胎儿宫内发育迟缓与丙二醛及红细胞滤过指数的关系

目的　探讨胎儿宫内发育迟缓 (IUGR)与丙二醛及红细胞滤过指数的关系。方法　以核孔滤膜红细胞变形能力测定仪 ,分别测定IUGR组 5 0例孕妇静脉血及新生儿脐血的红细胞滤过指数 (IF) ,用硫代巴比妥酸(TBA)法检测丙二醛 (MDA)的浓度。以同期住院的正常孕妇 5 0例作为对照组 ,并以常法测定孕妇红细胞计数(RBC)、血红蛋白 (Hb)、红细胞压积 (Ht)、平均红细胞体积 (MCV)、平均红细胞血红蛋白浓度 (MCH)。结果　IUGR组IF为 0 5 0± 0 2 6 ,正常孕妇组IF为 0 2 1± 0 0 7(P <0 0 1)。IUGR组脐血IF为 0 2 3± 0 0 8,正常孕妇组脐血IF为 0 2 0± 0 0 5 (P >0 0 5 )。血浆丙二醛 (MDA)浓度IUGR组 (8 2 6± 1 4 2 )nmol/L ,正常对照组为(4 96± 0 75 )nmol/L(P <0 0 1) ,脐血MDA两者间差异无显著性 (P >0 0 5 )。IUGR组Hb、Ht、MCV、MCH均明显高于正常对照组 ,差异有显著性 (P <0 0 1)。IF与新生儿平均出生体重呈负相关 (r =- 0 36 6 ,P <0 0 1)。结论　血浆中MDA含量升高可导致红细胞滤过指数升高 ,从而导致胎儿宫内发育迟缓 ,红细胞变形能力下降是胎儿宫内发育迟缓的原因之一。     

乙型肝炎病毒母婴垂直传播与Th1/Th2型细胞因子相关性研究

目的 :研究乙型肝炎病毒 (HBV)母婴垂直传播与T辅助细胞 1、2型细胞因子的相关性。方法 :将研究对象分为两组 :研究组为 78例乙型肝炎病毒表面抗原 (HBsAg)阳性孕妇 ;对照组为 40例正常孕妇。采用双抗夹心酶联免疫吸附法 (DAS-ELISA)检测孕妇外周静脉血及其新生儿脐静脉血血清中乙型肝炎五项指标 (HBVM)及细胞因子干扰素γ(IFN γ)、白细胞介素 12 (IL 12 )、白细胞介素 6 (IL 6 )水平。结果 :研究组孕妇分娩的新生儿有 10例宫内感染 ,宫内感染率为 12 82 %。胎儿宫内感染组孕妇血清中IFN -γ、IL - 12水平显著低于宫内未感染组及对照组孕妇 ,IL - 6水平则显著高于宫内未感染组及对照组孕妇 (P <0 0 5 )。宫内未感染组与对照组相比 ,上述三种细胞因子水平差异均无显著性(P >0 0 5 )。上述各组孕妇血清中IFN -γ与IL - 12水平均呈显著正相关 (P <0 0 1,P <0 0 5 ,P <0 0 5 ) ;IL - 12与IL -6呈显著负相关 (P <0 0 1,P <0 0 5 ,P <0 0 5 ) ;IFN -γ与IL - 6亦呈显著负相关 (P <0 0 1,P <0 0 5 ,P <0 0 5 )。各组新生儿脐血清中IFN -γ、IL - 12、IL - 6水平差异无显著性 (P >0 0 5 )。结论 :孕妇细胞免疫功能紊乱导致Th1型细胞因子IFN -γ、IL - 12水平下降 ,而Th 2型细胞因子IL - 6水平上升     

羊水过少静脉输液加饮水治疗前后脐血流变化及妊娠结局

目的　探讨静脉输液加饮水在羊水过少治疗中对脐血流及妊娠结局的影响。方法　妊娠 35周前后B超诊断为羊水过少孕妇 4 5例 ,每天用能量合剂 ,生理盐水 ,林格氏液各 5 0 0ml静脉点滴 ,并适量饮水10 0 0ml,5d一个疗程 ,共 1～ 2个疗程。监测治疗前后羊水指数 (AFI)和脐血流收缩期最大血流速度 舒张期末血流速度的比值 (S D)、阻力指数 (RI)、波动指数 (PI)、快速血流比 (FVR)情况 ;观察出生后羊水污染 ,新生儿窒息 ,吸入性肺炎等指标 ;并与羊水正常组孕妇 5 0例进行比较。结果　羊水过少组治疗前后比较 ,并与羊水正常组比较 ,AFI、S D、FVR差异有统计学意义 (P <0 0 1) ,而羊水污染、新生儿窒息、吸入性肺炎等发生率无明显差异 (P >0 0 5 )。但羊水过少治疗有效组 (38例 )与治疗无效组 (7例 )比较 ,羊水污染和新生儿窒息差异明显 (P <0 0 1) ,治疗无效组胎儿宫内发育迟缓 (IUGR)占 85 7%。结论　静脉输液加适量饮水法治疗羊水过少可增加羊水量 ,降低脐血流阻力 ,改善妊娠结局 ,治疗同时应注意纠正IUGR。     

