钳夹子宫血管致宫内生长迟缓幼鼠小脑皮层神经生长因子改变的研究

目的　了解宫内发育迟缓 ( IUGR)幼鼠脑发育过程中神经生长因子 ( NGF)在不同阶段的变化 ,探讨 IU GR所致脑损伤的发生机理。方法　采用钳夹孕鼠子宫血管 30分钟的方法建立 IU GR幼鼠动物模型 ,用免疫组化染色检测 IUGR幼鼠出生时及生后第 6天小脑皮层 NGF蛋白变化。结果　 1IUGR幼鼠出生体重较正常对照组降低 16 .1% (小于 2个标准差 ,P<0 .0 0 0 1) ;2 IU GR幼鼠出生时脑重较正常对照组脑重降低 ( P<0 .0 5 ) ;3IU GR幼鼠生后第 6天体重与正常对照组无差异 ( P>0 .0 5 ) ,但脑重仍有差异 ( P<0 .0 5 ) ;4IU GR幼鼠出生时小脑皮层 NGF蛋白较正常对照组降低 ( P<0 .0 0 5 ) ,且在生后第 6天仍有差异 ( P<0 .0 5 ) ,此改变与脑重改变一致。结论　本方法成功建立了 IU GR动物模型 ,且该模型所致 IUGR幼鼠伴有脑发育迟缓。IU GR幼鼠脑发育落后的发生可能与脑内 NGF水平下降有关 ,且 NGF的降低持续时间长 ,影响持久。本研究还发现 :IU GR幼鼠体格发育存在追赶生长 ,而脑发育迟缓不易恢复     

The relationships of the serum concentrations of insulin-like growth factors in fetal rats with intrauterine growth retardation]

OBJECTIVE: To observe the alterations of serum insulin-like growth factor-I,-II (IGF-I, IGF-II) in rat fetus and to investigate the relationship of serum IGFs with intrauterine growth retardation (IUGR). METHODS: 21 pregnant SD rats were randomly divided into control group (n = 9) and experimental group (IUGR group, n = 12). On day 14 of gestation, the bilateral uterine arteries and veins of experimental group were clamped for 20 minutes to build the rat IUGR models and sham surgeries were performed on control group. Fetal serum concentrations of IGFs, birth weight, the length and weight of fetal liver, lung, brain and placenta of all rats in the two groups were measured and compared. RESULTS: The serum concentrations of IGF-I,-II of IUGR group were 117.92 +/- 26.58 ng/ml and 223.19 +/- 33.35 ng/ml, respectively, which were significantly lower than those of control group (234.43 +/- 70.65 ng/ml and 397.74 +/- 23.69 ng/ml, respectively, P < 0.01). Likewise, birth weight, the length and weight of liver, lung, brain and placenta in IUGR group were significantly lower than those in control group (P < 0.05). CONCLUSION: The decrease of fetal serum concentrations of IGF-I,-II may be one of the internal factors contributing to fetal IUGR, and IGFs may play an important role in fetal growth.     

胰岛素样生长因子I受体在宫同内发育心缓胎鼠中的表达研究

目的 探讨宫内发育迟缓（IUGR）时胰岛素样生长因子I受体（IGFD－1R）表达的变化及其在组织和细胞中的定位。方法 将21只SD孕鼠随机分为实验组12只和对照组9只。钳夹实验组孕鼠双侧子宫动、静脉20分钟,建立宫内发育迟缓动物模型。对照组仅作开腹和关腹术。两组均于孕22天剖宫取出胎鼠,采用免疫组化法观察孕晚期胎鼠肝脏和肺组织中IGF－1R的表达。结果 实验组胎鼠的体重、身长及胎盘、肝、肺组织重量按对照组明显降低（P＜0．05）;实验组胎鼠肝脏IGF－1R表达面积比较对照组明显增加,平均灰度明显降低（P＜0．01）;实验组胎鼠肺组织IGF－1R表达面积也比较对照组明显增加（P＜0．05）,但平均灰度则无显著性差异（P＞0．05）。结论 宫内发育迟缓时IGF－1R在肝脏和肺组织的表达增加,可能是机体对IGF－1降低的代偿机制。     

