Distribution of constitutive nitric oxide synthase in the jejunum of adult rat

AIM: To study the distribution of the constitutive nitric oxide synthase (NOS) in the jejunum of adult rat. METHODS: The distribution of endothelial NOS (eNOS) was detected by immunohistochemistry. Immunofluorescence histochemical dual staining technique were used for studying the distribution of neuronal NOS (nNOS) and eNOS. The dual stained slides were observed under a confocal laser scanning microscope. RESULTS: Positive neuronal NOS (nNOS) and endothelial NOS (eNOS) cells were found to be distributed in lamina propria of villi, and the epithelial cell was not stained. eNOS was mainly located in submucosal vascular endothelia, while nNOS was mainly situated in myenteric plexus. Some cells in the villi had both nNOS and eNOS. More than 80% of the cells were positive for both nNOS and eNOS, the rest cells were positive either for nNOS or for eNOS. CONCLUSION: The two constitutive nitric oxide synthases are distributed differently in the jejunum of rat. nNOS distributed in myenteric plexus is a neurotransmitter in the non-adrenergic non-cholinergic (NANC) inhibitory nerves. eNOS distributed in endothelial and smooth muscle cells of blood vessels plays vasodilator role. eNOS and nNOS are coexpressed in some cells of lamina propria of villi. NO generated by those NOS is very important in the physiological and pathological process of small intestine.

Distribution of nitric oxide synthase in stomach myenteric plexus of rats

AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus. METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique. RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus.The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62+/-38 cells mm(2) (antrum), 43+/-32 cells/mm(2) (body), and 32+/-28 cells mm(2) (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels. CONCLUSION: Nitric oxide might be involved in the modulation of motility, secretion and blood circulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach.

The Role of Nitric Oxide in Hyperoxic Lung Injury in Premature Rats

To investigate the role of nitric oxide (NO) in hyperoxic lung injury, the 3 day old preterm rats were randomly assigned to four groups: group I (hyperoxia group), group Ⅱ (hyperoxia+N w nitro L arginine methyl ester (L NAME) group), group Ⅲ (air group), and group Ⅳ (air+L NAME) group. Group Ⅰ and Ⅱ were exposed to ≥90 % O 2 for 3 or 7 days. Group Ⅱ and Ⅳ received subcutaneous L NAMEy on daily basis (20 mg/kg). After 3 day or 7 day exposure, the lung wet weight/dry weight ratio (W/D), total protein and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF) and lung pathology were examined in all groups. NO content, expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in lungs were measured in group Ⅰ and Ⅲ. Our results showed that after 3 day exposure, group Ⅰ appeared acute lung injury characterized by the increase of MDA content ( P <0.01) and the presence of hyperaemia, red cell extravasation and inflammatory infiltration; after 7 day exposure, except MDA, total protein and W/D were also increased in comparison with group Ⅲ ( P <0.01, 0.05), pathological changes were more severe than those after 3 day exposure. After 3 and 7 day exposure, total protein in group Ⅱ was significantly increased as compared with group Ⅰ ( P <0.01 for both). The pulmonary acute inflammatory changes were more obvious in group Ⅱ than in group Ⅰ. Occasionally, mild hemorrhage was detected in the lungs of group Ⅳ. BALF protein content in group IV was higher than that in group Ⅲ after 7 day exposure ( P <0.01). After 3 and 7 day exposure, NO content in BALF were all significantly elevated in group Ⅰ as compared with group Ⅲ ( P <0.01 for all). In the lungs of group Ⅰ, strong immunostaining for iNOS was observed in airway and alveolar epithelia, inflammatory cells, which were stronger than those in group Ⅲ. Expression of iNOS in rats after 7 day hyperoxic exposure was stronger than that after 3 day exposure. Shortly after 7 day exposure, stronger immunostaining for eNOS in airway epithelia in group Ⅰ than that in group Ⅲ was seen. Our study suggested that treatment with L NAME worsened acute hyperoxic lung injury in preterm rats and also had a deleterious effect on the rats exposed to air, indicating that endogenous nitric oxide may play a protective role in rats under both physiological and hyperoxic status. Hyperoxia can significantly upregulate the expression of iNOS and eNOS in inflammatory cells, epithelia in the lungs of preterm rats, promote NO generation, which suggests that endogenous NO may mediate the hyperoxic pulmonary damage. Over stimulation of iNOS may contribute to the pathogenesis of hyperoxic lung injury. NO may have dual roles in pulmonary oxygen toxicity.

