舒血宁注射液治疗缺氧缺血性脑病的临床观察

目的:观察舒血宁注射液对新生儿缺氧缺血性脑病的治疗效果,为其临床治疗方案提供一种参考。方法:我院2011年4月至7月,共发生32例新生儿缺氧缺血性脑病(HIE)患者,随机将其分为对照组和观察组各16例。对照组患儿采用一般治疗方法进行治疗,观察组患儿采用舒血宁注射液进行治疗,分别于治疗前及治疗7天后检测所有患儿的血小板(PLT)值。评价临床疗效。结果:两组患儿经过7天治疗后,两组患儿的血小板均明显升高,但观察组患儿血小板升高率明显高于对照组患儿,两组比较差异显著,有统计学意义(P<0.05)。结论:血小板指数随着患儿缺血缺氧病情的加重而呈不断下降趋势,舒血宁注射液具有有效防止血小板聚集而增加血液中的血小板指数,达到提高患儿脑血流量,改善脑部微循环,减轻脑损伤,保护脑神经组织的作用。     

新生儿缺氧缺血性脑损伤脑脊液氨基酸含量的变化及临床意义

缺氧缺血性脑损伤是导致永久性神经损伤的重要原因之一。兴奋性氨基酸(EA A)和抑制性氨基酸 (IAA)在缺氧缺血性脑损伤的发病中所起的作用 ,已引起国内外学者的注意。我们检测了 2 6例新生儿缺氧缺血性脑病 (HIE)的患儿和8例正常新生儿脑脊液氨基酸含量的变化 ,探讨新生儿缺氧缺血性脑损伤患儿脑脊液 EAA和 IAA含量的变化及其与脑损伤程度的关系。一、对象和方法1.研究对象 :2 6例患儿系我院新生儿科 1998年 3～ 6月收治的足月新生儿 ,均因窒息复苏后 2 4h内出现神经系统症状转入我科治疗 ,待病情稳定后头颅 CT检查。根据 CT结果将其…     

非蛋白结合铁在新生儿缺氧缺血性脑病发生机制中的作用

关于铁介导的氧自由基 ( OFR)在新生儿缺氧缺血性脑损伤 ( HIBD)发生机制中作用的研究少见报道。本研究在于探讨窒息对足月新生儿铁代谢的影响和窒息后血浆非蛋白结合铁 ( nonprotein-bound iron,NPBI)浓度改变及其与新生儿缺氧缺血性脑病 ( HIE)发病机制的关系。一、对象共 4     

血红素氧合酶1在新生儿缺氧缺血性脑病中的变化

近年来研究显示缺氧缺血时脑细胞血红素氧合酶1(heme oxygenase-1，HO-1)表达增强，推测和一氧化氮(nitric oxide，NO)一样，HO-1可能参与了缺氧缺血性脑损伤的发病过程。本研究观察了新生儿缺氧缺血性脑病(hypoxic-ischemic encephalopathy，HIE)患儿HO-1活性的变化，以探讨其在HIE中的作用。     

缺氧缺血性脑病新生儿血清白细胞介素-1受体拮抗剂与高敏C反应蛋白的变化及临床意义

新生儿缺氧缺血性脑病(hypoxie-isel3emie encephalopa-thy,HIE)是围产期各种因素引起脑缺氧、缺血所导致的脑损伤综合征,是造成儿童中枢神经系统损害最常见的原因之一.近年来免疫系统在HIE发病中的作用日益受到重视,但确切机制尚未完全阐明~([1]).国内外研究表明缺氧缺血性脑损伤时有免疫异常及炎症反应,缺氧缺血与炎症反应相互作用,可能是引起新生儿围产期脑损伤的主要机制~([2]).白细胞介素-1受体拮抗剂(interleukin-1 receptor antagonist,IL-lra)是与炎症有关的细胞因子,而高敏C反应蛋白(high-sensitivity C-reactive protein,hsCRP)是全身炎症反应的一种标志物.本研究动态检测HIE及正常足月新生儿血清中IL-lra和hsCRP的水平,探讨其与新生儿HIE的相互关系.     

