Y-1型计测板对红细胞微量压积测量效果的初步评价

Ｙ－１型计测板对红细胞微量压积测量效果的初步评价袁光孚，保菊英，王冀湘，耿广献西宁市一医院ＥＶＡＬＵＡＴＩＯＮＯＦＡＣＡＬＣＵＬＡＴＩＮＧＰＬＡＴＥＭＯＤＥＬＹ－ＩＦＯＲＴＨＥＭＥＡＳＵＲＥＭＥＮＴＯＦＭＩＣＲＯ－ＨＥＭＡＴＯＣＲＩＴ．￥ＹｕａｎＧｕ...     

内源性一氧化氮调节大鼠低氧性肺血管结构的重建

目的 研究内源性一氧化氮对低氧性肺血管结构重建形成的调节作用。方法 大鼠随机分为４组;常氧组（ｎ＝８）、低氧组（ｎ＝８）、低氧＋Ｌ－精氨酸（Ｌ－Ａｒｇ）组（ｎ＝８）、低氧＋Ｎ＾ω－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ组）９ｎ＝６）。以光镜观测各组大鼠肺中、小肌型动脉的相对中膜厚度（ＲＭＴ）及相对中膜面积（ＲＭＡ）和三型肺小血管百分比。结果 低氧组大鼠肺中、小型动脉ＲＭＴ及ＲＭＡ和肺小血管肌型动脉百分     

血小板质控初探

血小板质控初探袁光孚，张玉芳，保菊英，秦振庭西宁市第一人民医院ＣＡＭＰＡＲＩＳＩＯＮＯＦＤＩＦＦＥＲＥＮＴＭＥＴＨＯＤＳＦＯＲＰＬＡＴＥＬＥＴＣＯＵＮＴＩＮＧＡＴＨＩＧＨＡＬＴＩＴＵＤＥＱＩＮＧＨＡＩ￥Ｋｕａｎｇ－ＦｕＹｕａｎ．ｅｔａｌ（Ｘｉ－Ｎｉｎ...     

不同日龄、不同病情新生儿血小板数量的观察

不同日龄、不同病情新生儿血小板数量的观察秦振庭，王广方北京医科大学第一临床医学院妇儿医院ＰＬＡＴＥＬＥＴＣＯＵＮＴＳＡＴＤＩＦＦＥＲＥＮＴＡＧＥＧＲＯＵＰＳＯＦＮＥＷＢＯＲＮＳ￥Ｃｈｅｎ－ＴｉｎｇＣｈｉｎｅｔａｌ（Ｗｏｍｅｎ＆Ｃｈｉｌｄｒｅｎｈｏｓｐ...     

小儿急性白血病患者血浆纤维结合蛋白测定的临床意义

小儿急性白血病患者血浆纤维结合蛋白测定的临床意义张宝玺，郭稳捷河北医学院附属二院儿科ＴＨＥＣＬＩＮＩＣＡＬＳＩＧＮＩＦＩＣＡＮＣＥＯＦＰＬＡＳＭＡＦＩＢＲＯＮＥＣＴＩＯＮＤＥＴＥＣＴＩＯＮＩＮＣＨＩＤＨＯＯＤＡＣＵＴＥＬＥＵＫＥＭＩＡ￥ＺｈａｎｇＢａ...     

急性下呼吸道感染患儿一氧化氮,循环内皮细胞改变及相关性研究

研究目的：急性下呼吸道感染（ＡＬＲＩ）时血管内皮细胞损伤机制及其临床意义。研究方法：ＡＬＲＩ患儿３６例，正常健康儿童３０例为对照组。测定一氧化氮（ＮＯ）水平及循环内皮细胞（ＣＥＣ）数量。研究结果：ＮＯ的稳定代射产物一循环亚硝酸／硝酸根离子（ＮＯ＾－２／ＮＯ＾－３）水平，对照组为２４．５±１４．１μｍｏｌ／Ｌ，ＡＬＲＩ组为４４．６±２２．６μｍｏｌ／Ｌ，差异显著（Ｐ＜０．０５）。ＣＥＣ数量对照组５．     