Spatio-temporal expression of inducible nitric oxide synthase in and surrounding a region of rat frontal lobe damaged with a sharp instrument

BACKGROUND： Inducible nitric oxide synthase （iNOS） cannot be detected in the neurons and glial cells of normal rats, but iNOS can be found in some neurons and glial cells of rats following ischemic, traumatic, neurotoxic or inflammatory damage. OBJECTIVE： To investigate iNOS expression and iNOS-positive cell types at various time points following damage to the rat frontal lobe using a sharp instrument. DESIGN： A nerve molecular biology, randomized, controlled study. TIME AND SETTING： This experiment was performed at the Department of Human Anatomy, Institute of Neurobiology, Medical School of Nantong University, between April 2006 and December 2007. MATERIALS： Rabbit anti-iNOS antibody （Santa Cruz, USA）, biotin labeled goat anti-rabbit antibody （Sigma, USA）, reverse transcription kit （Biouniquer, Hong Kong, China） and horseradish peroxidase labeled goat anti-rabbit antibody （Pierce, USA） were used for this study. METHODS： A total of 112 healthy rats aged 3 months were randomly assigned into a sham operation group （n = 28） and a damage group （n = 84）. Rat models of frontal lobe damage were induced in the damage group using a sharp instrument to make an incision in the frontal lobe cortex. In the sham operation group, the rat bone window was opened but brain tissues were left intact. MAIN OUTCOME MEASURES： Parameters were measured at 3, 6, 12, 24, 72, 120 and 168 hours following damage in both groups. Pathological changes were observed using Nissl staining and hematoxylin-eosin staining. Expression of iNOS mRNA, iNOS protein and iNOS-positive cells were examined by RT-PCR, Western blot analysis and immunohistochemistry, respectively. RESULTS： A large number of inflammatory cells infiltrated the damaged region 12 and 24 hours following damage, iNOS mRNA and iNOS protein expression increased in and around the damaged region 3 hours following damage, reached a peak at 24 hours, and then gradually decreased. The changes in iNOS-positive cell number reflected the changes in iNOS mRNA and iNOS protein expression after damage, iNOS was mainly found in neural cells at 3 and 6 hours, in macrophages at 12 and 24 hours, and in glial cells at 72 and 120 hours after damage. iNOS-positive cells were few in and surrounding the damaged region at 168 hours. There were a few iNOS-positive neural cells in the rat frontal lobe cortex in the sham operation group. CONCLUSION： Neurons, macrophages and glial cells can express iNOS following rat frontal lobe damage caused by a sharp instrument. The levels of iNOS expression, and the cell types expressing iNOS, change with time.

COLOCALIZATION OF NITRIC OXIDE SYNTHASE IN GNRH NEURONS OF RAT FOREBRAIN AND HYPOTHALAMUS

In order to gain more information about the effect of nitric oxide (NO) on GnRH release, double NADPH diaphorase histochemistry GnRH immunohistochemistry staining was used to investigate the morphological relationship between NO synthase (NOS) containing cells and GnRH neurons in the forebrain and hypothalamus of rats. The results showed that some of the GnRH neurons in the diagonal band of Broca, olfactory tubercle and deeper part of temporal cortex had the NOS activity, suggesting GnRH secretion can be rapidly regulated by NO derived from GnRH neurons themselves in an autocrine manner.

