川芎嗪对熏烟致宫内发育迟缓胎鼠脑发育的影响

目的：宫内发育迟缓(IUGR)患儿常有脑发育的异常。川芎嗪能改善脑部微循环,已被应用于新生儿缺氧缺血性脑损伤的治疗。被动吸烟法造大鼠IUGR模型,母鼠在孕8～20d给予川芎嗪,了解其对胎鼠宫内发育迟缓及其脑发育的影响,并探讨其作用机理。方法：孕鼠随机分为4组(均n=9):对照组,模型组,小剂量(40mg/kg)川芎嗪治疗组、大剂量(80mg/kg)川芎嗪治疗组。后3组孕鼠予以被动吸烟导致胎鼠宫内发育迟缓。孕21d剖宫取胎,观测胎鼠体重、脑重、肝重、身长及尾长;检测胎鼠脑组织中一氧化氮(NO)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果：对照组、模型组与小剂量、大剂量川芎嗪治疗组胎鼠IUGR发生率分别为3.9%(4/105),55.0%(50/106),11.8%(11/103)和5.4%(5/99)。模型组胎鼠体重(3.1±0.3gvs3.8±0.6g)、脑重(0.144±0.012gvs0.176±0.018g)、肝重(0.29±0.06gvs0.34±0.07g)均较对照组明显降低,差异有显著差异(均P<0.01),小、大剂量川芎嗪治疗组与模型组相比各指标均有所改善。模型组胎鼠脑组织NO(52.4±1.4μmol/gvs43.7±6.7μmol/g)和MDA(273.5±8.5μmol/gvs249.6±6.2μmol/g)水平较对照组明显增高(均P<0.01),而SOD活性比对照组明显降低29.7±2.6U/mgvs36.5±3.9U/mg(P<0.01)。川芎嗪治疗组与模型组相比,MDA水平降低而SOD活性增高(均P<0.01),较模型组进一步增高。结论：川芎嗪可有效防治被动吸烟诱导的胎鼠IUGR及其脑发育障碍,其机制可能与其纠正机体的氧化与抗氧化失衡有关。     

基于"多重打击"理论建立SD大鼠认知功能障碍模型及相关机制研究

目的通过脑发育早期脂多糖(LPS)重复刺激, 建立SD大鼠认知障碍模型, 探讨炎症反应介导下的"多重打击"对其组织学、行为学的影响及相关的分子机制。方法本研究的实验设计类型为成组设计。通过腹腔注射LPS构建SD大鼠"多重打击"认知障碍模型, 将24只孕鼠按照随机数字表法分为对照组、LPS1组、LPS2组、LPS3组, 每组6只。对照组孕18 d孕鼠和20日龄仔鼠均腹腔注射9 g/L盐水;LPS1组孕18 d孕鼠腹腔注射9 g/L盐水;LPS2组孕18 d孕鼠腹腔注射0.05 mg/kg LPS;LPS3组孕18 d孕鼠注射0.1 mg/kg LPS。LPS1～3组仔鼠均在20日龄时腹腔注射1 mg/kg LPS。通过前肢悬吊、网格和水迷宫等行为学实验, 对仔鼠运动和认知功能进行整体评估。组织学和蛋白免疫印迹(WB)实验检测仔鼠脑组织中胶质纤维酸性蛋白(GFAP)、Notch1和Jagged1的相对表达量。采用单因素方差分析进行多组数据之间比较, 采用独立样本t检验进行2组数据之间比较。结果 1.行为学实验:与对照组比较, LPS1～3组仔鼠的前肢悬吊时间递减[(34.81±5.66) ...     

宫内生长迟缓的分子调控机制

宫内生长迟缓(intrauterine growth retardation,IUGR)是指出生体重低于相应孕周胎儿平均体重第10百分位数或平均体重两个标准差的婴儿.它的发病率在活产婴儿中占10%左右,在低出生体重儿中占30%以上,其围产期死亡率是正常出生体重儿的4～10倍.     