新生儿肺炎尿NO2^—／NO3^—和血浆内皮素的变化及其临床意义

为了解新生儿肺炎内源性一氧化氮（ＮＯ）和内皮素（ＥＴ）的动态变化及其在重症肺炎发病机理中所起的作用，对４０例肺炎新生儿进行尿ＮＯ２＾－／ＮＯ３＾－和血浆ＥＴ水平的测定。结果示尿ＮＯ２＾－／ＮＯ３＾－在轻症肺炎儿明显升高，而重症肺炎儿却明显下降，随着疾病的恢复，尿ＮＯ＾２－／ＮＯ３＾－相应下降或升高，血浆ＥＴ在轻症和重症肺炎儿均高于对照组，病情越重，ＥＴ越高，随着疾病恢复，ＥＴ水平下降。本研究提示内     

一氧化氮对缺氧性肺血管结构重建大鼠肺动脉血小板源生长因子表达的影响

目的 探讨一氧化氮对缺氧性肺血管结构重建大鼠肺动脉中血小板源生长因子 （ＰＤＧＦ）表达的影响。方法 将大鼠随机分为４组：常氧组（６只）、低氧组（６只）、低氧＋Ｌ－精氨酸组（低氧＋Ｌ－Ａｒｇ组）（７只）及低氧＋Ｎ＾ω－硝基－Ｌ－精氨酸甲酯组（低氧＋Ｌ－ＮＡＭＥ组）（６只）。以光学显微镜观测４组大鼠肺中、小肌型动脉的相对中膜厚度（ＲＭＴ）。应用ＰＤＧＦ的单克隆抗体经免疫组织化学技术对４组大鼠肺动脉ＰＤ     

窒息新生儿血浆内皮素和一氧化氮水平的动态变化及其临床意义

为探讨正常新生儿早期和窒息后患儿血浆中内皮素（ＥＴ）和一氧化氮（ＮＯ，以ＮＯ－２／ＮＯ－３值代表）的变化，采用放射免疫法和镉柱比色法测定４２例窒息新生儿和１８例正常新生儿血浆ＥＴ、ＮＯ水平变化。结果表明，窒息急性期ＥＴ增高，ＮＯ－２／ＮＯ－３值降低，尤以重度窒息儿显著；恢复期ＥＴ降低，ＮＯ－２／ＮＯ－３值在足月儿窒息组表现为持续增加，早产窒息儿则降低；ＮＯ－２／ＮＯ－３值与各围产因素无显著相关。提示ＥＴ和ＮＯ水平与窒息严重程度呈正相关。     

小儿血液病骨髓活检的临床意义

小儿血液病骨髓活检的临床意义屠立明，沈亦逵，王若洁广东省人民医院儿科ＣＬＩＮＩＣＳＩＧＮＩＦＩＣＡＮＣＥＯＦＢＯＮＥＭＡＲＲＯＷＢＩＯＰＳＹＩＮＣＨＬＬＤＲＥＮＨＥＭＡＴＯＬＯＧＩＣＤＩＳＥＡＳＥＳ￥ＴｕＬｉｍｉｎｇ，ｅｔａｌ．（ＧｕａｎｇｄｏｎｇＰ...     

儿童血管瘤内皮细胞功能测定及病因学意义

目的　探讨血管瘤内皮细胞功能及其病因学意义。方法　采用放射免疫和硝酸还原酶法测定儿童血管瘤 30例瘤体内皮素 (ET)、一氧化氮 (NO)及外周血ET、NO水平 ,以 2 0例斜疝患儿外周血作为对照。结果　血管瘤患儿瘤体ET(6 6 .3± 12 .5 )pg/ml显著高于外周血 (5 5 .3± 13.1)pg/ml(P <0 .0 1) ,外周血ET与对照组 (5 4 .4± 15 .1) pg/ml相比差异无显著性意义 (P >0 .0 5 )。增生期血管瘤体ET(75 .6± 12 .5 ) pg/ml高于退化期 (6 5±10 .2 ) pg/ml及退化完成期 (6 2 .5± 7.3) pg/ml(P <0 .0 5 )。血管瘤体NO(32 .5± 9.3) pg/ml与外周血 (37.5± 5 .2 ) pg/ml和正常对照组 (39.5±8.8) pg/ml无差异 (P >0 .0 5 ) ,但增生期瘤体NO(2 7.9± 2 .1) pg/ml降低 (P <0 .0 1)。结论　增生期血管瘤内皮细胞具有活跃的合成分泌ET的功能 ,而合成分泌NO功能改变不明显 ,局部ET与NO水平的失调 ,可能与血管内皮的过度增生有关     