Immunohistochemical Analysis of Citrulline-Nitric Oxide Cycle Enzymes and Glutamine Synthetase in Different Regions of Brain in Epilepsy Rat Model

The aim of this study was to determine the immunoreactivity of neuronal and inducible nitric oxide synthetase, argininosuccinate synthetase, argininosuccinate lyase, glutamine synthetase in different regions of brain in rats of kainic acid mediated epilepsy. Male Sprague-Dawley rats were used in this study. The acute group animals were sacrificed after 2 hours and the chronic group animals were sacrificed after 5 days of a single subcutaneous injection of kainic acid (15 mg/kg body weight). The cerebral cortex, cerebellum and brain stem slices were fixed and immunohistostained for the above enzymes. Images were captured and analyzed. In acute group, argininosuccinate synthetase and inducible nitric oxide synthetase were increased in cerebral cortex and cerebellum, neuronal nitric oxide synthetase increased in cerebral cortex and brain stem, and there was no change in argininosuccinate lyase immunoreactivity compared to control group. In chronic group, glutamine synthetase was decreased and all other enzymes immunoreactivity was increased in all the brain regions tested. This study demonstrated the up-regulation of citrul-line-nitric oxide cycle enzymes and may contribute to enhancing recycling of citrulline to arginine to support the increased production of nitric oxide in epilepsy. The decreased glutamine synthetase may increase glutamate in chronic epilepsy and may lead to neurodegeneration.

Immunohistochemical localization of nitric oxide synthase in gastrointestinal tract of rats

Objective: To investigate the distribution of the three subtypes of nitric oxide synthase (NOS) inthe gastrointestinal tract of rats. Methods: Immunohistochemical ABC methods were used. Results: Neuronal NOS(nNOS)-positive substance was localized in epithelial cells, endocrine cells, endothelial cells andneuronal cell bodies in the intermuscular plexus and submucous plexus. Inducible NOS(iNOS)-positive substance was located in smooth muscle cells in gastric corpus, intestinal mucosa epithelium and endocrine cells.Endothelial NOS(eNOS)-positive substance was distributed mainly in vascular endothelial cells. Conclusion:The distribution patterns of the three subtypes of NOS exhibited specificity and overlapping profile in the gastrointestinal tract of rats.

诱导型一氧化氮合酶对肺纤维化形成的促进作用

目的 :研究纤维化肺内诱导型一氧化氮合酶上调及其与肺纤维化形成的关系。方法 :气管内滴注平阳霉素 (BLMA55mL/kg) ,观察注后 7、14、30d肺组织诱导型一氧化氮合酶 (iNOS)阳性细胞数和Ⅰ、Ⅲ型胶原纤维的变化 ;用氨基胍 (AG)阻断iNOS合成NO后 ,观察出肺血中NO-2 /NO-3 和肺组织中羟脯氨酸含量以及肺组织形态结构的变化。结果 :①注BLMA57d、14d和 30d组大鼠肺间质iNOS阳性细胞数明显多于对照组 (P <0 .0 1) ,并且 ,BLMA57d组和BLMA514d组还多于BLMA530d组 (P <0 .0 1)。BLMA514d和 30d组大鼠肺间质胶原纤维的出现多于对照组 ,BLMA514d组以Ⅲ型胶原纤维增多为主 ,BLMA530d组以Ⅰ型胶原纤维增多为主。②AG缓解出肺血NO-2 /NO-3和肺组织中羟脯氨酸含量的升高 ;AG还阻止肺间质或纤维细胞和巨噬细胞的增多。结论 :在肺纤维化形成过程中 ,肺内iNOS上调 ,大量生成NO ,有促肺纤维化的作用。

一氧化氮合酶同功异构酶在大鼠中枢神经系统的分布

本文采用免疫组织化学技术观察三种一氧化氮合酶同功异构酶在正常大鼠中枢神经系统的分布。结果显示：ＮＯＳ１ 阳性神经元分布于中枢神经系统的广泛区域，包括大脑皮质Ⅱ、Ⅲ、Ⅵ层，海马分子层，齿状回多形层，尾壳核，中脑上丘，小脑皮质分子层和颗粒层，脊髓Ⅰ、Ⅱ层、侧角、中央灰质和前角。脊髓中央管室管膜上皮也为阳性。ＮＯＳ３ 阳性神经元的分布区域与前者有部分重叠，但也有差别：大脑皮质相同层次内的ＮＯＳ３ 阳性神经元的形态和染色不同于ＮＯＳ１；密集分布于海马锥体细胞层和齿状回颗粒细胞层；小脑浦肯野细胞ＮＯＳ３ 阳性；另外，ＮＯＳ３ 阳性神经元弥散分布于脊髓内，其胞体和核仁均呈阳性。ＮＯＳ２ 阴性。广泛的分布表明ＮＯ 与中枢神经系统的诸多功能有关，而ＮＯＳ１ 与ＮＯＳ３ 分布的差异又说明中枢神经系统不同神经元内ＮＯ的产生是由此两种同功异构酶分别参与而完成的。