孕鼠尾静脉注射脑源性神经营养因子对宫内发育迟缓新生大鼠体质量及脑质量的影响

目的探讨孕鼠尾静脉注射脑源性神经营养因子(BDNF)对宫内发育迟缓(IUGR)新生大鼠体质量及脑质量的影响。方法选取适龄SD大鼠进行交配,以观察到阴道栓确定为妊娠第1天,随机分为IUGR组和假手术组,于孕第17天开腹行孕鼠双侧子宫动脉钳夹术,以微小动脉血管夹钳夹双侧子宫血管,30 min后恢复血供,手术缝合;假手术组孕鼠仅开腹不予血管钳夹。IUGR组术后孕鼠尾静脉注射BDNF 1μg(BDNF干预组)或9 g/L盐水(IUGR组),持续5 d。待自然分娩后对各组新生大鼠进行体质量及脑质量分析。结果与假手术组相比,IUGR组新生大鼠出生体质量减轻24.9%,脑质量减轻17.3%,差异均具有显著性(Pa<0.000 1);与IUGR组相比,BDNF干预组新生大鼠体质量增加约11.9%,脑质量增加约10.7%,差异均具有显著性(Pa<0.05)。结论孕鼠尾静脉注射BDNF干预可明显改善因IUGR所引起的新生大鼠体质量及脑质量减轻,提示外周静脉注射外源性BDNF,早期干预IUGR有一定效果。     

建立大鼠宫内生长迟缓模型的方法

建立大鼠宫内生长迟缓模型在研究宫内生长迟缓 (IUGR)发生机制、疾病发生过程及病理改变起着重要作用。目前造模的方法有孕期营养干预法、子宫动脉结扎法、被动吸烟法、更生霉素药物法、低氧吸入法等 ,营养干预法、子宫动脉结扎法是最常用的。不同方法的难度不一样 ,效果也不同。由于即使同一种方法、同一种大鼠 ,其仔鼠的出生体质量也有很大的差异 ,因此均采用低于对照组出生体质量减 2倍标准差作为判断试验组仔鼠是否是IUGR的条件。     

含CpG基序的寡聚脱氧核糖核苷酸辅助乙肝疫苗对孕鼠和仔鼠的免疫效果

目的　观察不同剂量CpG 182 6联合乙肝疫苗注射孕鼠后 ,对孕鼠本身及其仔鼠的特异性免疫效果。方法　分别用不同剂量 (10、2 0、4 0 μg/只 )CpG 182 6作为乙肝疫苗佐剂辅助免疫孕鼠 ,ELISA方法检测孕鼠和仔鼠血清乙肝表面抗体 (HBsAb)水平 ,并观察仔鼠存活数量和生长发育指标 (体质量、身长、胎脑和胎仔体质量系数 )变化。结果　给孕鼠注射CpG 182 6 乙肝疫苗或单纯乙肝疫苗后 ,孕鼠血清HBsAb水平总是高于仔鼠水平 (P <0 .0 1) ,但孕鼠与仔鼠血清HBsAb水平间无相关性存在 (r =0 .379　P >0 .0 5 ) ;CpG 182 6 乙肝疫苗免疫孕鼠后 ,2 0 μg/只剂量组孕鼠和仔鼠血清HBsAb含量均高于 10、4 0 μg/只剂量组 ,单纯乙肝疫苗组及空白对照组 (P <0 .0 5 ) ,但仔鼠存活数量及体质量、身长、胎脑和胎仔体质量系数等生长发育指标间均无显著差异 (P均>0 .0 5 )。结论　CpG 182 6 (2 0 μg/只 )联合乙肝疫苗免疫孕鼠时 ,既能显著提高孕鼠及其仔鼠血清特异性免疫抗体水平 ,又不对仔鼠生长发育造成不良影响 ,是一种在妊娠期即可刺激免疫系统不成熟个体免疫活性的理想免疫佐剂。     