新生儿呼吸衰竭时内源性一氧化氮及内皮素的动态观察

目的　了解新生儿呼吸衰竭时内源性一氧化氮（ＮＯ） 和内皮素（ＥＴ） 的动态变化及其在新生儿呼衰的发病中所起的作用。方法　测定了３８ 例新生儿呼衰患儿的尿ＮＯ代谢产物亚硝酸和硝酸根离子（ＮＯ２ － ＋ ＮＯ３ － ＝ ＮＯｘ） 和血浆ＥＴ 水平,同时监测患儿的动态肺顺应性和计算氧合指数（ＯＩ） 。结果　呼吸衰竭的患儿尿ＮＯｘ （２６４．９８±２１８．３２ μｍｏｌ／ｍｇ Ｃｒ） 水平明显降低,血浆ＥＴ（７３ ．０１ ±１０．０６ ｎｇ／Ｌ）水平明显升高,其中的ＲＤＳ组（２０８ ．６４ ±８８．５３ μｍｏｌ／ｍｇ Ｃｒ,８２．３６ ±１７ ．８３ ｎｇ／Ｌ） 变化最为明显。对照组尿ＮＯｘ 和血浆ＥＴ 水平分别为３９７ ．２６ ±２０６ ．６１ μｍｏｌ／ｍｇ Ｃｒ,４０ ．６６ ±１６．８６ ｎｇ／Ｌ。随着疾病的恢复,存活者尿ＮＯｘ 水平上升,而血ＥＴ水平下降,逐渐恢复正常。相关性分析显示尿ＮＯｘ 与ＯＩ呈负相关,与肺顺应性呈正相关,而血ＥＴ与ＯＩ呈正相关,与肺顺应性呈负相关。结论　肺部疾病越重,尿ＮＯｘ 水平越低,血ＥＴ水平越高;严重缺氧所致的内源性ＮＯ合成不足和ＥＴ 合成增加在新生儿呼吸衰竭的发生中可能起了重要的作用。     

L-精氨酸及L-硝基精氨酸对缺氧肺动脉内皮细胞内皮素的影响

目的探讨Ｌ精氨酸（一氧化氮合成的前体物质）及Ｌ硝基精氨酸（一氧化氮合酶抑制剂）对缺氧肺动脉内皮细胞内皮素１分泌及基因表达的影响。方法采用斑点杂交、Ｎｏｒｔｈｅｒｎ杂交及放射免疫分析，对常氧、缺氧、缺氧加Ｌ精氨酸及缺氧加Ｌ硝基精氨酸组的猪肺动脉内皮细胞进行了内皮素１的测定。结果缺氧能增加肺动脉内皮细胞的内皮素１的分泌及基因表达，此作用能被Ｌ精氨酸所抑制。Ｌ硝基精氨酸能增加缺氧时肺动脉内皮细胞的内皮素１分泌及基因表达。结论本实验间接提示，一氧化氮对肺动脉内皮细胞内皮素１的分泌及基因表达起调节作用     