大鼠胃肠道一氧化氮合酶分布的免疫组织学研究

目的：研究一氧化氮合酶（ＮＯＳ）三种不同类型在大鼠胃肠道的分布．方法：采用兔抗人ＮＯＳ抗血清免疫组织化学ＡＢＣ法．结果：神经组成型ＮＯＳ（ｎ－ｃＮＯＳ）阳性物质分布于胃肠道粘膜层的上皮细胞、内分泌细胞、血管内皮细胞、固有层中的组织细胞和肌间神经丛及粘膜下神经丛的神经节细胞；诱导型ＮＯＳ（ｉＮ－ＯＳ）阳性物质分布于胃体的平滑肌细胞、十二指肠腺及肠粘膜上皮细胞和内分泌细胞中；内皮组成型ＮＯＳ（ｅ－ｃＮＯＳ）分布于血管内皮及胃肠道粘膜固有层的组织细胞内．结论：三种类型的ＮＯＳ分布部位有一定的特异性，又有一定程度重叠，提示三种ＮＯＳ可能在生理病理活动中作用有所不同，又有协同效应．

高脂血症大鼠海马nNOS及NT-3免疫阳性神经元的变化

目的 观察高脂血症大鼠海马中神经元型一氧化氮合酶 (nNOS)及神经营养因子 3(NT 3)的变化 ,并探讨其临床意义。方法 采用HE和SABC免疫组织化学染色方法 ,结合计算机图像分析系统 ,比较两组海马各区平均光密度(MOD)值。结果 与对照组相比 ,实验组血清总胆固醇(6 6 5mmol/L)及血清低密度脂蛋白胆固醇 (4 4 1mmol/L)升高明显 ,差异有显著性。实验组海马各区nNOS免疫阳性神经元MOD升高 ,尤以CA3区明显 ;NT 3免疫阳性神经元MOD降低 ,以CA1区最为显著。结论 高脂血症大鼠海马中nNOS表达增强而NT 3表达减弱 ,表明高脂血症可导致海马神经元功能改变。

大鼠额叶损伤后诱导型一氧化氮合酶的表达变化

为了探讨大鼠额叶损伤后不同时间诱导型一氧化氮合酶(iNOS)的表达变化及意义,本研究采用大鼠额叶锐器损伤模型,经Nissl和H.E.染色观察伤后的病理变化过程,RT-PCR及免疫组织化学染色方法检测伤后iNOSmRNA和iNOS阳性细胞的表达变化。结果显示:伤后12、24h创伤区炎症细胞大量浸润;创伤区及周边iNOSmRNA的表达3h开始上升,24h达到高峰;伤后iNOS阳性细胞数量也增多,伤后3、6h主要由神经细胞表达iNOS,在12、24h主要由巨噬细胞表达iNOS,而72、120h则主要由胶质细胞表达iNOS。上述结果说明大鼠额叶锐器伤后iNOS的表达增加,iNOS阳性细胞的种类和数量变化与伤后时程有关。

氨基胍干预对创伤性面瘫大鼠外周面神经及周围组织一氧化氮合酶表达的影响

目的 研究诱导型一氧化氮合酶抑制剂氨基胍对创伤性面瘫大鼠外周面神经及周围组织一氧化氮合酶表达的影响。方法 通过大鼠面瘫前后腹膜内小剂量给予氨基胍 ,在伤后各个时间点切取损伤面神经和软组织 ,采用兔抗大鼠一氧化氮合酶 (NOS)抗血清免疫组织化学ABC法对面神经和肌肉软组织内NOS表达的变化进行研究。结果 氨基胍组面神经和肌肉软组织伤后诱导型一氧化氮合酶免疫反应性明显降低。结论 氨基胍慢性干预明显抑制面神经和肌肉软组织内诱导型一氧化氮合酶的表达 。