胎鼠血清胰岛素样生长因子水平改变与宫内生长迟缓的关系研究

目的　观察胎鼠血清胰岛素样生长因子 和 (IGF- 和 IGF- )的变化 ,探讨 IGFs与胎儿宫内发育迟缓 (IUGR)发生的关系。方法　 2 1只 SD孕鼠被随机分为对照组 9只 ,实验组 (IUGR) 12只。实验组于第14天行双侧子宫动、静脉钳夹 2 0分钟以建立胎鼠 IUGR模型。对照组仅行开腹和关腹术。比较两组胎鼠血清 IGFs的浓度及体重、身长和肝、肺、脑及胎盘的重量。结果　实验组血清 IGF- 、 浓度分别为 117.92± 2 6 .5 8ng/ ml和2 33.19± 33.35 ng/ ml,明显低于对照组 (分别为 2 34 .43± 70 .6 5 ng/ m l和 397.74± 2 3.6 9ng/ m l) (P均 <0 .0 1) ,其体重、身长及肝、肺、脑、胎盘组织的重量亦明显低于对照组 (P均 <0 .0 5 )。结论　胎鼠血 IGF- 和 IGF- 水平的降低是 IU GR发生的内在因素之一 ,IGFs在胎儿生长发育中有重要的作用。     

胎盘血流量下降对大鼠胎仔生长和胎盘结构的影响——宫内生长迟缓动物模型的研究

本实验采用 SD 大鼠,在孕后期行孕鼠一侧子宫动脉中段完全结扎,另一侧作对照.23只孕鼠(150只胎仔)分成未结扎上、下(CU 和 CL)与结扎上、下(LU、LL)四组.结果表明,LU 组宫内胎仔体重、胎盘重、脑肝重均较其它三组有显著下降(P<0.01);LU 组脑/肝重比值及脑/体重比值较其它三组有显著增加(P<0.01).其胎仔呈不均称性宫内生长迟缓(IUGR)。52只胎盘作了光镜观察,12只胎盘作了电镜观察。在已知子宫胎盘血流不足,且胎仔发生 IUGR 的情况下,其胎盘的改变与以往报道的人类 IUGR 胎盘病理改变相一致,从而证实了子宫胎盘血流量下降是 IUGR 发病的重要原因之一。     

EFFECTS OF EARLY NUTRITION INTERVENTION ON IGF1, IGFBP3, INTESTINAL DEVELOPMENT, AND CATCH-UP GROWTH OF INTRAUTERINE GROWTH RETARDATION RATS

Objective To investigate the effects of early nutritional intervention on the serum insulin-like growth factor-1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3), intestinal development, and catch-up growth of intrauterine growth retardation (IUGR) rats by giving the IUGR new born rats different protein level diet. Methods IUGR rat model was built by starvation of pregnant female rats. Twenty-four IUGR pups and 8 normal pups were divided randomly into 4 groups: normal control group (C group); IUGR control group(S group), IUGR low-protein diet group (SL group), and IUGR high-protein diet group (SH group). Detected the serum IGFI, IGFBP3, body weight, body length, intestinal weight length, intestinal villi height (VH), crypt depth (CD), villi absorbing area (VSA), mucous thickness (MT), and disaccharidase at the 4th week. Results (1) The SH group showed the fastest catch-up growth, serum IGF1, IGFBP3, VH, and VSA were significantly higher than those of normal control group and IUGR control group. The intestinal weight and length, and the activities of lactase and saccharase of the SH group also reached the normal control group level. (2) The SL group kept on small size, the serum IGF1, IGFBP3, and most of intestinal histological indexes were all significantly lower than other groups. (3) IGF-1, IGFBP3 were positively correlated to intestinal VH, VSA, saccharase, body weight and length. Conclusions The serum IGF1 was a sensitive index to the catch-up growth. The early nutritional intervention of highprotein diet after birth is helpful for the catch-up growth of IUGR through promoting the intestinal development and the absorption of nutrition.     

Establishment of a new rat model of intrauterine growth retardation]

OBJECTIVE: To establish intrauterine growth retardation (IUGR) models in rats for study of the etiology, pathology and therapy of this disease. METHOD: Partial ligation of the medial segment of the uterine artery and vein was performed in 10 Sprague-Dawley rats with pregnancy (17 d) to establish IUGR models, and another 9 rats with pregnancy of the same length which did not receive the operation were used as control. On day 21 of pregnancy, the fetuses and placentas in both groups were surgically taken and weighted, and the incidence of IUGR and mortality in the fetus were observed. RESULTS: Significant decrease in the average weight of the fetuses (3.32+/-0.54 g) and placentas (0.38+/-0.05 g) occurred in the ligated group as compared with those of the control group (4.55+/-0.76 g and 0.44+/-0.11 g, P<0.005). An incidence of IUGR as high as 33.33% was resulted in the fetus of ligation group, significantly higher than that in the control group (1.14%, P<0.005), but no significant difference was observed in the mortality between the 2 groups (4.94% vs 3.41%, P>0.05). CONCLUSION: IUGR models can be successfully established in SD rats by partial ligation of the medial segment of the uterine artery and vein.     