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目的 探讨先天性心脏病(CHD)患儿肺动脉高压(PH)形成的影响因素.方法 研究对象均为2003-06-2005-02于北京大学深圳医院收集病例,以健康者30名为对照组(A组),以肺动脉压正常和并发PH的左向右分流的CHD患儿各30例为观察组(B组、C组).以高效液相色谱法、硝酸还原法及放射免疫法测定其血清精氨酸(L-Arg)、一氧化氮(NO)、血浆内皮素(ET-1)的浓度.结果 血清L-Arg浓度对照组(A组)为(72.00±18.01)nmol/mL,肺动脉压正常的患儿(B组)为(30.74±8.97)nmol/mL,伴PH的患儿(C组)为(23.51±12.37)nmol/mL.血清NO浓度A组为(76.10±17.10)nmol/mL,B组(90.55±26.57)nmol/mL,C组(60.05±17.60)nmol/mL.血浆ET-1浓度A组(50.82±7.58)pg/mL,B组(64.90±16.28)pg/mL,C组(69.64±10.66)pg/mL.结论 血清NO浓度和血浆ET-1浓度及其之间的平衡关系共同影响PH的形成及其程度.血浆ET-1浓度的升高是肺动脉压升高的直接因素,血清NO浓度的降低是间接因素,而血清NO浓度降低是由血清L-Arg浓度的降低引起.     

不同干预方法对实验性肥胖大鼠早期血管内皮功能障碍作用的比较

目的 观察单纯控制食谱、控制食谱联合有氧运动或降脂药对实验性肥胖大鼠血脂和血管内皮功能的影响。方法 Wistar大鼠随机分为：F组：饲予高脂饲料;N组：饲予基础饲料;A组：高脂饲养8周后予单纯控制食谱12周,B组：高脂饲养8周后予控制食谱联合游泳12周,C组：高脂饲养8周后予控制食谱联合藻酸双酯钠12周。干预12周后,处死全部大鼠,测定Lee指数;血脂指标：总胆固醇（TC）、甘油三酯（TG）;血管内皮因子：血浆内皮素（ET）、血清一氧化氮（NO）,血浆血管性假血友病因子（vWF）,免疫组化法检测腹主动脉细胞间黏附分子1（ICAM-1）蛋白的表达,逆转录-聚合酶链反应（RT-PCR）法检测腹主动脉ICAM-1mRNA的表达。结果 A组的TC、TG、ET低于F组（均P〈0．05）;B、C组的Lee指数、TC、TG、ET、vWF、ICAM-1蛋白和mRNA表达水平均低于F组（均P〈0．05）;A、C两组NO均高于F组（均P〈0．05）,与N组比较差异无统计学意义（均P〉0、05）,B组NO同时高于F组和N组（P〈0．01）。结论 单纯控制食谱能改善血脂和血管舒缩功能,控制食谱联合有氧运动或联合降脂药藻酸双酯钠在减重、降脂和改善血管舒缩、凝血、黏附功能方面均有效,而控制食谱联合有氧运动改善舒缩功能的效果更为显著,因此是单纯肥胖早期血管内皮功能障碍的最佳干预选择。     

Age-related endothelium-dependent vascular relaxation in rat thoracic aorta in response to colforsin

BACKGROUND: Colforsin, a novel water-soluble forskolin derivative, increases intracellular cyclic AMP by direct stimulation of adenylate cyclase and has strong positive inotropic and vasodilative effects. However, it is not known whether colforsin causes nitric oxide (NO) release and enhances endothelium-dependent vascular relaxation. METHODS: We studied NO production and relaxation on exposure to colforsin in thoracic aorta from rats aged 4, 12 and 60 weeks. RESULTS: When a low concentration of colforsin was added to a solution bathing ring segments of aorta from 12-week-old rats, relaxation was greater in the ring segments with intact endothelium than in those from which the endothelium had been removed. A high concentration of colforsin induced the same degree of relaxation of ring segments with or without endothelium, probably by a direct effect on vascular smooth muscle cells. Production of NO in response to colforsin by cultured endothelial cells from 12-week-old rat aorta was demonstrated by the electron paramagnetic resonance spin trapping method. A low concentration of colforsin relaxed aortic segments with intact endothelium from 4-week-old rats more than those from 12-week-old or 60-week-old rats. Reversal of relaxation by NG-nitro L-arginine, an NO synthesis inhibitor, was most significant in arteries from 4-week-old rats. Production of NO after exposure to colforsin was greater in aortic segments from 4-week-old rats than older rats, as detected by an NO-selective electrode. CONCLUSIONS: Colforsin induces vasodilation in part by releasing NO from the endothelium in rat thoracic aorta. In addition to a direct vasodilative effect on the vascular smooth muscle cells, an endothelium-dependent vasodilative effect is also important in younger arteries.     