硝酸甘油对妊高征母脐血血清NO2-/NO3-及围生儿预后的影响

目的　研究硝酸甘油对妊高征母、脐血清NO2 /NO3 及围生儿预后的影响。方法　选取 1999～ 2 0 0 0年晚期妊娠正常妇女 (正常组Ⅰ组 :12例 ) ,中、重度妊高征患者 36例 [妊高征组 ,其中单用硫酸镁 (Mg)治疗Ⅱ组 :12例 ;单用硝酸甘油 (Ng)治疗Ⅲ组 :12例 ;联合用药 (Mg +Ng)治疗Ⅳ组 :12例 ]。采用硝酸还原酶法测母、围生儿脐血清NO2 /NO3 ,并对围生儿预后进行评价。结果　母血NO2 /NO3 浓度 :产前PIH组低于Ⅰ组 ,差异有显著性意义 (P <0 0 5 ) ,产后各组差异无显著性意义 ;脐静脉血各组NO2 /NO3 浓度均小于产前 ,但PIH组与Ⅰ组比较 ,脐血间差异小于母血间差异 ,用药后Ⅲ、Ⅳ组上升 ,差异有显著性意义 (P <0 0 5 ) ,Ⅱ组差异无显著性意义 (P >0 0 5 )。围生儿预后不良者百分率 ,PIH组比Ⅰ组增高 ,但差异无显著性意义 (P >0 0 5 ) ,PIH组间差异无显著性意义 (P >0 0 5 )。结论　硝酸甘油作为NO供体治疗妊高征时 ,能改变母、脐血NO含量 ,从而降低胎儿 -胎盘循环阻力 ,可能对PIH引起的胎儿宫内发育迟缓 (IUGR)有治疗作用     

辅助生育技术受孕双胎与自然受孕双胎妊娠结局的分析

目的　探讨辅助生育技术受孕 (助孕 )双胎与自然受孕双胎围产期的结局。方法　选择 10 4例助孕双胎孕妇 (助孕组 )和 173例自然受孕双胎孕妇 (自然受孕组 ) ,比较两组孕妇一般情况、妊娠合并症、分娩情况和新生儿预后等方面的差异。结果　 (1)助孕组孕妇平均年龄 (31 2± 3 7)岁 ,自然受孕组孕妇为 (2 7 8± 3 5 )岁 ,两组比较 ,差异有显著性 (P <0 0 5 )。 (2 )助孕组孕妇早产 70例(6 7 3% ) ,自然受孕组孕妇早产 78例 (45 1% ) ,两组比较 ,差异有极显著性 (P <0 0 1)。助孕组孕妇患妊娠期糖尿病或糖耐量异常 16例 (15 4 % ) ,自然受孕组孕妇仅 4例 (2 3% ) ,两组比较 ,差异有极显著性 (P <0 0 1)。(3)助孕组孕妇剖宫产率为 76 0 % (79/10 4 ) ,明显高于自然受孕组的 6 5 3% (113/173)。(4)两组围产儿死亡率、畸形发生率和新生儿窒息率等比较 ,差异无显著性 (P <0 0 5 )。结论　助孕双胎孕妇年龄较大 ,早产率及妊娠期糖尿病或糖耐量异常发生率高 ;分娩方式以剖宫产为主。助孕双胎孕妇的围产儿结局与自然受孕双胎相似     