邻苯二甲酸二丁酯干预雄激素依赖性FGF8信号通路致尿道下裂发生的实验研究

目的 通过检测邻苯二甲酸二丁酯(DBP)孕期染毒所致尿道下裂雄性大鼠仔鼠睾酮(T)、雄激素受体(AR)及成纤维细胞生长因子8(FGF8)的表达,研究DBP干预雄激素依赖性FGF8通路致尿道下裂发生的相关机制.方法 20只孕鼠随机分为两组,孕14～18 d,分别予大豆油及DBP 750 mg·kg-1 ·d-1灌胃.仔鼠出生第一天,统计仔鼠出生数、尿道下裂发生率.第七天时,称量雄性仔鼠体重,拍摄尿道下裂图片,分别取两组中尿道下裂仔鼠及正常仔鼠血清和生殖结节(GT),用放射免疫法检测仔鼠血清睾酮含量;用定量逆转录聚合酶链式反应(Real-time quantitative PCR)及WesternBlot检测AR与FGF8表达水平.结果 染毒组及对照组产仔数分别为9.10±0.99和12.60±1.26,仔鼠体重(g)分别为9.53±0.12和11.93±0.15,DBP的生殖毒性作用导致染毒组孕鼠产仔数及仔鼠体重明显减少(P＜0.05),雄性仔鼠尿道下裂发生率为37.2％.染毒组仔鼠血清睾酮浓度(41.85±8.38) ng/L、生殖结节中AR0.404±0.040及FGF 80.036±0.004的表达均明显低于对照组睾酮浓度( 107.40±24.28) ng/L、AR表达1.669±0.124及FGF8表达0.168±0.004(P＜0.05).结论 DBP对孕鼠有明显的生殖毒性,DBP通过干预雄激素依赖性FGF8信号通路,导致尿道下裂的发生.     

Lipin基因表达与宫内发育迟缓大鼠肝脏脂肪含量的相关性研究

目的 探讨宫内发育迟缓（intrauterine growth retardation,IUGR）大鼠肝脏Lipin2基因和内脏脂肪组织Lipin1基因的表达与肝脏脂肪含量的相关性。 方法 使用母孕期低蛋白（10%蛋白）饮食法喂养孕鼠制造IUGR仔鼠模型,对照组孕鼠在孕期使用正常蛋白饲料喂养（蛋白含量21%）。分别在两组仔鼠生后1 d、1周、3周、8周和12周时称体重并留取仔鼠的肝脏组织,在生后3周、8周和12周留取两组仔鼠的内脏脂肪组织。采用3.0T氢质子磁共振波谱法检测两组大鼠生后3周、8周、12周时肝脏脂肪含量;采用Real-time PCR法检测两组大鼠各时间点肝脏组织Lipin2、内脏脂肪组织Lipin1基因的mRNA表达水平;采用Western blot法检测两组大鼠肝脏组织Lipin2、内脏脂肪组织Lipin1蛋白表达水平。采用Pearson相关分析Lipin mRNA及其蛋白表达与肝脏脂肪含量的相关性。 结果 生后3周、8周、12周时,IUGR组仔鼠内脏脂肪组织Lipin1 mRNA及其蛋白表达水平均高于对照组（P<0.05）。生后1 d时IUGR组肝脏组织Lipin2 mRNA及其蛋白表达水平低于对照组（P<0.05）,而生后1周、3周、8周、12周时Lipin2 mRNA及其蛋白表达水平均高于对照组（P<0.05）。生后3周时IUGR仔鼠和对照组肝脏脂肪含量比较差异无统计意义（P>0.05）,生后8周、12周时IUGR组仔鼠肝脏脂肪含量显著高于对照组（P<0.05）。Lipin1蛋白和mRNA表达与肝脏脂肪含量呈正相关（分别r=0.628、0.521,P<0.05）,Lipin2蛋白和mRNA表达与脂肪含量呈正相关（分别r=0.601、0.524,P<0.05）。 结论 IUGR大鼠内脏脂肪组织Lipin1和肝脏组织Lipin2 mRNA及其蛋白表达上调可引起肝脏脂肪含量增加,可能与导致IUGR大鼠成年期肥胖有关。     