新生儿缺氧缺血性脑病低钠血症与血浆脑利钠肽相关性研究

目的探讨新生儿缺氧缺血性脑病(HIE)低钠血症与血浆脑利钠肽(BNP)相关性；HIE病理过程中的BNP及低钠血症生理和病理作用机制。 方法枣阳市第一人民医院于2002年10月至2004年10月，动态观察22例低钠血症HIE患儿3日龄、7日龄和2周时血浆BNP和血钠水平，并进行相关性分析。同时与血钠正常的52例HIE患儿及血钠正常非HIE患儿(对照组)进行比较。 结果3日龄HIE患儿BNP显著高于对照组(P<001)；7日龄时，血钠正常的HIE患儿与对照组之间已无明显统计学差异，而低钠血症HIE组明显高于血钠正常HIE组(P<001)；低钠血症组的三个时间段BNP之间差异均具有显著性(P<001)；低钠血症组各时间段的血钠浓度呈递减，依次比较差异有显著性。低钠血症HIE组与血钠正常HIE组相应时间段行为神经(NBNA)测定比较差异具有显著性(P<001)；低钠血症组的HIE患儿在三个时间段NBNA比较差异具有显著性(P<005)。低钠血症组BNP水平与血钠离子在各时间段具有负相关性。 结论BNP参与和导致了HIE低钠血症，并直接和经过低钠介导在HIE病理过程中起重要作用。     

谷氨酸和一氧化氮在新生儿缺氧缺血性脑病发病中的作用

目的　研究新生儿缺氧缺血性脑病 (HIE)患儿脑脊液谷氨酸和一氧化氮 (NO)水平变化 ,探讨二者在新生儿 HIE中的作用及相互关系。　方法　对 2 4例新生儿 HIE脑脊液谷氨酸和 NO水平进行检测 ,并与 8例对照组比较。　结果　重度 HIE组脑脊液谷氨酸和 NO水平明显高于对照组[(分别为 92± 42和 148.7± 5 .4,高于 45± 5和 83.3± 2 7.5 )μmol/ L ],谷氨酸和 NO水平呈显著正相关(r=0 .6 2 ,P<0 .0 1)。　结论　谷氨酸和 NO在新生儿 HIE的发生和发展过程中具有重要意义。     

硫酸镁对窒息新生儿缺氧缺血性脑损伤保护作用的观察

新生儿窒息后缺氧缺血性脑损伤常遗留严重的后遗症。由于病因及发病机制复杂 ,尚无有效药物能改善这种损伤 [1 ] 。近年有许多实验室研究表明 ,硫酸镁具有神经保护作用 ,但临床应用报道尚少见 [2 ] 。本研究旨在探讨硫酸镁对窒息新生儿缺氧缺血性脑损伤的保护作用及安全性 ,为新生儿缺氧缺血性脑病的治疗提供新的思路。一、资料与方法1.病例选择 :2 0 0 0年 8月～ 2 0 0 1年 12月我院 NICU收住的患儿 ,符合以下条件入选 :(1)足月新生儿 ;(2 )生后1min Apgar评分≤ 7分或 5 m in Apgar评分≤ 6分 ;(3)无严重先天畸形 ;(4)孕母在产科无特殊…     

