妊娠高血压综合征患者胎盘绒毛组织内皮素1和内皮型一氧化氮合成酶的基因表达及其脐动脉血流变化

目的　研究妊娠高血压综合征 (简称妊高征 )患者胎盘绒毛组织内皮素 1(endothelin- 1,ET- 1)及内皮型一氧化氮合成酶 (endothelial nitric oxide synthase,e NOS)的基因表达 ,探讨 ET- 1及一氧化氮在妊高征患者胎儿胎盘循环中对脐动脉血流变化的作用。　方法　对妊高征患者及正常妊娠孕妇的胎盘绒毛组织 ,用地高辛标记的 ET- 1及 e NOS互补脱氧核糖核酸 (com plem entary deoxyri-bonucleotide,c DNA)探针进行点印迹杂交 ,利用 L eica QWIN图象处理系统测量每个杂交点的平均光密度值。在分娩前一日用彩色超声多普勒仪测定其脐动脉血流 S/ D值。　结果　妊高征患者胎盘绒毛组织 ET- 1基因表达明显增多 ,其平均光密度值妊高征组为 0 .43± 0 .0 3,正常组为 0 .2 3± 0 .44两组间差别显著 P<0 .0 5。而妊高征组胎盘绒毛组织 e NOS基因的表达明显低于正常对照组 ,其平均光密度值妊高征组为 0 .19± 0 .2 2 ,正常组为 0 .38± 0 .0 2 ,两组间差别显著 P<0 .0 5。妊高征组脐动脉S/ D值明显高于正常对照组 ,分别为 5 .92± 2 .13和 2 .11± 0 .2 2 ,两组间差别显著 P<0 .0 5。　结论　妊高征患者胎盘绒毛组织 ET- 1的表达明显增加 ,而内 e NOS的表达明显减少 ,脐动脉血流阻力亦明显增加。妊高征患者脐动脉血流     

妊娠高血压综合征患者胎盘和脐带血管内皮细胞损伤与肿瘤坏死因子的关系

目的　探讨妊娠高血压综合征 (妊高征 )患者胎盘和脐带血管内皮细胞损伤及功能变化与肿瘤坏死因子 (TNF)的关系。方法　采用放射免疫分析法 ,测定 41例妊高征患者 (妊高征组 )和 35例正常妊娠妇女 (对照组 )血浆TNF、内皮素和一氧化氮的水平 ;采用透射电镜观察两组胎盘和脐带血管内皮细胞的超微结构 ,并与在体外人重组TNF(rTNF)作用下培养的脐带血管内皮细胞形态相比较。结果　 (1)妊高征组血浆TNF和内皮素分别为 (2 .2 7± 0 .42 ) μg/L和 (73.31± 9.98)ng/L ,一氧化氮为(10 4.93± 2 0 .5 4) μmol/L ;对照组血浆TNF和内皮素分别为 (1.72± 0 .2 5 ) μg/L和 (5 2 .32± 10 .44 )ng/L ,一氧化氮水平为 (138.2 5± 2 2 .16 ) μmol/L。妊高征组TNF及内皮素增高 ,一氧化氮减少。两组比较 ,差异有显著性 (P <0 .0 5 )。(2 )电镜显示 ,妊高征组中除轻度患者的胎盘及脐带血管未见异常改变外 ,中、重度患者的胎盘和脐带血管内皮细胞均有损伤性表现。与rTNF作用下于体外培养的脐带血管内皮细胞形态学的改变相似。结论　TNF可引起胎盘和脐带血管内皮细胞损伤 ,可导致血管调节因子失衡 ,在妊高征的发病中有一定作用。     