左旋精氨酸对低出生体重仔鼠PI3K和PKB的影响

目的：生命早期应用左旋精氨酸（L-Arg）干预低出生体重仔鼠,检测其肝脏磷脂酰肌醇-3-激酶（PI3K）和蛋白激酶B(PKB)的表达,探讨L-Arg对改善胰岛素抵抗的影响。方法：以孕期低蛋白饮食法建立低出生体重仔鼠模型,18只孕鼠随机分为对照组、模型组和干预组,每组6只。对照组孕期给予21%正常蛋白饲料建立正常出生体重仔鼠模型,模型组及干预组孕期给予10%低蛋白饲料建立低出生体重仔鼠模型,3组孕鼠所生仔鼠分别纳入仔鼠对照组、模型组、干预组。生后21 d 仔鼠的哺乳期内,3组孕鼠均给予21%正常蛋白饲料喂养,对照组及模型组给予正常饮用水喂养,干预组给予富含L-Arg（200 mg/kg.d）的饮用水喂养。断乳后,3组仔鼠均给予21%正常蛋白饲料及正常饮用水喂养。于仔鼠生后1 周、3 周、8 周时,分别留取3组仔鼠的肝脏标本,用Western blot法检测肝脏PI3K和PKB的蛋白表达。结果：1 周时干预组仔鼠肝脏PI3K的蛋白表达高于模型组（P=0.045）,且与正常组相比差异无统计学意义（P=0.503）。8 周时干预组仔鼠肝脏PKB蛋白表达明显高于模型组（P=0.039）,且与正常组比较差异无统计学意义（P>0.05）。结论：生命早期补充L-Arg可促进蛋白质的合成,增加肝脏PI3K及PKB的蛋白表达,促进胰岛素信号传导,改善胰岛素抵抗。     

L-精氨酸对宫内发育迟缓大鼠肾脏Pax2表达的影响

目的：研究L-精氨酸（L-Arg）对宫内发育迟缓(IUGR)大鼠肾脏 Pax2表达的影响。方法：孕鼠随机分为 3 组：正常对照组、IUGR 组和干预组。正常对照组母鼠全程以普通饲料（含 21％ 蛋白）喂养。IUGR 组和干预组大鼠孕期均采用低蛋白饲料（含 10% 蛋白）喂养。仔鼠出生后,IUGR 组母鼠常规饲料喂养;干预组母鼠在常规饲料喂养的基础上,于部分饮水中每日添加 L-Arg 200 mg/kg。取 7 d、21 d、2月和 3月龄仔鼠肾脏组织,用免疫组化和 Western blot 法检测 Pax2 表达。结果：免疫组化显示正常对照组仔鼠在各时间点均未见明显 Pax2 表达。IUGR 组、干预组仔鼠2月龄和 3月龄时,两组大鼠在肾小球和肾小管区可见 Pax2 阳性细胞,且 3月龄鼠的 Pax2 表达比 2月龄的更显著（P<0.05）;干预组的 Pax2 表达低于同龄IUGR组（P<0.05）。Western blot 检测发现,3 组仔鼠肾脏在 7 d 和 21 d 均未见 Pax2 蛋白明显表达。到 2月龄和 3月龄时,干预组和 IUGR 组仔鼠肾组织 Pax2 蛋白表达均较正常对照组显著增多,但干预组的表达低于 IUGR 组（P＜0.01）。结论：IUGR 大鼠成年后肾脏 Pax2 基因有再表达现象;用L-Arg 干预后Pax2 表达明显减少。     

Cerebral and adrenal monoamine metabolism in the growth-retarded rat fetus under normoxia and hypoxia.