胰岛素样生长因子I、生长抑素在新生儿缺氧缺血性脑病血液中水平变化的研究

目的　观察胰岛素样生长因子 I(insulin- like growth factor- I,IGF- I)、生长抑素(som atostatin,SS)在新生儿缺氧缺血性脑病 (hypoxic- ischemic encephalopathy,HIE)极期和恢复期血液中的变化 ;探讨 IGF- I、SS在 HIE发病机制中的作用。　方法　 (1)用放射免疫分析法 (RIA)测定正常对照组、HIE极期、恢复期血浆 SS的水平。(2 )用免疫放射分析 (IRMA)测定上述标本血清中 IGF- I的水平。　结果　 (1) HIE极期、恢复期与正常对照组 IGF- I、SS水平有显著差异 (F=78.7,P<0 .0 1;H=33.3,P<0 .0 1) ,HIE极期 IGF- I、SS水平下降 ,恢复期 IGF- I、SS水平升高。(2 ) HIE轻、中、重度组间 IGF- I、SS水平比较 ,均有显著差异 (F=3.38,P<0 .0 5 ;H=6 .46 ,P<0 .0 5 ) ,病情越重 ,IGF- I、SS水平越低。　结论　 (1) HIE极期 IGF- I、SS水平下降 ,恢复期 IGF- I、SS水平升高 ,提示 IGF- I、SS在 HIE的发病机制中可能具有重要作用。(2 ) HIE时 IGF- I、SS水平下降程度与疾病轻重程度有关。IGF- I、SS检测对临床疾病严重程度的判断可能具有指导意义并可作为病情恢复与否的一个监测指标。     

早期干预改善宫内缺氧缺血性脑损伤新生大鼠学习记忆能力的效果评价

新生儿缺氧缺血性脑病(HIE)发病率高，常导致智能迟缓等严重后遗症。对急性期发生的脑损伤尚缺乏有效的治疗方法。有研究发现早期干预可改善宫内缺氧缺血性脑损伤(HIBD)新生大鼠的脑功能。本研究对宫内HIBD干预组及正常干预组新生大鼠进行早期干预28d，通过“Y”臂迷宫检测学习分辨能力、记忆保持百分率判断干预效果，并观察额皮质和海马CA2区、     

缺氧缺血性脑病血和脑脊液LDH、CK及同工酶分析和相关性研究

目的　探讨不同程度缺氧缺血性脑病（ＨＩＥ） 新生儿血清乳酸脱氢酶（ＬＤＨ） 、肌酸激酶（ＣＫ）和同工酶活性变化及与脑脊液酶活性的相关性。　方法　４７ 例轻、中、重度ＨＩＥ 和３９ 例正常儿均于生后４８ 小时内进行血清ＬＤＨ 及同工酶ＬＤＨ１,２,３,４,５ 、ＣＫ 及同工酶ＣＫＭＭ,ＣＫＭＢ和ＣＫＢＢ活性检测。其中２４ 例患儿同时作血清和脑脊液酶活性的相关性分析。　结果　ＨＩＥ中度和重度组血清ＬＤＨ、ＣＫ、ＬＤＨ３ ,４,５ 和ＣＫＢＢ活性明显高于正常组和轻度组（Ｐ＜ ０．０５）,以ＬＤＨ３ 升高为著（ Ｐ＜０．０１）。血清和脑脊液ＬＤＨ３ ,４,５ 、ＣＫ 和ＣＫＢＢ活性呈良好正相关（ Ｐ＜ ０．０５）,其中ＣＫＢＢ 呈高度正相关（ Ｐ＜ ０ ．０１） 。　结论　血清ＬＤＨ、ＣＫ 和同工酶,尤其ＣＫＢＢ、ＬＤＨ３ 活性测定可代替脑脊液酶活性的检查,可作为缺氧缺血性脑损伤及程度评价的参考指标。     