椎管内阻滞麻醉与笑气吸入用于分娩镇痛的效果比较

目的　比较椎管内阻滞麻醉和笑气吸入两种方法的分娩镇痛效果和对产妇及新生儿的影响。方法　随机选取 30 0例产妇分为笑气组、椎管内阻滞组和对照组 ,每组各 10 0例。在分娩过程中 ,笑气组给予吸入含 5 0 %笑气与 5 0 %氧气的混合气体 ;椎管内阻滞组给予蛛网膜下腔 +硬膜外腔联合注入芬太尼和布比卡因 ;对照组未给予镇痛药物。并分别观察 3组产妇的镇痛效果、产程时间、分娩方式、产后出血量、产妇桡动脉血及新生儿脐血的血气分析以及新生儿窒息情况。结果　 (1)镇痛效果比较 :椎管内阻滞组镇痛分级 0级为 88例 ,笑气组为 12例 ,对照组为 0例。 3组之间比较 ,差异有极显著性 (P <0 0 1)。 (2 )产程时间比较 :第一产程和总产程时间 ,椎管内阻滞组短于对照组和笑气组 (P <0 0 5 ) ,笑气组与对照组比较 ,差异无显著性 (P >0 0 5 ) ;第二产程时间椎管内阻滞组长于对照组和笑气组 ,但差异无显著性 (P >0 0 5 )。 (3)剖宫产术后出血量比较 :笑气组为 (373± 77)ml,椎管内阻滞组为 (2 5 9± 78)ml,对照组为 (2 39± 89)ml,笑气组与其他两组比较 ,差异有极显著性 (P<0 0 1)。(4)血气分析结果比较 :3组产妇桡动脉血及新生儿脐血血气分析结果各组之间比较 ,差异均无显著性 (P >0 0 5 )。 (5 )分娩方式比较     

妊娠高血压综合征患者胎盘血管内皮生长因子的表达及其意义

目的　探讨胎盘血管内皮生长因子 (VEGF)在妊娠高血压综合征 (妊高征 )患者中的表达及其与胎盘血管网络构建、胎盘重量及新生儿体重的关系。方法　采用蛋白免疫印迹技术测定 2 5例正常妊娠妇女 (正常妊娠组 )及 2 5例妊高征患者 (妊高征组 )的胎盘组织中VEGF的表达。采用免疫组织化学法 ,用抗F8因子抗体标记两组孕妇胎盘中的血管密度。两组孕妇分娩后 ,测量新生儿身长、体重 ,并胎盘称重。结果　 (1)妊高征组和正常妊娠组孕妇胎盘VEGF积分吸光度值分别为2 4793± 6 5 79、4190 3± 110 0 9;胎盘血管密度分别为 (6 1± 11)和 (78± 11)个 / 40 0×视野。两组比较 ,差异均有极显著性 (P <0 0 1) ,且与妊高征患者病情严重程度相关。 (2 )妊高征组胎盘重量 [(4 6 0±5 9)g]较正常妊娠组 [(5 73± 99)g]显著下降 (P <0 0 1)。 (3)妊高征组新生儿体重为 (3176± 5 0 3)g,较正常妊娠组的 (34 6 8± 493)g显著下降 (P <0 0 5 ) ;而新生儿身长在两组间比较 ,差异无显著性(P >0 0 5 )。(4 )正常妊娠组中 ,胎盘VEGF的表达与血管密度、胎盘重量和新生儿体重的相关系数分别为 0 82 3、0 6 71、0 888;妊高征组分别为 0 90 5、0 85 9、0 732 ,两者均呈显著正相关 (P <0 0 1)。而VEGF表达与新生儿身长不相关     

乙型肝炎病毒母婴垂直传播与人类白细胞抗原-DR区域基因相关性的研究

目的　探讨人类白细胞抗原 (HLA)DR区域基因HLA DR3、HLA DR4、HLA DR13、HLA DR15与乙型肝炎病毒 (HBV)母婴垂直传播的关系。方法　采用聚合酶链反应 序列特异性引物 (PCR SSP)方法 ,检测 78例乙型肝炎表面抗原 (HBsAg)阳性孕妇 (研究组 )和 4 0例正常孕妇 (对照组 )外周静脉血中HLA DR3、HLA DR4、HLA DR13、HLA DR15基因表型分布及频率。结果　 (1)研究组孕妇HLA DR3基因频率为 19 2 % ,显著高于对照组的 5 0 % (P <0 0 5 ) ;HLA DR13基因频率为 2 6 % ,显著低于对照组孕妇的 17 5 % (P <0 0 5 ) ;两组孕妇HLA DR4、HLA DR15的基因频率比较 ,差异无显著性 (P >0 0 5 )。 (2 )研究组孕妇中 ,HBV高复制状态者的HLA DR3基因频率为30 0 % ,显著高于低复制状态者的 7 9% (P <0 0 5 )。 (3)将研究组孕妇分娩的新生儿 ,根据脐血清HBsAg、HBVDNA的检测结果分为 :宫内感染组和宫内未感染组 ,宫内感染组孕妇HLA DR3的基因频率为 5 0 0 % ,显著高于宫内未感染组的 14 7% (P <0 0 5 )。其余各基因表型比较 ,差异无显著性(P >0 0 5 ) ;宫内感染组新生儿HLA DR3基因频率为 30 0 % ,明显高于宫内未感染组的 7 4 % ,但差异无显著性 (P >0 0 5 )。结论　孕妇HBsAg携带与HLA DR3和HLA DR13表达有明显相关     