一氧化氮和内皮素-1在新生儿缺氧缺血性脑病中的作用

目的　研究新生儿缺氧缺血性脑病(HIE)患儿脑脊液一氧化氮(NO)和内皮素-1(ET-1)水平变化,探讨NO 和ET-1在HIE中的作用及相互关系。方法　检测24 例HIE患儿脑脊液NO和ET-1 水平,并与8 例对照组比较。结果　HIE组患儿脑脊液NO 和ET-1 水平明显高于对照组(P< 0.05),中、重度HIE组患儿脑脊液NO 和ET-1水平明显高于轻度HIE组(P< 0.05),头颅CT异常HIE患儿脑脊液ET-1 水平明显高于CT正常者(P< 0.01)。结论　NO和ET-1 参与新生儿HIE的病理生理过程,脑脊液NO和ET-1 是反映脑实质损伤的重要指标     

Influence of morphine and naloxone on endothelin and its receptors in newborn piglet brain vascular endothelial cells: clinical implications in neonatal care

The present study examines the hypothesis that morphine exposure alters newborn brain vascular endothelial cell production of endothelin (ET)-1, as well as the mRNA expression of its receptors. Newborn piglet vascular endothelial cells were treated with morphine (100 ng/mL media), naloxone (100 ng/mL media), or drug-free media (control) for 6, 24, 48, and 96 h. Media was analyzed for ET-1 and big ET-1 levels and the cells were assessed for ETA and ETB receptor mRNA expression. Morphine exposure progressively increased ET-1 production from 6 to 96 h with concurrent reductions in big ET-1 levels starting at 24 h to almost undetectable levels by 96 h. Whereas ETA receptor mRNA expression increased 2-fold at 6 h and 4-fold at 96 h, ETB receptor mRNA expression remained unchanged. Naloxone exposure caused significant decreases in ET-1 levels, whereas an opposite effect was noted in big ET-1 levels, which increased from 6 through 96 h. Naloxone caused a progressive decrease in ETA receptor mRNA expression at 6 h through 96 h and a 2-fold increase in ETB receptor mRNA expression at 48 and 96 h. Increased ET-1 and its receptors in response to morphine may suggest altered cerebrovascular perfusion and brain metabolism in the immature piglet brain.     

Zinc as a potential enteroprotector in oral rehydration solutions: its role in nitric oxide metabolism

Zinc has been recognized as an antioxidant with potential for chronic and acute effects. Oxidative damage produced by free radicals, including nitric oxide (NO), is responsible for certain types of intestinal malabsorption syndromes and diarrhea. Under physiologic or mildly stimulatory conditions for NO synthesis, the small intestine characteristically is in a proabsorptive state; however, an excessive production of NO triggers formation of cyclic nucleotides, which cause secretion and malabsorption. In this study, we hypothesized that low-molecular-weight, soluble zinc chelates could modulate the effects of induced NO excess on the small intestine. In vitro experiments demonstrated that zinc-citrate or zinc-histidine at > or =0.66 mM, as well as a known NO scavenger, 2-[carboxyphenyl]-4,4,4,4-tetramethylimidazoline-1-oxyl-3-oxide, at 2 microM, were effective at removing chemically generated NO. In vivo jejunal perfusions, conducted in healthy rats under anesthesia, showed that c-PTIO reduced the proabsorptive effects produced by 1 mM L-arginine, the precursor of NO. In a standard oral rehydration solution, 1 mM zinc-citrate partially reversed the antiabsorptive effects on potassium caused by an excess of NO generated from 20 mM L-arginine but did not alter sodium or water absorption. The data are consistent with the view that soluble zinc compounds incorporated into an oral rehydration solution may deserve further attention as a means to scavenge NO with fluids used for the treatment of chronic or acute diarrhea, especially in malnourished children who are often zinc deficient.