重度妊娠高血压综合征患者表皮生长因子及其受体水平的研究

目的　研究孕晚期重度妊娠高血压综合征 (妊高征 )并发及未并发胎儿生长受限(FGR)者的血浆表皮生长因子 (EGF)水平、胎盘组织 EGF受体 (EGFR)表达情况 ,探讨 EGF与妊高征的关系、EGF在妊高征及 FGR发生中的作用、EGF对妊高征胎儿生长发育的影响 ,为妊高征及FGR的病因研究及治疗提供依据。　方法　血浆 EGF及血清胎盘生乳素 (HPL )采用放射免疫分析法测定 ,胎盘组织 EGFR采用免疫组织化学方法测定。　结果　 (1)血浆 EGF浓度 ,重度妊高征组为(96± 46 ) ng/L ,明显低于对照组 (144± 36 ) ng/L ,(t=4.16 9,P<0 .0 1)。重度妊高征并发 FGR组为(89± 37) ng/L ,重度妊高征未并发 FGR组为 (10 1± 5 4) ng/L ,均明显低于对照组 ,Dunnett t=3.94、3.2 0 ,P<0 .0 1,但此二者之间差异无显著性 ,(t=0 .792 ,P>0 .0 5 )。(2 )血清 HPL与血浆 EGF呈正相关。(3)胎盘 EGFR染色情况。重度妊高征胎盘 EGFR的表达比对照组强 ,妊高征组染色通光度为 114± 8,对照组为 12 5± 9(t=4.74,P<0 .0 1) ,且无论妊高征并发或未并发 FGR,其胎盘 EGFR的表达都比对照组强 ,FGR组为 115± 8,NFGR组为 114± 7,Dunnett t值分别为 3.6 4、4.35 ,P值均 <0 .0 1。但在妊高征者 FGR组与 NFGR组之间差异无显著性 ,(t=0 .5 5 ,P>0 .0 5 )。     

妊娠高血压综合征患者血浆C-型利钠肽水平变化的相关性研究

目的　探讨妊娠高血压综合征 (妊高征 )患者血浆C 型利钠肽水平的变化 ,及其与妊高征发病的关系。方法　采用放射免疫分析法测定了 89例妊高征患者 (妊高征组 )、193例正常妊娠妇女 (正常妊娠组 )和 46例正常孕龄妇女 (正常妇女组 )血浆C 型利钠肽水平。结果　妊高征组血浆C 型利钠肽水平明显升高 ,为 (30 .5 1± 33.6 1)ng/L ;正常妊娠组为 (19.43± 5 .13)ng/L ,正常妇女组为(17.15± 3.82 )ng/L。妊高征患者血浆C 型利钠肽水平明显高于正常妊娠妇女。妊高征组轻、中、重患者之间 ,血浆C 型利钠肽水平亦有极显著差别 ,分别为 (9.88± 2 .74)ng/L、(2 2 .15± 8.90 )ng/L和(6 4.2 6± 44 .0 3)ng/L ,3者比较 ,差异有极显著性 (P <0 .0 1)。结论　血浆C 型利钠肽水平由低到高的变化反映妊高征的疾病严重程度 ,可作为判断妊高征病情发展的一个生化指标。     

妊高征患者白细胞介素6与免疫球蛋白的相关性研究

目的　探讨妊高征患者白细胞介素 6 (IL- 6 )与免疫球蛋白 (Ig)的相关性。　方法　用放射免疫法检测妊高征患者 5 0例 (妊高征组 ,其中中度 2 4例 ,重度 2 6例 )及正常足月妊娠 30例 (正常足月妊娠组 )的母血、脐血中的 IL- 6含量 ,采用速率散射比浊法检测同样标本中的 Ig G、Ig M、Ig A的含量。　结果　重度妊高征患者母血中 IL- 6的含量为 (16 7.2 0± 72 .5 2 ) ng/ L,脐血中 IL- 6含量为 (133.2 0±85 .5 5 ) ng/ L,均较正常孕妇显著增高 ,差异显著 (P<0 .0 1,P<0 .0 1) ,中度妊高征患者母血中 IL- 6的含量为 (12 4.40± 86 .37) ng/ L,脐血中 IL- 6含量为 (97.33± 74.16 ) ng/ L,均较正常孕妇显著增高 ,差异显著 (P<0 .0 5 ,P<0 .0 5 )。中度妊高征母血 Ig G含量为 (7.0 1± 2 .0 9) g/ L,而重度妊高征母血 Ig G含量为 (7.43± 1.6 6 ) g/ L,均显著低于正常妊娠组 (P<0 .0 1,P<0 .0 1) ,与母血 IL- 6含量呈显著负相关关系 (r=- 0 .779,P<0 .0 1;r=- 0 .80 6 ,P<0 .0 1)。　结论　 IL- 6与 Ig G协同作用 ,共同参与了妊高征的免疫损伤过程 ,提示 :如能使母血中 IL- 6降低 ,Ig G升高 ,有可能防治妊高征。     