急性心肌梗死大鼠心脏一氧化氮合酶表达的改变

目的通过建立大鼠心肌梗死模型,观察急性心肌梗死对大鼠心脏内皮型一氧化氮合酶mRNA和诱导型一氧化氮合酶蛋白表达的影响。方法48只健康成年SD大鼠(体重200～250g)随机分为假手术组和缺血组,取1、2、8和24h四个不同时间点观察。采用开胸结扎冠状动脉左前降支建立心肌缺血模型,逆转录聚合酶链反应检测大鼠心肌梗死后1、2及24h三个时段缺血心肌内皮型一氧化氮合酶mRNA的表达;免疫组织化学染色检测冠状动脉结扎后8h缺血心肌诱导型一氧化氮合酶蛋白的表达。结果冠状动脉结扎后2h,缺血组大鼠缺血心肌组织内皮型一氧化氮合酶mRNA表达下降(P<0.05),并持续至结扎后24h;结扎后24h组内皮型一氧化氮mRNA的表达与结扎后2h组相比无显著性差异(P>0.05)。冠状动脉结扎后8h,梗死区存活心肌组织细胞诱导型一氧化氮合酶蛋白大量表达,而假手术组未见诱导型一氧化氮合酶蛋白表达。结论正常大鼠心肌组织有内皮型一氧化氮合酶基因表达,无诱导型一氧化氮合酶蛋白表达。在心肌梗死早期缺血心肌内皮型一氧化氮合酶mRNA表达减少。心肌急性缺血刺激早期诱导大鼠缺血心肌组织诱导型一氧化氮合酶蛋白大量表达。

大鼠异种原位肝移植急性排斥反应中一氧化氮合酶细胞定位的意义

目的 探讨一氧化氮合酶（ｃＮＯＳ，ｉＮＯＳ） 在金黄地鼠至大鼠异种原位肝移植急性排斥反应中的细胞定位及其意义．方法 我们应用金黄地鼠至大鼠异种原位肝移植急性排斥反应及大鼠同基因原位肝移植动物模型，应用ＮＡＤＰＨ 黄递酶组化染色及免疫组化染色观察移植肝组织ＮＯＳ 的活性及ｃＮＯＳ，ｉＮＯＳ 的蛋白表达．结果 大鼠异种原位肝移植急性排斥反应时血浆ＮＯ 代谢产物ＮＯ－ｘ 明显增高，环孢菌素Ａ 可显著抑制ＮＯ 的合成． 异种肝移植急性排斥反应时，ＮＡＤＰＨ＿ｄ 组化染色及其兔抗大鼠多克隆抗体ｉＮＯＳ，ｃＮＯＳ 免疫组化染色均呈强阳性表达，但以ｉＮＯＳ表达为主．ｉＮＯＳ 主要在肝细胞、肝窦内皮细胞及Ｋｕｐｆｆｅｒ 细胞等炎性细胞表达，而同基因组及免疫抑制治疗组则不表达．结论 原位肝移植肝细胞ＮＯ 产物可随移植肝的免疫状态不同而异，肝细胞ＮＯ 很可能具有重要的免疫保护作用，ＮＯ 合酶及其代谢产物ＮＯ－ｘ 在肝移植急性排斥反应中可具有早期的免疫学监测作用．

L-NAME对肝硬化大鼠胃肠道中一氧化氮合酶亚型表达的影响

目的 研究一氧化氮合酶亚型 (NOS1 ,NOS2 ,NOS3)在肝硬化大鼠胃肠道中的表达 ,并探讨 NOS抑制剂左旋硝基精氨酸甲基酯 (L- NAME)对其表达的影响 .方法 制作大鼠四氯化碳中毒肝硬化模型 ,肝硬化模型大鼠随机分为 NO合酶 (NOS)抑制剂治疗组和未治疗组 ,模型治疗组用 L - NAME0 .5 mg· kg- 1· d- 1 ,胃内注入 ,每日 1次 ,治疗 10 d.免疫组织化学染色显示胃肠道组织中各型 NOS的染色强度和分布 ,Western blot法检测胃肠道组织中各型 NOS的表达 .结果 模型组大鼠胃、小肠、结肠组织中的 NOS染色强度显著弱于正常对照组和 L- NAME治疗组大鼠 .Western blot显示在肝硬化模型大鼠胃、小肠、结肠组织中的各型 NOS表达均明显降低 ,L - NAME治疗后又恢复至接近正常 .结论 肝硬化大鼠胃肠道组织中各型 NOS的表达明显减少 ,L-