The dynamic changes of plasma neuropeptide y and neurotensin and their role in regulating cerebral hemodynamics in neonatal hypoxic-ischemic encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is a common cause of neonatal encephalopathy and is one of the most important causes of neonatal death and disabilities, especially those infants with moderate to severe encephalopathy. However, the pathogenesis of HIE still remains unclear. The purpose of this study was to explore the dynamic changes in plasma neuropeptide Y (NPY) and neurotensin (NT) as well as their role in regulating cerebral hemodynamics in HIE patients. The plasma levels of NPY and NT in the umbilical artery and peripheral blood on the first, third, and seventh days after birth in 40 term infants with HIE and 40 healthy controls were measured using radioimmunoassay. On the first day of life, the blood samples were collected immediately when ultrasound examinations were finished. The ultrasound transducer was placed on the temporal fontanelle to detect the hemodynamic parameters of the middle cerebral artery, including peak systolic flow velocity, end-diastolic flow velocity, time-average mean velocity, pulsatility index, and resistance index (RI) in both groups were measured by pulse Doppler ultrasound in the first day after birth. The relationship between RI and NPY or NT was analyzed by linear regression analysis. NPY levels in umbilical blood ([mean +/- standard deviation] 615.5 +/- 130.7 ng/L) and first-day peripheral blood (355.9 +/- 57.4 ng/L) in neonates with HIE were significantly higher than those in normal newborns' blood (199.1 +/- 63.2 and 214.4 +/- 58.0 ng/L, respectively; P < 0.01). NPY levels in HIE neonates then declined to control levels on the third day after birth ( P > 0.05). However, the levels of plasma NT in umbilical blood and peripheral blood were much higher in the HIE group than those in normal newborns during the first week ( P < 0.01). The results of Doppler ultrasound examinations showed that cerebral blood flow velocity significantly decreased, whereas RI increased markedly in HIE patients compared with healthy controls ( P < 0.01). Linear regression analysis revealed that the RI was positively correlated with NPY levels ( R = 0.614; P < 0.01) and negatively correlated with NT levels ( R = -0.579; P < 0.01). The results of this study showed that there was a significant increase in plasma NPY and NT levels in HIE patients and this was strongly related to the severity of HIE, and the hemodynamic parameter RI was significantly correlated with NPY and NT. Therefore, we believe that the dynamic changes in plasma NPY or NT levels participate in the mechanisms of HIE by regulating cerebral hemodynamic changes after neonatal asphyxia occurs.     

Effect of phenobarbital on free radicals in neonates with hypoxic ischemic encephalopathy--a randomized controlled trial

BACKGROUND: Phenobarbital is one of the oldest, cheapest and easily available cerebroprotective drugs for the hypoxic brain. However, its potential and various actions have not been fully explored. AIM: To evaluate the effects of Phenobarbital on levels of oxidants and anti-oxidants in term and near term neonates with hypoxic ischemic encephalopathy. METHODS: Design--randomized controlled trial. Setting--tertiary care referral perinatal centre. Procedure--asphyxiated neonates (gestation > or = 34 weeks) with HIE were randomized to receive Phenobarbital 20 mg/kg i.v. within first six hours of life or to control group. CSF levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx) and blood levels of vitamins A and E were estimated at 10-12 hours of age. RESULTS: CSF levels of MDA, SOD, GPx and blood levels of vitamins A and E were significantly lower in the Phenobarbital group (p<0.001). There was a trend towards lower levels of CSF MDA, SOD, GPx and blood vitamins A and E in babies with normal outcome as compared to babies with adverse outcome (death or neurologically abnormal at discharge). CONCLUSION: Phenobarbital in the dose of 20 mg/kg i.v. given within 6 hours of life in term and near-term neonates with HIE, was associated with a decrease in lipid peroxides, anti-oxidant enzymes and anti-oxidant vitamins.     