妊高征孕妇血清β-HCG及HPL水平测定

目的 :探讨血清 β绒毛膜促性腺激素 (β HCG)及胎盘泌乳素 (HPL)水平与妊娠高血压综合征 (妊高征 )之间的关系。方法 :用放射免疫法测定 1 1 8例正常妊娠妇女及 42例妊高征妇女血清 β HCG及HPL水平。结果 :正常妊娠妇女血清 β HCG为 1 2 .0 4± 5.62 μg/L ,妊高征妇女血清 β HCG为 2 2 .32± 9.40 μg/L,两组比较差异有显著性 (P <0 .0 5)。β HCG水平与妊高征病情严重程度呈正相关 (γ=0 .56P <0 .0 5) ;正常妊娠妇女血清HPL为 6.1 8± 3 .2 7mg/L ,妊高征妇女为 6 .35± 2 .79mg/L ,妊高征组与正常妊娠妇女组比较 ,差异无显著性 (P >0 .0 5)。结论 :β HCG可反映妊高征时胎盘滋养细胞功能紊乱程度及病情的严重程度     

妊高征患者血清瘦素水平变化的研究

目的 :探讨妊娠高血压综合征 (妊高征 )患者血清瘦素 (leptin)水平的变化及其与妊高征发病的关系。方法 :采用放射免疫分析法测定了 36例妊高征患者 (妊高征组 )和 30例正常孕妇 (正常妊娠组 )产前及产后血清瘦素水平。结果 :中、重度妊高征患者产前瘦素水平为 15 .19± 6 .74 ng/ ml明显高于正常妊娠组的 10 .11± 2 .80 ng/ m l(P<0 .0 5 ) ;轻度妊高征组患者产前瘦素水平 12 .77± 4 .6 8ng/ ml与正常妊娠组比较 ,差异无显著性 (P>0 .0 5 )。妊高征患者产后瘦素水平为 5 .91± 2 .6 8ng/ ml,与产前 14 .5 6± 6 .30 ng/ ml相比 ,差异显著 (P<0 .0 5 )。妊高征组产后瘦素水平与正常妊娠组 5 .74± 2 .38ng/ ml相比 ,差异无显著性。结论 :妊高征患者血清瘦素水平升高 ,与妊高征的发生有关     

妊娠高血压综合征患者血浆止凝血分子标志物水平变化的意义

目的探讨妊娠高血压综合征(妊高征)患者血浆止凝血分子标志物水平变化的意义.方法对45例妊高征孕妇(妊高征组,其中轻度20例、中度15例、重度10例)及20例正常孕妇(正常妊娠组)分娩前后的血浆止凝血分子标志物进行检测.其中,采用酶联免疫吸附试验(ELISA)检测两组孕妇分娩前后的P-选择素、凝血酶原片段1+2(F1+2)、D-二聚体、纤溶酶抗纤溶酶复合物(PAP);采用发色底物法检测两组孕妇分娩前后的抗凝血酶活性.结果 (1)P-选择素妊高征组中、重度孕妇分娩前分别为(66±24)μg/L、(80±30)μg/L,正常妊娠组为(49±15)μg/L,两组比较,差异有显著性(P<0.05).分娩后妊高征组重度孕妇为(65±34)μg/L,正常妊娠组为(40±12)μg/L,两组比较,差异有显著性(P<0.05).(2)F1+2妊高征组轻、中、重度孕妇分娩前分别为(2.2±0.2)nmol/L、(2.3±0.4)nmol/L、(2.2±0.2)nmol/L,均明显高于正常妊娠组的(1.2±0.3)nmol/L,两组比较,差异有显著性(P<0.05).(3)D-二聚体妊高征组轻、中、重度孕妇分别为(0.7±0.1)mg/L、(0.7±0.3)mg/L、(0.8±0.2)mg/L,正常妊娠组为(0.4±0.1)mg/L,妊高征组显著高于正常妊娠组(P<0.05),且妊高征组重度孕妇D-二聚体水平高于中度及轻度孕妇.(4)PAP妊高征组轻、中、重度孕妇分娩前分别为(0.7±0.4)mg/L、(0.8±0.4)mg/L、(0.8±0.4)mg/L,均高于正常妊娠组的(0.7±0.3)mg/L(P<0.05),且妊高征组轻、中、重孕妇PAP的升高水平与疾病的严重程度呈正相关(P<0.05).两组孕妇分娩后PAP水平比较,差异无显著性(P>0.05).(5)抗凝血酶活性正常妊娠组为(108±17)%,而在妊高征组则显著降低,其中重度孕妇为(44±37)%、中度孕妇为(64±25)%、轻度孕妇为(83±39)%,两组比较,差异有极显著性(P<0.01).妊高征组中、重度孕妇又显著低于轻度孕妇(P<0.01).结论 P-选择素及 F1+2可用于高危妊娠的筛查,D-二聚体可作为妊高征孕妇早期DIC的监测,抗凝血酶活性是反映妊高征疾病严重程度的有效指标.以上这些止凝血分子标志物可作为妊高征患者血栓前状态的监测指标.     