The effect of intrauterine growth retardation (IUGR) on cerebral and adrenal monoamine metabolism was studied in the fetuses of eight nulliparous rat dams after unilateral uterine artery ligation on d 18 of gestation. On d 22 (term = 23 d), four dams were subjected to normoxia and four to hypoxia (10% O2) for 58 min while their hemodynamics and blood gases were monitored. An inhibitor of L-aromatic-decarboxylase (3-hydroxybensylhydrazine) was infused to measure monoamine synthesis rate. After decapitation of the dam, fetuses were delivered by sectio, decapitated, and dissected at -5 degrees C. The body, liver, forebrain, brainstem, and adrenal glands were weighed, and concentrations of monoamine precursors, transmitters, and metabolites were assessed in the three latter organs. The weights of liver and forebrain were reduced in fetuses with IUGR, whereas brainstem and adrenal weights were unaltered. Epinephrine content in adrenals was reduced in proportion to body weight under normoxia but failed to increase under hypoxia as it did in appropriately grown fetuses. There were only minor changes in monoamine metabolism in the brainstem. In the forebrain, however, marked changes were seen, mainly in serotonin metabolism: under normoxia, fetuses with IUGR had decreased levels of serotonin and its metabolite 5-hydroxyindole acetic acid. Under hypoxia, appropriately grown fetuses reduced their concentrations of these substances, whereas fetuses with IUGR paradoxically increased their synthetic activity. It is concluded that a disturbance of central nervous serotonin metabolism prevails in growth-retarded rat fetuses in late gestation and that this disturbance depends on the degree of growth retardation and the degree of perinatal stress.     

Etiological factors and perinatal risks in symmetrical and asymmetrical intrauterine growth retardation

Fetuses with intrauterine growth retardation (IUGR) are of two types—symmetrical and asymmetrical, and it is important to differentiate between the two types antenatally. Ultrasound studies on 22 patients with IUGR were done after 28 weeks of gestation. The fetuses were distinguished as symmetrical and asymmetrical on the basis of ratio of head to abdominal circumference. It was found that the ratio of head to abdominal circumference differentiated well between the two types of IUGR after 36 weeks of gestation. The etiology and perinatal behaviour in the two groups were also different. A single head: abdominal circumference ratio may be useful in differentiating between symmetrical and asymmetrical IUGR after 36 weeks.     

Foetal nutrition, foetal growth restriction and health later in life

Retarded intrauterine growth has been linked to increased risk of perinatal mortality and morbidity, sudden infant death and poorer health later in life. The independent variables used in these studies are mainly neonatal size parameters, such as weight, ponderal index and ratios of head and abdominal measures. These are, in terms of foetal development and growth, crude parameters. This paper discusses the concepts of growth retardation used in most clinical and epidemiological studies. It is again emphasized that small for gestational age (SGA) and intrauterine growth retardation (IUGR) are different concepts. SGA is a size parameter that may or may not reflect restricted foetal growth and is therefore of limited value. Even IUGR, defined as retarded foetal growth rate, may be a too crude a criterion to select foetuses with short- and long-term health risks. Other biophysical measurements, such as foetal blood flow patterns and biochemical parameters, may be helpful in a better selection of these foetuses and infants. Furthermore, different causes of IUGR, e.g. poor maternal nutrition versus insufficient placental function, may not have the same effects on the foetus. The discrepancies in the results of studies on the relationship between IUGR or foetal malnutrition and short- and long-term health risks may be explained by the crudeness of the independent variables used. In the future, research on the biology of the developing human foetus should be more focused in the studies of the relationship between the intrauterine environment and nutrition and risk of poor health later in life.     

Foetal nutrition, foetal growth restriction and health later in life.