新生儿缺氧缺血性脑病血清肌酸激酶及其同工酶动态变化的临床研究

摘要】目的探讨新生儿缺氧缺血性脑病(HIE)时血清肌酸激酶(CK)和心型同工酶 (CK MB)、脑型同工酶(CK BB)的动态变化及其意义。方法对2004 05—2005 01的32例HIE患儿和30例正常新生儿分别在生后24h内、第3天、 第7天采集股静脉血，测定血清中总CK、CK MB及CK BB。结果(1)HIE组血清CK、CK MB、CK BB水平均高于对照组(P<0.05)。HIE各组血清CK 、CK MB、CK BB水平均随着病情加重而升高，生后24h内均达到峰值，第3天开始下降，第7天中度组CK、CK MB、CK BB降至正常水平，重度 组CK、CK MB、CK BB仍明显高于对照组(P<0.01)。(2)中、重度HIE组血清CK、CK MB与对照组和轻度HIE组比较有显著性差异(P<0.01)。轻度 HIE组血清CK、CK MB与对照组比较无统计学意义(P>0.05)。轻、中、重度HIE组血清CK BB与对照组比较差异均显著(P<0.01)。结论(1)HIE血 清中CK、CK MB、CK BB水平与HIE程度密切相关，HIE程度越重其水平越高。(2)血清CK、CK MB、CK BB是HIE患儿心、脑损伤的早期敏感指 标，可作为对HIE的早期诊断、病情严重程度判定常用的指标；对临床进行干预治疗和早期估计预后具有重要的意义。     

超声监测围产期胎儿、新生儿脑损伤及颅内出血的研究

目的　早期诊断围产期缺血缺氧所造成的脑损伤及颅内出血。　方法　对 1987年 4月至 1999年 4月间在我院出生的高危新生儿 880例用高分辨力超声仪行颅脑检查 ,对高危妊娠患者产前超声检查时着重观察胎儿颅内结构。　结果　发现异常者 36 5例 (4 1.5 % ) ,其中缺血缺氧性脑病(包括脑水肿 ,脑室周围回声增强 ) 110例 ,颅内出血 2 33例 (其中 6例是在产前检查时发现胎儿颅内出血 ,生后进一步证实 ) ,脑积水 7例 (2例在宫内诊断 ) ,先天性胼胝体发育不良 2例 (1例宫内诊断 ) ,脑肿瘤 1例 ,其他 12例。颅内出血在小于胎龄儿及有妊娠合并症的新生儿中发病明显增高。　结论　常规对高危胎儿及新生儿行颅脑超声检查有利于早期诊断、恰当处理及估计预后     

新生儿重度缺氧缺血性脑病预后因素临床分析

目的探讨新生儿重度缺氧缺血性脑病的预后因素。方法 2011年1月至2014年12月湖南省儿童医院新生儿科收治住院的重度新生儿缺氧缺血性脑病患儿131例,对其预后影响因素进行相关和回归分析。结果单因素分析显示5min Apgar评分、惊厥、昏迷、pH值、剩余碱值、脏器损伤是影响重度新生儿缺氧缺血性脑病预后的危险因素;多因素Logistic分析结果表明,5 min Apgar评分3分(OR=4.256,95%CI1.501~15.432)、剩余碱≤-10mmol/L(OR=37.208,95%CI6.053~42.105)是影响重度新生儿缺氧缺血性脑病预后的独立性危险因素(P0.05),入院日龄72h(OR=0.098,95%CI 0.032~0.367)是重度新生儿缺氧缺血性脑病保护因素。结论影响重度新生儿缺氧缺血性脑病预后的因素很多,及时发现这些因素,是预防重度新生儿缺氧缺血性脑病的关键所在,临床医师应该引起重视和早期干预。     

Status of vitamin D,antioxidant enzymes,and antioxidant substances in neonates with neonatal hypoxic-ischemic encephalopathy

Objective: To investigate the concentration of vitamin D (VD), glutathione peroxidase (GP), superoxide dismutase (SOD), malondialdehyde (MDA), and advanced oxidation protein products (AOPP) in neonates with hypoxic-ischemic encephalopathy (HIE).

Material and methods: This study was performed prospectively in term neonates treated for HIE. Samples were collected from the neonates in study and control groups at 6–14 h and on day 5 of their lives for 25-OH vitaminD3, antioxidant enzymes including GP and SOD and oxidants substances including MDA and AOPP.