妊娠高血压综合征患者外周血单个核细胞产生Th1、Th2型细胞因子失衡的研究

目的　研究妊娠高血压综合征 (简称妊高征 )患者外周血单个核细胞 (peripheral bloodmononuclear cell,PBMC)产生 Th1、Th2型细胞因子的功能变化。　方法　妊高征组 4 3例 ,正常孕妇组 15例 ,健康非孕组 15例 ,采用 EL ISA方法检测外周血 PBMC体外培养上清液中白细胞介素 2(interleukin- 2 ,IL- 2 )、干扰素 γ(interferon- γ,IFN- γ)及白细胞介素 4 (interleukin- 4 ,IL- 4 )水平。　结果　 PBMC体外培养上清液中 ,IL- 2在正常妊娠组为 (14 0 .3± 73.2 ) ng/ L,与健康非孕组 (2 5 9.5± 114 .4 ) ng/ L 相比水平下降 (P<0 .0 1) ;在妊高征组为 (2 34.6± 10 7.2 ) ng/ L,与正常妊娠组相比水平升高 (P<0 .0 1)。IFN- γ在正常妊娠组为 (30 7.5± 10 6 .4 ) ng/ L,与健康非孕组 (4 83.7± 177.8) ng/ L相比水平下降 (P<0 .0 1) ;在妊高征组为 (4 13.5± 14 9.7) ng/ L,与正常妊娠组相比水平升高 (P<0 .0 1)。IL- 4在正常妊娠组为 (4 1.9± 11.4 ) ng/ L,与健康非孕组 (2 7.4± 8.3) ng/ L 相比水平升高 (P<0 .0 0 1) ;在妊高征组为 (32 .1± 12 .0 ) ng/ L,与正常妊娠组相比水平下降 (P<0 .0 1)。IL- 2 / IL- 4比值在正常妊娠组为 3.5± 1.9,与健康非孕组 10 .1± 4 .8相比比值下降 (P<0 .0 0 1) ;在     

肝细胞生长因子与妊娠高血压综合征发病的关系

目的 :探讨肝细胞生长因子 (HGF)与妊娠高血压综合征 (妊高征 )发病的相关性。方法 :采用逆转录 -聚合酶链式反应 (RT PCR)检测 2 0例重度妊高征患者 (妊高征组 )胎盘组织中HGFmRNA表达水平 ,并以 2 0例健康孕妇 (对照组 )为对照。结果 :妊高征组胎盘组织HGFmRNA表达峰度为 0 .19± 0 .0 7,较对照组 ( 0 .3 3± 0 .0 5 )显著降低 (P <0 .0 5 )。结论 :妊高征患者HGF表达异常发生于转录水平 ,HGF异常表达在妊高征胎盘缺氧中有重要作用     

Toll样受体与子宫内膜及子宫内膜异位症

子宫内膜异位症(EMs)发病机制尚未完全阐明.大量研究表明,免疫因素在EMs的发病机制中起重要作用.EMs免疫应答异常主要是巨噬细胞数量和活性增加及其分泌产物,如生长因子、细胞因子和血管生成因子的改变.Toll样受体(TLRs)识别特异性的病原体相关分子模式,启动和介导免疫应答,在固有免疫中发挥重要作用,并诱导产生适应性免疫反应.TLRs在正常子宫内膜中的生理作用以及在EMs中的相关研究已逐步开展,对其深人认识和研究将为EMs诊断、治疗和预后判断提供新思路和手段.     

