新生儿缺氧缺血性脑病脑脊液谷氨酸变化

利用高压液相色谱法测定了１８例缺氧缺血性脑病（ＨＩＥ）新生儿脑脊液谷氨酸含量。结果显示：中重度ＨＩＥ脑脊液谷氨酸浓度明显高于轻度ＨＩＥ及对照组，轻度ＨＩＥ与对照组比较差异无显著性。中重度ＨＩＥ中有无惊厥者脊液谷氨酸浓度无显著性差异。提示脑内谷氨酸的增加与ＨＩＥ患儿脑损伤的程度有关。本资料结果为谷氨酸受体拮抗剂在拮抗剂在新生儿窒息、ＨＩＥ的临床应用提供了初步依据。     

内皮素和一氧化氮与新生儿缺氧缺血性脑病的研究

目的 探讨血浆与脑脊液中内皮素,一氧化氮在新生儿缺氧缺血性脑病中的作用及其相互关系。方法 对３５例ＨＩＥ患儿分别采用放射免疫法测定血浆和ＣＳＦ中ＥＴ－１,硝酸根不原酶法测定血浆和ＣＳＦ中ＮＯ＾－２／ＮＯ＾－３值ＮＯ水平,并观察其急性期,恢复期的动态变化。     

一氧化氮在新生儿缺氧缺血性脑病中的作用

新生儿缺氧缺血性脑病(HIE)是因围产期宫内缺氧缺血及产后窒息影响新生儿脑细胞能量代谢，导致缺氧性脑病变，出生后出现的一系列脑部症状。其发病率高，重症患儿将会发生脑瘫等严重后遗症，给家庭和社会带来沉重负担。但是其发病机制到日前为止     

新生儿缺氧缺血性脑病与胎龄关系的探讨

本文对２７７例新生儿缺氧缺血性脑病（ＨＩＥ）与胎龄的关系进行探讨,结果发现： 儿ＨＩＥ与足月儿ＨＩＥ临床分度与ＣＴ分度之间的差异均呈显著性意义（ｘ＾２＝８．８７、７．６７,Ｐ均〈０．０５）,早产儿ＨＩＥ分度较足月儿严重。早产儿ＨＩＥ的临床分度与ＣＴ分度基本呈一致性,以中度为主,足月儿ＨＩＥ的临床分度与ＣＴ分度一致性较差。早产儿ＨＩＥ与足月儿ＨＩＥ之间合并颅内出血的发生率、出血类型及其他并发症发生率     

新生儿缺氧缺血性脑病血浆一氧化氮一氧化氮合成酶水平及临床意义

目的 探讨新生儿缺氧缺血性脑病（ＨＩＥ）时一氧化氮（ＮＯ）、一氧化氮合成酶（ＮＯＳ）的变化及意义。方法 采用比色等方法测定３２例ＨＩＥ及３０例正常新生儿血浆ＮＯ、ＮＯＳ活性水平。结果 ＨＩＥ急性期ＮＯ、ＮＯＳ水平较正常新生儿明显升高（Ｐ〈０．０５）,中、重度ＨＩＥ升高更显著（Ｐ〈０．０１）, 中、重度ＨＩＥ患儿ＮＯ、ＮＯＳ较轻度ＨＩＥ患儿明显升高。结论 ＮＯ、ＮＯＳ水平高低与ＨＩＥ患儿脑损伤程度和     

新生儿缺氧缺血性脑病的预后探讨

本文对47例新生儿缺氧缺血性脑病（以下简称HIE）的预后进行了探讨。对存活者年龄在12～36月的幼儿32例进行了随访。应用首儿所0～4岁小儿精神发育量表进行了发育商（DQ）测查。结果表明：临床分度为轻度者DQ正常；中度者DQ25％低于正常，部分伴有神经系统后遗症；重度者不但病死率高且存活者DQ55．6％低于正常，部分伴有严重神经系统后遗症，轻至中度脑水肿伴蛛网膜下胜出血者来发现神经系统后遗症且DQ均在正常范围，应作为积极抢救及早期干预的对象。     

缺氧缺血性脑病新生鼠中枢神经系统一氧化氮合酶的变化

一氧化氮合酶（ＮＯＳ）催化Ｌ精氨酸分解生成一氧化氮（ＮＯ）和瓜氨酸,ＮＯＳ活性的变化反映组织内ＮＯ含量的变化。ＮＯ是一种具有广泛生理活性的物质,除血管内皮细胞、巨噬细胞等能合成内源性ＮＯ外、脑组织也是内源性ＮＯ合成的重要场所。本研究缺氧缺血性脑病（ＨＩＥ）新生鼠中枢神经系统中ＮＯＳ的变化,以探讨脑组织局部ＮＯ的变化。材料和方法：１－实验动物：正常７日龄、体重１８～２２ｇ的ＳＤ新生鼠４５只,随机分成三组,每组１５只：正常对照组;急性缺氧组：吸入氧浓度（ＦｉＯ２）为０－０８的氧１０～１５分钟;ＨＩ…     