Results: This study was performed with 31 term neonates with HIE and 30 healthy term neonates. Maternal VD level was statistically lower in the study group (9.8±6.8 ng/mL) than the control (16.4±8.7?ng/mL) (p?=?0.002). SOD and MDA levels were significantly high, and VD level was significantly low in the study group on the first day of life (p?=?0.001 and p?=?0.028, respectively). SOD and GP levels were significantly high in the study group on day 5 (p?<?0.05). VD was significantly low in the study group on day 5 and the proportion of subjects with VD below 5 ng/ml was significantly lower in the control group (p?=?<0.05).

Conclusion: VD has neuroprotective and antioxidant properties. We detected VD levels were low in infants with HIE and their mothers. This finding may be useful for decreasing of brain damage.     

宫内窘迫新生儿脐动脉血超氧化物歧化酶及丙二醛检测的临床意义

目的　探讨脂质过氧化与胎儿窘迫,以及与新生儿缺血缺氧性脑病(HIE)的关系。方法　将产程中发生宫内窘迫的新生儿60例作为研究对象其中出生后无窒息者39例为检测Ⅰ组,有窒息者21例为检测Ⅱ组;取同期正常新生儿30例为对照组。检测各组新生儿脐动脉血超氧化物歧化酶(SOD)、丙二醛水平,观察各组新生儿HIE发生情况;分析宫内窘迫持续不同时间的新生儿SOD、丙二醛的变化及HIE发生情况。结果　(1)SOD水平检测:检测Ⅰ组为(12 896±247)U/gHb,检测Ⅱ组为(9846±268)U/gHb,对照组为(17 282±134)U/gHb。检测Ⅰ、Ⅱ组SOD水平分别与对照组比较,均显著降低,差异有统计学意义(P<0 01)。检测Ⅰ、Ⅱ组共发生HIE9例(HIE组),SOD水平为(7486±245)U/gHb,未发生HIE51例(非HIE组),SOD水平为(13 878±257)U/gHb,两组比较,差异有统计学意义(P<0 01)。检测Ⅰ、Ⅱ组宫内窘迫持续时间≤30min共19例,SOD水平为(17 411±324)U/gHb,持续时间31~120min共26例,SOD水平为(12 076±230)U/gHb,持续时间≥121min共15例,SOD水平为(9786±249)U/gHb。(2)丙二醛水平检测:检测Ⅰ组为(6 3±0 4)μmol/L,检测Ⅱ组为(8 6±1 5)μmol/L,对照组为(4 1±0 5)μmol/L,检测Ⅰ、Ⅱ组丙二醛水平显著高于对照组,两者比较,差异有统计学意义(P<0 01)。HIE组为     

Low adjusted serum ionized calcium concentration shortly after birth predicts poor outcome in neonatal hypoxic-ischemic encephalopathy

AIM: Hypoxic-ischemic reperfusion injury causes either necrosis or apoptosis, and the influx of ionized calcium into cells is the major cause of both types of cell death. The aim of this study was to investigate whether or not the serum ionized calcium concentration in neonates with hypoxic-ischemic encephalopathy (HIE) could be used to predict their outcome. METHODS: Serum samples were obtained shortly after birth from 20 HIE neonates who had not urinated or received treatment with calcium. Serum ionized calcium concentrations were adjusted for pH using a correction formula. Twelve neonates without any disease were selected as a control. The results were compared between nine HIE neonates who made a full recovery, 11 who died or had neurologic deficits, and 12 normal neonates. RESULTS: Considered together, the two HIE groups had lower serum ionized calcium concentrations (1.05 +/- 0.10 mmol/L) than the control group (1.22 +/- 0.07 mmol/L; P < 0.0001). Moreover, serum ionized calcium concentrations in the group with the poor outcome (0.99 +/- 0.07 mmol/L) were lower than those in the group that made a full recovery (1.13 +/- 0.06 mmol/L; P=0.0016). CONCLUSIONS: The serum ionized calcium concentrations shortly after birth were significantly lower in neonates with HIE who had a poor outcome. Low concentrations may reflect multiple organ damage, particularly involving the brain.