Retarded intrauterine growth has been linked to increased risk of perinatal mortality and morbidity, sudden infant death and poorer health later in life. The independent variables used in these studies are mainly neonatal size parameters, such as weight, ponderal index and ratios of head and abdominal measures. These are, in terms of foetal development and growth, crude parameters. This paper discusses the concepts of growth retardation used in most clinical and epidemiological studies. It is again emphasized that small for gestational age (SGA) and intrauterine growth retardation (IUGR) are different concepts. SGA is a size parameter that may or may not reflect restricted foetal growth and is therefore of limited value. Even IUGR, defined as retarded foetal growth rate, may be a too crude a criterion to select foetuses with short- and long-term health risks. Other biophysical measurements, such as foetal blood flow patterns and biochemical parameters, may be helpful in a better selection of these foetuses and infants. Furthermore, different causes of IUGR, e.g. poor maternal nutrition versus insufficient placental function, may not have the same effects on the foetus. The discrepancies in the results of studies on the relationship between IUGR or foetal malnutrition and short- and long-term health risks may be explained by the crudeness of the independent variables used. In the future, research on the biology of the developing human foetus should be more focused in the studies of the relationship between the intrauterine environment and nutrition and risk of poor health later in life.     

Effect of respiratory acidosis on glucose homeostasis in experimental intrauterine growth retardation in rats

Hypoglycemia and asphyxia account for a significant proportion of morbidity in the infant with intrauterine growth retardation (IUGR). The purpose of this study was to evaluate changes in glucose homeostasis in IUGR rats during acute respiratory acidosis. IUGR was produced by bilateral uterine artery ligation at 17 days of gestation in 14 pregnant rats with 23 successfully delivered pups. The normal pups (n = 31) were those whose mothers were sham operated at the same gestational period. The IUGR and normal pups were studied at 2 days of age. One group of pups was studied under room air while another was subjected to 20 min of exposure to a gas mixture of 10% O2/15% CO2, balanced with N2. Gluconeogenesis in the liver and carcass, as well as plasma glucose and catecholamines were determined before and after the exposure to the gas mixture. The results showed that the 2-day-old IUGR rats have lower body weight (P less than 0.001), liver weight (P less than 0.001), plasma glucose (P less than 0.001), and rate of gluconeogenesis (P less than 0.01) when compared with the normally grown rats. During respiratory acidosis, the normally grown rats showed an increase in plasma epinephrine (P less than 0.005) without significant change in plasma glucose and rate of gluconeogenesis. The IUGR rats on the other hand, demonstrated a decrease in rate of gluconeogenesis (P less than 0.02), an increase in plasma glucose (P less than 0.001) while the plasma epinephrine level remained unchanged. We speculate that respiratory acidosis blunted cellular metabolism in the IUGR rat resulting in decreased peripheral glucose utilization.(ABSTRACT TRUNCATED AT 250 WORDS)     

IUGR大鼠胰岛素样生长因子与小肠及体格发育关系的研究

目的：生后早期的生长主要受营养的调控,营养物质-胰岛素-胰岛素样生长因子(IGF)轴在胎儿宫内发育迟缓(IUGR)生长追赶及胃肠发育中起着重要的作用,而胃肠发育又与营养物质的吸收、生长追赶关系密切。目前国内有关IUGR出生时小肠发育状况报道甚少,且仅限于IUGR出生时胃肠形态结构的观察。该研究探讨生后早期不同蛋白质和热卡水平的营养干预如何调控IGF系统及影响IUGR大鼠的小肠发育和体格生长追赶,并追踪至成年期。方法：采用孕母饥饿法建立IUGR模型。64只IUGR新生鼠随机分为4组：IUGR正常饮食组(SC组),饮食中蛋白含量20%;IUGR高蛋白组(SH组),饮食中蛋白含量占30%;IUGR低蛋白组(SL组),饮食中蛋白含量为10%;IUGR高热卡组(SA组),饮食中热卡较其它组高20%。16只正常新生鼠为正常对照组(C组)予以正常饮食。幼鼠3周断乳后继续予原饮食模式1周,第4周起各组均予正常饮食喂养。分别于出生时及生后第4周、12周测定各组大鼠的血清IGF-1、胰岛素生长因子结合蛋白-3(IGFBP-3)浓度及体重、身长和小肠重量、长度。结果：IUGR大鼠虽然宫内营养不良,但SH组及SA组呈快速小肠发育和体格生长追赶伴IGFs水平明显升高,其中4周时SH组IGFs水平显著高于其余各组(P0.05)。SL组4周和8周的体重、身长、小肠长度和重量均低于其它4组(P0.05)。结论：4周时血清IGF-1是反映生长追赶的灵敏指标,与小肠和体格的生长追赶呈正相关,至成年期这种相关性消失。     