新生儿缺氧缺血性脑病与分娩方式探讨

目的探讨新生儿缺氧缺血性脑病（HIE）与分娩方式之间的关系。方法对于我院妇产科2000-2005年娩出的3433例活产儿发生HIE的90例进行临床分析。结果顺产儿HIE的发生率为0．22％，难产儿中HIE发生率为2．35％，两者差异有非常显著性（P〈0．01）。结论重视围产期保健，加强产科、儿科之间的密切联系，提高新法复苏是减少围产期窒息、预防HIE的重要措施。     

新生儿缺氧缺血性脑病与NO、NOS、PRL水平的相关性研究

采用放免法和比色法测定68例新生儿缺氧缺血性脑病(HIE)及30例正常新生儿血浆一氧化氮(N0)、一氧化氮合酶(NOS)及血清催乳素(PRL)活性水平,以探讨NO、NOS及PRL在HIE中的发病机理、病情进展及预后中的作用。结果;HIE急性期NO、NOS、PRL水平较正常新生儿明显升高(P<0.05),中度和重度HIE的3项水平升高更显著(P均<0.01);HIE惊厥组急性期血清PRL水平显著高于非惊厥组(P<0.01),且与惊厥发作持续时间呈正相关(r=0.485,P<0.01)。提示:NO、NOS、PRL水平高低与HIE患儿脑损伤严重程度有关,可作为判断病情、预后及惊厥是否发作的指标。     

窒息新生儿肾损害及一氧化氮保护作用

为了解机械通气治疗的窒息新生儿肾损害的发生情况，比较不同窒息程度与肾损害的关系。并探讨一氧化氮（NO）吸入治疗对肾脏的影响。对机械通气治疗的41例窒息新生儿（轻度窒息19例，重度窒息22例），进行回顾性分析，其中13例同时予以NO吸入治疗。结果显示：41中17例（占41．5％），有不同程度的肾损害，重度窒息患儿肾损害发生率明显高于轻度窒息患儿（P＝0．014）。予以NO吸入治疗的窒息患儿肾损害的改善较未予以NO吸入治疗者明显，9例未用NO吸入治疗的肾损害患儿在机械通气治疗后2例肾损害好转，5例无好转，另2例未随访，8例用NO吸入治疗的肾损害患儿在NO吸入治疗后肾损害好转6例，另2例未随访，提示窒息新生儿肾损害的发生率相当高，而NO吸入治疗能较明显的改善窒息后的肾损害。     

足月新生儿缺氧缺血性脑病的早期评估

目的　 探讨通过临床分度 ,新生儿行为测定 ,脑部CT对足月新生儿缺氧缺血脑病的患儿进行早期评估 ,判断预后 ,以便早期干预治疗。 方法 　按照 1996年杭州会议修定的HIE临床分度标准 ,轻度 13例 ,中度 2 7例 ,重度 14例 ,同时对其采用新生儿行为神经测定进行评估 ,头颅CT扫描检查 ,并随访至 6个月时进行发育商评估 ,以DQ≥ 90为达标水平。 结果　临床分度为轻、中度HIE者在 6个月时DQ达标率无显著差异。轻、中、重度HIE患儿在不同日龄NBNA评分有显著差异性 (P <0 0 0 1) ,临床分度越重 ,NBNA评分越低。 14d时NBNA≥ 35分和 <35分者在 6个月时DQ达标率有显著差异性 ,对判断HIE预后有较大的价值。临床分度与颅脑CT分度符合率 80 8% ,CT分度轻、中度在 6个月时DQ达标率无显著差异性 ,中与重度有显著差异性 ,与预后有关。 结论 　只有将临床分度、NBNA评分、头颅CT三者结合起来 ,综合分析才能早期准确地判断HIE的程度和预后。     

一氧化碳和一氧化氮在新生儿缺氧缺血性脑病发病中的作用

目的：探讨一氧化碳（ＣＯ）和一氧化氮（ＮＯ）在新生儿缺氧缺血性脑病（ＨＩＥ）中的作用。方法：对２８例新生儿ＨＩＥ血浆ＣＯ和ＮＯ水平进行检测，并与３０例正常新生儿对照组比较。结果：与正常对照组比较，２８例新生儿ＨＩＥ患儿血浆ＣＯ、ＮＯ水平显著增高；与轻、中度新生儿ＨＩＥ患儿比较，重度者血浆ＣＯ、ＮＯ水平显著增高；ＣＯ和ＮＯ呈显著正相关。结论：ＣＯ和ＮＯ在新生儿ＨＩＥ的发病过程中具有重要意义。     

Serum total magnesium and ionized calcium concentrations in asphyxiated term newborn infants with hypoxic-ischaemic encephalopathy