妊娠合并糖代谢异常并发先兆子痫对母儿结局影响的分析

目的 :探讨妊娠合并糖代谢异常并发先兆子痫母、儿的结局。方法 :收集1981至 2 0 0 3年糖代谢异常孕妇 12 0 2例的临床资料 ,其中 15 1例孕妇并发先兆子痫 ,按照有无先兆子痫的发生将孕妇分为先兆子痫组 (Ⅰ组 )和非先兆子痫组 (Ⅱ组 )。回顾分析比较两组孕妇、新生儿的结局。结果 :(1)I组孕妇早产、羊水过多、酮症、手术产的发生率明显高于II组 ,发生率分别为 2 1.2 %vs 6 .0 %、13.9%vs 6 .2 %、15 .2 %vs 7.4 %、71.5 %vs6 0 .7% (P <0 .0 1) ;两组孕妇胎死宫内、胎儿窘迫、宫内感染、产后出血的发生率比较 ,差异无统计学意义 (P >0 .0 5 ) ;(2 )I组与II组的新生儿结局比较 :两组新生儿患病率有明显差异 (P <0 .0 5 ) ,新生儿窒息、畸形、红细胞增多症、低血糖和高胆红素血症发生率分别为12 .0 %vs 3.9%、7.3%vs 3.1%、8.7%vs 2 .2 %、15 .3vs 5 .7%和 18.0 %vs 12 .3% ;两组大于胎龄儿和小于胎龄儿发生率分别为 17.2 %vs 11.3%、10 .6 %vs 1.9% ;新生儿转科(41.0 %vs 19.6 % ) ,差异有显著性 (P <0 .0 5 ) ;新生儿呼吸窘迫综合征 (NRDS)及围产儿死亡的发生率两组无统计学差异 (P >0 .0 5 )。结论 :妊娠合并糖代谢异常的孕妇一旦并发先兆子痫将增加糖代谢异常孕妇的并发症及新生儿的患病率。     

腹腔镜下治疗休克型输卵管妊娠的临床观察

目的　探讨腹腔镜手术治疗休克型异位妊娠的可行性与安全性。方法　回顾性分析我院 1996年 1月至 2 0 0 1年 1月 5年间收治的经腹腔镜手术治疗的输卵管妊娠病例 2 15例的临床资料。其中有休克症状及腹腔内出血量超过 10 0 0ml的 2 1例为研究组 ,其余 194例为对照组 ,分析两组患者围手术期情况。结果　研究组与对照组的一般情况无明显差异 ;输卵管破裂的发生率分别为 81%(17/2 1)、16% (3 1/194) ,两组比较 ,差异有极显著性 (P <0 0 1) ;腹腔内出血量分别为 (1775± 5 3 1)与(13 3± 176)ml (P <0 0 1) ,自体输血量分别为 (1141± 13 2 7)与 (2 5± 83 )ml (P <0 0 1) ,自体输血率分别为 95 %与 9% ,两组比较 ,差异均有极显著性 (P <0 0 1) ;术中出血量分别为 (40± 2 2 )与 (5 6±5 8)ml,两组比较 ,差异无显著性 (P >0 0 5 )。研究组与对照组输卵管切除术的比例分别为 86%与5 1% ,两组比较 ,差异有极显著性 (P <0 0 1) ;手术时间分别为 (5 0± 2 4)与 (43± 2 4)min ,两组比较 ,差异无显著性 (P >0 0 5 ) ;术后住院时间分别为 (3 0± 0 8)与 (2 3± 0 8)d ,两组比较 ,差异无显著性 (P>0 0 5 )。两组均无腹腔镜操作引起的围手术期并发症。结论　具备熟练的腹腔镜操作技术对休克型输卵管妊娠     

Maternal and fetal atrial natriuretic peptide levels at delivery from normal and growth retarded pregnancies.