灵芝孢子对大鼠脊神经腹根切断后脊髓运动神经元存活及其NT-3、NOS表达的影响

目的探讨灵芝孢子(萌动激活赤灵芝孢子)对大鼠脊髓受损伤运动神经元存活和表达神经营养素_3(NT_3)及一氧化氮合酶(NOS)的影响。方法对单侧腹根切断后的大鼠胃饲不同剂量的灵芝孢子,计算受损伤运动神经元存活率;用免疫组织化学及原位杂交方法检测NT-3的表达;用酶组织化学方法检测NOS的活性。结果腹根切断后35 d,对照组运动神经元存活率为47.32%,灵芝孢子低、中、高剂量组的运动神经元存活率分别为67.11%、72.67%和81.67%;腹根切断后高剂量组存活的运动神经元NT_3和NOS的表达都高于对照组。结论灵芝孢子促进大鼠脊髓前角受损伤的运动神经元存活,其存活率与用药剂量有关;灵芝孢子促进大鼠脊髓存活的运动神经元表达NT-3和NOS。

与学习记忆相关的脑内cGMP的表达及其与一氧化氮的关系

学习记忆;;ｃＧＭＰ;;一氧化氮合酶抑制剂;;免疫组织化学;;

大鼠脑发育过程中神经型一氧化氮合酶的表达变化

目的用免疫组化方法探讨神经型一氧化氮合酶在大鼠脑发育过程中的表达变化。方法分别随机选取E12、E15、E18、P0、P5及P10期的SD大鼠,应用免疫组化方法,检测大脑皮层、纹状体及海马nNOS阳性细胞的密度。结果E12、E15及E18期大鼠脑组织未见nNOS阳性细胞;大脑皮层及纹状体区P0、P5及P10期均可见nNOS阳性细胞。nNOS阳性细胞密度,在P0、P5及P10期逐渐降低,两两比较,有显著性差异(P<0.05)。P0期海马偶见nNOS阳性细胞,P5期和P10期均可见较多nNOS阳性细胞,但nNOS阳性细胞密度P5和P10期之间无统计学差异(P>0.05)。结论胚胎期大鼠脑内nNOS染色呈阴性反应;生后大脑皮层及纹状体nNOS阳性细胞密度逐渐减小,海马nNOS阳性细胞密度则有所增加。

新生大鼠缺血缺氧后脑内一氧化氮合酶的动态表达

实验采用生后 14天 Wistar大鼠缺血缺氧 (HI)动物模型 ,用免疫组织化学方法观察 HI复苏 (HI/ R)后前脑一氧化氮合酶动态表达。结果显示 :神经元型一氧化氮合酶 (n NOS)阳性神经元主要分布于新生大鼠大脑皮层的 - 层 ,尾状核、隔核及嗅结节。 HI/ R早期其表达水平无明显变化 ;复苏 48小时及 5天后 ,可分别在右侧大脑顶皮层或右侧大脑顶皮层和尾状核区出现梗塞灶 ,该区 n NOS阳性神经元明显减少。而诱导型一氧化氮合酶 (i NOS)阳性细胞在 HI/ R后 12小时始现于损伤侧的侧脑室 ;随时间的推移在损伤侧缰核、皮层、尾状核以及丘脑背外侧核、丘脑腹侧核可见 i NOS阳性细胞逐渐增多并染色加深。用识别单核巨噬细胞的克隆 ED 1单克隆抗体检测可见 ED 1阳性细胞出现的时间和在脑区的分布与 i NOS阳性细胞相似。本实验提示 ,在局灶性脑缺血缺氧早期 ,脑内 NO的释放不依赖于 n NOS阳性神经元或 i NOS阳性细胞 ;而在局灶性脑缺血缺氧晚期 ,i NOS阳性细胞产生的