Total magnesium, ionized calcium, potassium and sodium concentrations in mixed umbilical cord blood and venous blood serum at a median (min.-max.) age of 33 h (24-48 h) were assessed colorimetrically in 46 asphyxiated and 35 healthy term infants. Asphyxiated infants without any signs or with signs of mild hypoxic-ischaemic encephalopathy (HIE) had significantly higher, and infants with severe HIE lower umbilical cord blood serum total magnesium (mean (95%CI) 0.81 (0.75-0.87) mmol/l and 0.64 (0.47-0.87) mmol/l, respectively, p < 0.05) compared with the control group (0.72 (0.69-0.76)mmol/l). An increase in serum total magnesium in spite of normalized acid-base status in asphyxiated infants suffering from severe HIE compared with the control group infants was found by the second day of life (0.97 (0.87-1.07) mmol/l and 0.86 (0.81-0.9) mmol/l, respectively, p < 0.05). At the age of 24-48 h hypermagnesaemia (>2 SD) was discovered in 36%, hyponatremia (<2 SD) in 38%, and hypocalcaemia (<2 SD) in 23% of asphyxiated infants. Derangements (>2 SD) in at least two electrolytes by the second day of life were significantly associated with poor outcome. CONCLUSIONS: Magnesium, calcium and sodium derangements are a frequent finding in asphyxiated infants, and these abnormalities are significantly associated with poor outcome. For a better outcome prediction, the routine determination of magnesium in addition to other electrolytes in asphyxiated infants is recommended.     

Nitric oxide inhalation and nitric oxide synthase inhibitor supplement for endotoxin-induced hypotension

BACKGROUND: This study was performed to determine whether a combined therapy of nitric oxide (NO) inhalation and nitric oxide synthase (NOS) inhibitor is effective in experimental animals with endotoxin-induced refractive hypotension accompanied by pulmonary hypertension. METHODS: Escherichia coli lipopolysaccharide (1 mg/kg) was administered to 10 newborn piglets to induce endotoxemia. The experiment then began 60 min later, when the systemic arterial pressure dropped. The inhalation of 20 p.p.m. NO at 60 and 120 min of endotoxemia created a control group. Another group was also administered N w-nitro-L-arginine (L-NNA; 5 mg) after the first NO inhalation at 60 min of endotoxemia (the L-NNA group). Pulmonary arterial pressure, systemic arterial pressure and cardiac output were measured and compared among the groups. RESULTS: Three of the 5 piglets in the control group died of hypotensive shock, while in the L-NNA group the systemic arterial pressure recovered to pre-endotoxin administration levels. The L-NNA group produced a further increase in pulmonary arterial pressure against which NO inhalation was effective. CONCLUSION: Nitric oxide inhalation alone carries a potential risk of further lowering systemic arterial pressure in a piglet with hypotension induced by endotoxin, whereas the combined therapy resulted in the recovery of the blood pressure to pre-endotoxin levels. The combined therapy was simultaneously effective against pulmonary hypertension.     

Concentrations of magnesium and ionized calcium in umbilical cord blood in distressed term newborn infants with hypoxic-ischemic encephalopathy

Magnesium and ionized calcium in mixed umbilical cord blood was assessed colorimetrically in 38 distressed and 21 healthy term newborn infants. Distressed infants with a severe or moderate degree of hypoxic-ischemic encephalopathy (HIE) ( n = 8) had significantly lower ( p < 0.001 (concentrations of magnesium (0.52 ± 0.08 mmol/L) compared to the control group (0.69 ± 0.06 mmol/L). No differences in concentrations of ionized calcium between distressed and control infants were detected.     

肾病综合征患儿血浆一氧化氮及内皮素检测及其意义

为探讨一氧化氮(NO)及内皮素(ET)与肾病综合征之间的关系,采用比色法和放免法分别检测了活动期肾病综合征患儿59例、治疗后48例的血浆NO及ET水平,并设24例健康儿童作为对照。结果发现肾病综合征活动期血浆NO与ET水平显著高于缓解期,活动期与缓解期血浆NO与ET水平均显著高于对照组(P均<0.01),NO水平与ET水平呈显著正相关(r=0.565,P<0.05),显示NO与ET和肾病综合征的发生有关。     

Endogenous nitric oxide in the upper airways of premature and term infants

Concentrations of endogenous nitric oxide (NO) were measured in premature ( n = 18) and term infants ( n = 7). Nasal gas was aspirated continuously and after timed occlusions, 15 s and 60 s, by a fast-response chemiluminescence analyser. The sampling flow rate was 20 ml min^-1. Typical NO recordings consisted of plateaux and postocclusive peaks. In term infants peak NO concentrations (60 s occlusion) were 2. 71 ± 0. 44 parts per million (ppm) within lOmin after birth, increasing ( p < 0. 05) to 3. 81 ± 0. 25 ppm at 4–7 d postnatally. Peak NO values (15 s occlusion) averaged 1. 22 ± 0. 16 ppm in premature infants (postconcep-tional age 25–37 weeks, body weight 623–2844 g) and the NO concentrations increased significantly with postconceptional age ( p < 0. 05). Nasal excretion rate, estimated from plateau NO concentrations and sampling flow rate, was 0. 10 ± 0. 01 nmol min^-1 kg^-1 in both groups. We conclude that premature and term newborn infants excrete considerable amounts of NO in the upper airways, with hitherto not fully known functions.