OBJECTIVE: To determine whether circulating fetal levels of the vasodilator atrial natriuretic peptide (ANP) are reduced in pregnancies complicated by intrauterine growth retardation (IUGR). DESIGN: Prospective observational study. SETTING: University teaching hospital and research laboratory. SUBJECTS: 25 normal singleton pregnancies delivered at term by spontaneous vertex delivery (n = 16) or by elective caesarean section (n = 9), and a series of 14 singleton pregnancies complicated by IUGR. INTERVENTION: Measurement of ANP by radio-immunoassay in maternal venous, umbilical artery, and umbilical vein plasma from a series of normal, and IUGR pregnancies. MAIN OUTCOME MEASURES: Comparison of plasma ANP levels between the three groups; relation between fetal ANP, PO2 and pH. RESULTS: Mode of delivery did not influence either maternal, umbilical artery or umbilical vein plasma ANP levels in normal term singleton pregnancies. Umbilical vein ANP levels were significantly higher in the IUGR group when compared with normal pregnancies at term (mean 66 95%, CI 36-122 vs mean 37, 95% CI 29-47 pg/ml, P = 0.03) and were inversely related to umbilical artery pH (R2 = 65%; P = 0.003). CONCLUSIONS: These data suggest that umbilical vein ANP levels are elevated in pregnancies complicated by IUGR, and rise appropriately in response to the stress of acidosis. In the absence of any receptor or second messenger defect within feto-placental vascular smooth muscle, these data suggest that ANP is not directly implicated in the vascular pathophysiology of IUGR.     

硫酸镁对胎儿生长受限孕鼠胎盘组织半胱氨酸天冬氨酸蛋白酶3表达的影响

目的探讨硫酸镁对胎儿生长受限(FGR)孕鼠胎盘组织半胱氨酸天冬氨酸蛋白酶3(caspase-3)表达的影响,及硫酸镁治疗FGR的机理。方法烟熏法构建FGR模型。实验对象分为对照组(10只)、治疗组(18只)、FGR组(10只)。治疗组中低剂量(硫酸镁300 mg／kg)治疗10只、高剂量(硫酸镁600 mg／kg)治疗8只,皮下注射给药。络合指示剂方法测孕鼠血清Mg2+(血镁)浓度。物理测量胎鼠的各项生理指标。链霉菌抗生物素蛋白-过氧化物酶连接(SP)法及RT-PCR法检测胎盘组织caspase-3的表达情况。结果(1)FGR组孕鼠血镁浓度为(0．55±0．03)mmol／L,高、低剂量治疗组孕鼠血镁浓度分别为(0．72±0．13)、(0．61±0．03)mmol／L,高、低剂量治疗组分别与FGR组比较,差异均有统计学意义(P<0．01)。(2)FGR组孕鼠胎盘重量为(0．63±0．05)g,其胎鼠体重为(2．95±0．46)g,高剂量治疗组分别为(0．80±0．16)、(3．58±0．10)g,两组分别比较,差异均有统计学意义(P<0．05、P<0．01)。(3)FGR组胎盘组织caspase-3 mRNA表达量为0．626±0．036,其蛋白表达量为199．5±4．7,高剂量治疗组分别为0．361±0．030、183．0±3．3,差异均有统计学意义(P< 0．05),低剂量治疗组caspase-3 mRNA表达量为0．525±0．029,与高剂量治疗组比较,差异也有统计学意义(P<0．05)。(4)孕鼠血镁浓度与胎鼠重量、胎盘组织caspase-3 mRNA及蛋白表达量有显著相关性(r=0．899,P=0．038;r=-0．747,P=0．033;r=-0．915,P=0．001)。结论硫酸镁能降低胎盘组织caspase-3 mRNA及蛋白表达,硫酸镁可能通过抑制胎盘caspase-3的表达,减少胎盘滋养细胞、血管内皮细胞等功能细胞的凋亡,从而改善FGR胎鼠的低体重现象。     