IGFBP-1在胎鼠生长发育中作用的研究

目的　探讨胰岛素样生长因子结合蛋白 - 1(IGFBP - 1)在正常胎鼠发育和胎鼠宫内发育迟滞(IUGR)发生中的作用。方法　钳夹孕鼠双侧子宫动、静脉 2 0min ,建立胎鼠IUGR模型 ,观察实验组 (IUGR组 )和正常对照组胎鼠血清IGFBP - 1水平与胎鼠血糖水平、生长参数 (身长、体重 )和器官重量 (胎盘、肺、脑、肝重 )的关系。结果　实验组胎鼠的体重、肺、脑、肝依次为 (1.93± 0 .2 3) g ,(0 .39± 0 .0 1) g ,(0 .10± 0 .0 1) g ,和 (0 .18±0 .0 2 )g ;身长为 (2 .70± 0 .16 )cm ,血糖水平为 (42 .49± 9.2 5 )mg/ml均明显低于对照组的 (3.87± 0 .85 )g ,(0 .47± 0 .0 4) g ,(0 .15± 0 .0 2 ) g ,和 (0 .2 2± 0 .0 6 ) g ,(3.6 1± 0 .44 )cm ,血糖 (6 7.31± 7.12 )mg/ml。血清IGFBP - 1(94.99± 16 .0 7)ng/ml较对照组 (33.2± 6 .96 )ng/ml明显升高 (均P <0 .0 1) ,血清IGFBP - 1与胎鼠血糖水平、生长参数、器官重量呈显著负相关 (均P <0 .0 1)。结论　血清IGFBP - 1作为生长抑制因子参与正常胎鼠发育及IUGR的发生。     

广州和佛山地区早产低出生体重儿出院时宫外生长迟缓发生情况调查

目的评价早产低出生体重儿出生时宫内生长受限(IUGR)和出院时宫外生长迟缓(EUGR)的发生情况。方法广州市、佛山市10家医院新生儿科出院的早产低出生体重儿(胎龄<37周,体重<2500g),分别以出生时、出院时生长发育指标在相应宫内生长速率期望值的第10百分位水平以下定义为IUGR、EUGR,分别计算各胎龄组、各体重组IUGR、EUGR发生率及总的发生率,并计算各胎龄组、各体重组EUGR发生率比IUGR发生率增加的比例。结果共595例早产低出生体重儿,出生时以体重、身长、头围为指标的IUGR发生率分别为20.2%、16.5%和24.4%,出院时以体重、身长、头围为指标的EUGR发生率分别为42.2%、28.1%和34.3%。不同出生胎龄(<31周、31～32周、33～34周、≥35周)出院时EUGR发生率较出生时IUGR发生率变化的情况:以体重为指标,EURG发生率各组分别增加36.8%、24.8%、19.1%、18.3%;以身长为指标,EUGR发生率各组分别增加26.5%、17.4%、8.2%、6.5%;以头围为指标,各组分别增加26.5%、14.0%、8.2%、3.2%,胎龄越小,增加率越高,组间比较差异有统计学意义(P<0.05)。不同出生体重(<1500g、1500～1999g、≥2000g)出院时EUGR发生率较出生时IUGR发生率变化的情况:以体重为指标,EUGR发生率分别增加45.3%、21.2%、17.4%;以身长为指标,EUGR发生率分别增加29.7%、14.8%、4.6%;以头围为指标,EUGR发生率分别增加26.6%、12.0%、4.3%,体重越低,增加率越高,组间比较差异有统计学意义(P<0.05)。结论早产低出生体重儿IUGR发生率较高,出院时EUGR发生率较IUGR发生率增高,且出院时EUGR发生率较出生时IUGR发生率的增加随出生胎龄和出生体重的降低而升高。