宫内发育迟缓雌性仔鼠早期营养对生长追赶的影响

【目的】探讨生命早期不同营养状态对宫内发育迟缓（IUGR）雌性大鼠体质量生长追赶、青春发育启动及肥胖的影响。【方法】SPF母鼠孕期限制饮食法建立仔鼠IUGR模型,采用雌性仔鼠进行实验,IUGR仔鼠哺乳期以小窝喂养（SL-IUGR）模拟过度喂养,同时设IUGR仔鼠常规哺乳（CF-IUGR）,正常对照组仔鼠常规哺乳（NC）,3组仔鼠均在21d断乳后以基础饲料喂养,分别于仔鼠生后1、7、14、21、35、42和75d称体质量,记录阴门开启时间,21、35d采血检测雌二醇（E2）、黄体生成素（LH）、卵泡雌激素（FSH）水平进行比较。【结果】IUGR组仔鼠出生体质量（4.9±0.2）g,低于对照组（6.0±0.3）g,差异有统计学意义（P<0.001）。IUGR大鼠生后14d均出现生长追赶,SL-IUGR组大鼠14~75d体质量均高于对照组,CF-IUGR组大鼠1~75d体质量均落后于对照组,差异有统计学意义（P<0.05）。SL-IUGR组雌性大鼠的阴门开启时间（29.88±1.81）d,较CF-IUGR组（32.03±2.11）d提前,差异有统计学意义（P=0.044）;21d体质量与IUGR大鼠阴门开启时间具有相关性,Rs=-0.174,P=0.039。SL-IUGR组大鼠青春期、成年期肥胖率为28.33%、21.67%,较CF-IUGR组7.5%、6.25%增加,差异有统计学意义（P=0.001、0.007）。青春期肥胖IUGR大鼠7d、21d体质量生长速度较不发生青春期肥胖者增加,成年期肥胖IUGR大鼠7d、35d体质量生长速度较不发生青春期肥胖者增加,差异有统计学意义（P<0.05）。IUGR组大鼠阴门开启时间和成年期肥胖二元Logistic回归分析OR=0.419,P=0.24,阴门开启时间不是成年期肥胖的独立因素。【结论】生命早期营养水平提高有利于IUGR体质量追赶;哺乳期体质量过度追赶可导致IUGR大鼠青春期肥胖及成年期肥胖和阴门开启时间提前。     

高压氧治疗胎儿宫内生长迟缓58例临床效果观察

目的：观察高压氧治疗胎儿宫内生长迟缓（IUGR）的临床效果。方法：对58例IUGR孕妇采用高压氧治疗，观察治疗前后胎儿大脑中动脉（MCA）、脐动脉（UA）血流速率RImcA和RIuA的变化，并设氨基酸组对照；在新生儿出生后对其体格发育、智能发育作为期一年的随访。结果：经高压氧治疗后胎儿RImcA明显上升，RIuA明显下降，接近于正常，较对照组有显著差异；随访一年新生儿的体格、智能发育指标，与正常新生儿无差异。结论：高压氧治疗能有效地改善IUGR胎儿异常的脑及脐动脉血流速率，纠正胎儿宫内缺氧，减少低体重、低智能儿的发生。     

宫内发育迟缓儿身长、体重、头围的追赶比较

目的 研究宫内发育迟缓儿（IUGR）生长发育模式,以指导IUGR的生长保健工作.方法 对本院及复旦大学附属妇产科医院确诊的210名IUGR儿的体重、身长、头围等指标,分别在其0、6、12和24个月时进行随访性调查.结果 成功随访188例,男孩为87例,女孩101例,平均出生体重为2.27 kg,共有102例儿童的出生体重＜2 500 g,占总数的54.25%.其中,早产儿为46例,占24.47%.在出生头2年中,IUGR体重、身长、头围均有追赶生长,尤其是出生后头6～12个月生长速度最快,而头围生长大于身长及体重,女孩生长追赶要早于男孩,但2岁之内除女孩头围外均未达正常水平（P＜0.01）.在2岁之内为生长追赶的良好时间段.结论 证实了IUGR有生长追赶现象.若2岁之前不能给予干预治疗,有一部分IUGR其最终的生长将落后于正常儿.加强孕期营养及提倡母乳喂养是保证IUGR早期发育的关键.