Magnesium sulfate protection of fetal rat brain from severe maternal hypoxia

OBJECTIVE: To determine whether severe maternal hypoxia affects fetal rat physical characteristics and causes neuronal damage, and whether magnesium sulfate can decrease these effects. METHODS: At 17 days gestation, rats were randomly assigned to one of four groups that received saline injections and room air (n = 6), magnesium sulfate and room air (n = 5), saline and hypoxia (n = 5) or magnesium sulfate and hypoxia (n =5). Maternal magnesium sulfate or saline injections were given for 4 hours. In groups 3 and 4 this was followed by a hypoxia chamber protocol that included a gas mixture of 9% oxygen and 3% carbon dioxide for 2 hours. After 72 hours of recovery, fetuses were delivered abdominally, perfused transcardially, and brains removed intact. Fetal body and brain weight and size were measured. Brains were embedded in paraffin, sectioned, and stained. A neuropathologist masked to the protocol performed histologic grading of brain regions. RESULTS: Exposure to the hypoxia chamber resulted in decreased maternal oxygen tension and pH (from 82.8 +/- 20.0 to 49.2 +/- 14.4 mmHg, and from 7.37 +/- 0.05 to 7.20 +/- 0.04, respectively; P <.005). Magnesium sulfate administration resulted in higher magnesium levels in blood (from 1. 52 +/- 0.2 to 3.77 +/- 0.7 mg/dL; P <.001). The hypoxia protocol resulted in a significant decrease in fetal body and brain size, but not weight. Hypoxia also caused an increase in the proportion of fetal rats that had brain injury, including shrinkage of cells and karyorrhexis in the hippocampus and thalamus (from 0% to 38.1% and 38.9%, respectively; P <.05). Magnesium sulfate reduced these effects on fetal brain histopathology and size. CONCLUSION: Severe maternal rat hypoxia resulted in significant fetal neuronal damage and decreased fetal body and brain size. Maternal magnesium sulfate administration reduced the effect of hypoxia on fetal brain histopathology and size without affecting body size.     

The effects of intrapartum magnesium sulfate therapy on fetal serum interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha at delivery: a randomized, placebo-controlled trial.

OBJECTIVE: Elevated levels of inflammatory cytokines in the fetus have been linked to neurologic morbidities in preterm neonates. Magnesium sulfate is currently being studied in clinical trials as a potential fetal neuroprotective agent. The purpose of this study was to determine whether intrapartum magnesium sulfate therapy has an effect on the umbilical venous concentrations of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha at delivery. STUDY DESIGN: Women with singleton gestations >32 weeks with no clinical indications for magnesium sulfate therapy (preeclampsia or tocolysis) and either clinical chorioamnionitis or prolonged rupture of membranes were recruited for the study. Consenting patients were randomly assigned, in a double-blinded fashion, to receive either magnesium sulfate (6-g load then 2 g/hr) or matched volumes of lactated Ringer's solution until delivery. Fetal blood specimens were obtained by aspiration of the umbilical vein after cord clamping but before placental separation. Umbilical cytokine levels were measured with a sensitive and specific immunoassay. RESULTS: Twenty-two patients were randomly assigned to groups and received either magnesium sulfate (n = 11) or placebo (n = 11). There were no differences in the demographic or clinical characteristics between groups. The umbilical venous ionized magnesium concentration was significantly higher in the magnesium sulfate group (2.32 +/- 0.27 mg/dL vs 1.23 +/- 0.15 mg/dL; P <.001). There were no statistically significant differences between groups with respect to umbilical levels of interleukin-1beta (1.5 pg/mL [1.5-58] vs 1.5 pg/mL [1.5-10]; P =.5); interleukin-6 (8.5 pg/mL [1-1000] vs 11.2 pg/mL [1-113]; P =.9); or tumor necrosis factor-alpha (16 pg/mL [7.6-20.3] vs 16.6 pg/mL [8.3-22.2]; P =.5). CONCLUSION: In this pilot study the intrapartum administration of magnesium sulfate does not appear to affect the concentration of inflammatory cytokines in fetal blood at delivery.     

The effects of intrapartum magnesium sulfate therapy on fetal serum interleukin-1β, interleukin-6, and tumor necrosis factor-α at delivery: A randomized, placebo-controlled trial

