an important role--in the pathophysiology of lumbar pain and radiculopathy. Mast cells are known to play an important role in acute and chronic inflammatory responses. It was therefore of interest to clarify their possible role in intervertebral disc herniation inflammation. METHODS: Fifty herniated lumbar discs from 50 patients who had undergone disc surgery and three normal control discs were obtained. Sections from every disc then were examined histologically and immunocytochemically for mast cells by using monoclonal antibodies to either of two types of specific proteases of mast cells, tryptase and chymase. RESULTS: By none of the methods could any mast cells be observed in any of the control disc samples. With toluidine blue staining, mast cells were observed in 9 of 50 (18%) of discs. Mast cells immunoreactive to either tryptase or chymase were observed in 10 of 50 disc samples (20%) and immunoreactive for tryptase and chymase simultaneously in 4 of 50 disc samples (8%). However, the majority of the samples studied (80%) demonstrated immunoreactivity to neither tryptase nor chymase. Among the samples studied were five disc protrusions that totally lacked mast cells. CONCLUSIONS: A minority of disc herniations exhibited mast cells, as verified by toluidine blue staining and immunocytochemistry. The results may suggest a role of mast cells in intervertebral disc herniation inflammation, but only in a subset of these cases. Massive infiltration by mast cells never was observed.     

前列腺素E2在突出腰椎间盘中的表达及其与坐骨神经痛的关系

目的探讨前列腺素(PG)E2在突出腰椎间盘组织中的表达及其在坐骨神经痛发病机制中的作用。方法 42个突出椎间盘标本取自42例腰椎间盘突出并有坐骨神经放射性疼痛症状的手术治疗患者,其中膨隆型12例,破裂型15例,游离型15例,取材部位为紧贴神经根突入椎管的椎间盘组织(A部位)和椎间隙内残存的椎间盘组织(B部位)。术前采用视觉模拟评分(VAS)对所有患者坐骨神经痛严重程度进行评分。应用酶联免疫吸附试验(ELISA)检测PGE2含量。结果 A部位PGE2含量自膨隆型、破裂型至游离型逐渐升高,差异有显著性(P<0.01);A部位PGE2含量高于B部位(P<0.01);PGE2含量与患者坐骨神经痛VAS评分存在明显相关性(r=0.848,P<0.01)。结论 PGE2参与了腰椎间盘退变、突出的发病机制,PGE2含量与坐骨神经痛程度呈正相关性。     

神经源性膀胱组织中一氧化氮合酶表达的特点和意义

目的 探讨神经元型一氧化氮合酶(nNOS)、诱导型NOS(iNOS)和内皮型NOS(eNOS)在神经源性膀胱组织中表达状况,探讨一氧化氮在神经源性膀胱组织中产生及作用特点.方法 神经源性膀胱患儿30例.男18例,女12例.年龄(6.3±3.1)岁.30例均行手术治疗,术中留取膀胱组织标本,采用免疫组织化学方法检测膀胱组织中nNOS、iNOS和eNOS表达状况,10例正常膀胱组织标本作对照. 结果 正常膀胱体部组织nNOS阳性表达,走行在平滑肌纤维之间,分布于平滑肌细胞表面,膀胱基质也有表达,组织化学评分(HS)为2.8～4.0和1.2～2.7;平滑肌细胞iNOS阴性表达,平滑肌细胞基质有少量稀疏表达,HS为0～0.4和0～0.1;eNOS表达分布于血管内皮细胞中,分布稀疏,平滑肌细胞无表达.膀胱颈部组织表达高于膀胱体部组织,以nNOS表达为主.神经源性膀胱组织中以iNOS表达为主,nNOS表达明显减少;eNOS主要分布于膀胱基质的内皮细胞,膀胱平滑肌、成纤维细胞阴性表达;病变膀胱组织血管稀疏,微血管密度100倍视野下可见到(6.8±3.2)个血管灶,低于正常膀胱组织的(16.7±6.3)个(P＜0.01).结论 正常膀胱组织nNOS主要分布在膀胱颈中,NO合成主要受nNOS调节.神经源性膀胱患者膀胱组织中氮能神经元分布稀疏,nNOS表达减少,iNOS表达上调,NO的合成与调节可能主要来源于iNOS,受iNOS水平调节,eNOS表达下降,提示膀胱组织血供不良.