Objective: Elevated levels of inflammatory cytokines in the fetus have been linked to neurologic morbidities in preterm neonates. Magnesium sulfate is currently being studied in clinical trials as a potential fetal neuroprotective agent. The purpose of this study was to determine whether intrapartum magnesium sulfate therapy has an effect on the umbilical venous concentrations of interleukin-1β, interleukin-6, and tumor necrosis factor-α at delivery. Study Design: Women with singleton gestations >32 weeks with no clinical indications for magnesium sulfate therapy (preeclampsia or tocolysis) and either clinical chorioamnionitis or prolonged rupture of membranes were recruited for the study. Consenting patients were randomly assigned, in a double-blinded fashion, to receive either magnesium sulfate (6-g load then 2 g/hr) or matched volumes of lactated Ringer’s solution until delivery. Fetal blood specimens were obtained by aspiration of the umbilical vein after cord clamping but before placental separation. Umbilical cytokine levels were measured with a sensitive and specific immunoassay. Results: Twenty-two patients were randomly assigned to groups and received either magnesium sulfate (n = 11) or placebo (n = 11). There were no differences in the demographic or clinical characteristics between groups. The umbilical venous ionized magnesium concentration was significantly higher in the magnesium sulfate group (2.32 ± 0.27 mg/dL vs 1.23 ± 0.15 mg/dL; P < .001). There were no statistically significant differences between groups with respect to umbilical levels of interleukin-1β (1.5 pg/mL [1.5-58] vs 1.5 pg/mL [1.5-10]; P = .5); interleukin-6 (8.5 pg/mL [1-1000] vs 11.2 pg/mL [1-113]; P = .9); or tumor necrosis factor-α (16 pg/mL [7.6-20.3] vs 16.6 pg/mL [8.3-22.2]; P = .5). Conclusion: In this pilot study the intrapartum administration of magnesium sulfate does not appear to affect the concentration of inflammatory cytokines in fetal blood at delivery. (Am J Obstet Gynecol 2001;184:1320-4.)     

表皮生长因子与胎儿宫内发育迟缓关系的研究

探讨表皮生长因子与胎儿宫内发育迟缓的关系。方法用放射免疫分析,测定８６例妊娠晚期妇女血清,羊水和脐静脉血ＥＧＦ浓度;根据新生儿出生体重,将研究对象分成对照组５４例,大于胎龄儿组１８例和ＩＵＧＲ组１４例。对照组中有１１例同时测定脐动脉血清ＥＧＦ浓度,比较各组间羊水和孕妇,脐血清ＥＧＦ水平及脐动,静脉血清间ＥＧＦ水平的差异。     

120例早发型子痫前期孕妇解痉抗凝治疗的临床分析

目的:探讨早发型子痫前期患者应用硫酸镁合并低分子肝素及丹参期待治疗的临床效果和安全性。方法:将2008年10月至2011年5月来我院就诊的早发型子痫前期孕妇随机分为4组(共120例)。A组:硫酸镁常规治疗;B组:硫酸镁+丹参(20ml/d)治疗;C组:硫酸镁+低分子肝素(4100U/d)治疗;D组:硫酸镁+丹参(20ml/d)+低分子肝素(4100U/d)治疗。通过临床症状、体征及辅助检查的变化判断各组的治疗效果及其对母婴的影响。结果:4组患者在治疗前临床各项指标差异无统计学意义(P>0.05);4组治疗后平均动脉压均较治疗前下降(P<0.05),24小时尿蛋白治疗前后差异无统计学意义;治疗后B、C、D3组的新生儿窒息率较A组显著降低(P<0.05),而在B、C、D各组间比较差异无统计学意义(P>0.05)。结论:硫酸镁联合低分子肝素或丹参治疗可改善早发型子痫前期患者新生儿的预后,安全有效。     

Endothelin 1 and leptin in the pathophysiology of intrauterine growth restriction.

OBJECTIVES: To evaluate the relationship of endothelin 1 (ET-1) and leptin concentrations in women and newborns following a pregnancy complicated with intrauterine growth restriction (IUGR). METHODS: Twenty-five women with a pregnancy complicated with IUGR at 19 different gestational ages were matched with women with uncomplicated pregnancies. Blood samples from the umbilical artery and maternal peripheral venous circulation were collected at delivery, and ET-1 and leptin levels were determined from the blood samples. Data relating to obstetric complications (e.g., pregnancy-induced hypertension), delivery (e.g. mode, birth weight, signs of intrapartum fetal distress, and Apgar scores) were also recorded. RESULTS: Mean maternal ET-1 (13.4+/-6.2-9.9+/-2.9 pmol/l) and mean fetal ET-1 (14.5+/-4.2-11.7+/-3.1 pmol/l) concentrations were significantly higher when women had experienced pregnancies complicated with IUGR than when they had had normal pregnancies. Mean fetal leptin concentration was significantly lower in the study group (6.8+/-2.2 ng/ml) than in the control group (10.6+/-3.6 ng/ml (P<0.05). However, fetal leptin per kilogram of fetal weight was not significantly different in the study group (3.16+/-1.18 ng/ml) than in the control group (3.23+/-0.96 ng/ml) (P>0.05, paired t-test). However, a statistically significant correlation was observed between fetal leptin concentrations per kilogram of fetal weight and fetal endothelin concentrations in pregnancies complicated with IUGR (r=0.546; P<0.05). CONCLUSIONS: These results suggest the intertwined roles of ET-1 and leptin in the pathophysiology of IUGR. Further studies concerning interaction between these peptides in different pregnancy conditions may provide important information about the actions of ET-1 and leptin on fetal growth.     

Endometriosis

OBJECTIVE: To identify prenatal events associated with cerebral palsy (CP) in infants born between 26 and 30 weeks of gestation. STUDY DESIGN: Case (n=22)-control (n=170) study was performed using a logistic regression model. RESULTS: Significant association of intrauterine infection with increased risk of CP was found in a logistic regression model that controlled for abnormal FHR patterns, placental infection, fetal acidosis at birth (umbilical artery pH<7. 1), and low Apgar score (<7) (odds ratio (OR) 5.47, 95% confidence interval (CI) 1.46-20.4). Magnesium sulfate exposure was associated with decreased risk (OR 0.13, CI 0.03-0.66) after exclusion of premature rupture of the membranes and abruptio placentae. In the magnesium exposure group, cases were infants born less than 28 weeks of gestation (3/21 vs. 0/61, P=0.015). CONCLUSION: In this case-control study, both intrauterine infection and magnesium sulfate exposure were significant factors related to the occurrence of cerebral palsy.     

妊娠肝内胆汁淤积症患者脐带血管病变及血管活性物质的表达与胎儿窘迫发生的关系

目的 探讨妊娠肝内胆汁淤积症(ICP)患者脐带血管病理改变、脐带血管活性物质表达的变化与胎儿窘迫发生的关系.方法 应用HE染色法制片,光镜下观察25例ICP伴有胎儿窘迫(ICP窘迫组)、25例ICP不伴胎儿窘迫(ICP对照组)以及27例正常妊娠妇女(正常妊娠组)新生儿脐带血管病理改变;应用免疫组化辣根过氧化物酶-生物素标记(SABC)法测定内皮型一氧化氮合酶(eNOS)、诱导型一氧化氮合酶(iNOS)及内皮素1(ET-1)蛋白在各组脐静脉内皮细胞中的表达量,以平均吸光度(A)值表示;应用循环酶法测定脐静脉血总胆酸水平并进行相关性分析.结果 (1)脐静脉血总胆酸水平:ICP窘迫组为(19.0±2.3)μmol/L,ICP对照组为(9.0±1.7)μmol/L,正常妊娠组为(4.4±1.5)μmol/L,各组分别比较,差异均有统计学意义(P＜0.05).(2)脐静脉病理改变:ICP患者脐静脉内皮细胞单层扁平结构丧失,细胞向管腔耸立,梭形排列,细胞排列不均甚至脱落.ICP窘迫组患者脐静脉内皮细胞出现此病理改变的发生率(92%,23/25)明显高于ICP对照组(68%,17/25),差异有统计学意义(P＜0.05).(3)脐静脉内皮细胞中eNOS蛋白表达量:ICP窘迫组为0.09±0.06,ICP对照组为0.21±0.08,正常妊娠组为0.47±0.07,各组分别比较,差异均有统计学意义(P＜0.05).脐静脉内皮细胞中iNOS蛋白表达量:ICP窘迫组为0.20±0.04,ICP对照组为0.21±0.05,正常妊娠组为0.26±0.04,两ICP组分别与正常妊娠组比较,差异均有统计学意义(P＜0.01,P＜0.05);而ICP窘迫组与ICP对照组间比较,差异无统计学意义(P＞0.05).(4)脐静脉内皮细胞中ET-1蛋白表达量:ICP窘迫组为0.49±0.08,ICP对照组为0.32±0.07,正常妊娠组为0.14±0.06,两ICP组分别与正常妊娠组比较,差异均有统计学意义(P＜0.01,P＜0.05).(5)脐静脉血总胆酸水平与其病理改变的关系:脐静脉血总胆酸水平升高是脐静脉病理改变的危险因素;且与脐血管内皮细胞eNOS、iNOS的蛋白表达量呈负相关关系(r1=-0.88、r2=-0.45,P＜0.01);与脐血管内皮细胞ET-1蛋白的表达量呈正相关关系(r3=0.79,P＜0.01).结论 ICP患者脐静脉血高胆酸状态可能损伤脐静脉内皮细胞,且与其eNOS、iNOS蛋白表达下调、ET-1蛋白表达上调有关,脐静脉的这些改变可能与ICP患者胎儿窘迫的发生有关.