Toll样受体与子宫内膜及子宫内膜异位症

子宫内膜异位症（EMs）发病机制尚未完全阐明。大量研究表明,免疫因素在EMs的发病机制中起重要作用。EMs免疫应答异常主要是巨噬细胞数量和活性增加及其分泌产物,如生长因子、细胞因子和血管生成因子的改变。Toll样受体（TLRs）识别特异性的病原体相关分子模式,启动和介导免疫应答,在固有免疫中发挥重要作用,并诱导产生适应性免疫反应。TLRs在正常子宫内膜中的生理作用以及在EMs中的相关研究已逐步开展,对其深入认识和研究将为EMs诊断、治疗和预后判断提供新思路和手段。     

Psychological and pharmacological treatments of mood and anxiety disorders during pregnancy and postpartum. Review and synthesis

The aim of this article is to review the main methods of treatment of anxious and depressive disorders during pregnancy and the postpartum. To this end, we analyse recent publications about the use and efficacy of psychotherapy and psychosocial interventions (cognitive behavioural therapy, interpersonal psychotherapy, psychoanalytical therapy) in the perinatal period. We also review recent papers about the use of psychotropic medication during pregnancy and breast-feeding, with special emphasis on clinical trials. We particularly focus on the risk/benefit assessment of antidepressants, mood stabilisers, antipsychotics and benzodiazepines, in terms of teratogenicity, and impact on neonatal adaptation and neuropsychological development. Various treatment modalities are presented and discussed. It appears that psychotherapies have proved their efficiency on most pre- and postpartum anxious and depressive disorders and represent a first line treatment in most cases. Psychopharmacological treatment is indicated for severe anxious and depressive disorders. The risks of such medication, especially antidepressants, may have been overestimated in the past. Provided reasonable precautions are taken and mothers and future mothers receive clear information on the potential risks and benefits, psychotropic medication could be more broadly prescribed during pregnancy and the breast-feeding period.     

Pharmacokinetics and endometrial and tubal tissue penetration of cefalotin and cefazolin

The pharmacokinetics and concentrations of the two antibiotics cefazolin and cefalotin were studied during gynecologic operations in endometrial and tubal tissue. The patients received 0.05 g/kg of the antibiotics by intravenous injection. Under the given conditions, pharmacokinetic calculation of the plasma elimination gave half-lives of 24.8 min for cefalotin and of 63 min for cefazolin. Fitting of the tissue levels to the Bateman function showed that the two antibiotics diffuse rapidly into both tubal and endometrial tissue and attain peak concentration levels between 10 and 25 min. In both tissues the concentrations of cefazolin were higher than those of cefalotin. Higher tissue concentrations of cefazolin could also be demonstrated in experiments of longer duration.     

Placental ischemia and changes in umbilical and uteroplacental arterial and venous hemodynamics

Objective: To relate Doppler velocimetry findings in fetoplacental and uteroplacental circulation to placental histomorphology. Material and methods: In 14 uncomplicated and 31 high-risk pregnancies Doppler velocimetry was performed in umbilical artery and vein, and in maternal uterine veins and arteries during the second half of gestation. Histopathology of the placentas was examined, especially for signs of ischemia and inflammation. Results: All fetuses in uncomplicated pregnancies had normal flow velocity waveforms in umbilical artery; in the high-risk group, 18 fetuses had abnormal flow (increased PI or absent/reverse end-diastolic flow). The latter group had more often high ischemic score and infarctions in the placenta than found in pregnancies with normal umbilical artery flow (p?<?0.001 and p?=?0.02, respectively). Similarly, the abnormal uterine artery flow pattern (uterine artery score 3–4) occurred more often with high ischemic score and placenta infarctions (p?<?0.001 and p?<?0.001, respectively). No significant associations were found between the uterine venous flow type and placental ischemia. Conclusion: Placental ischemic morphological changes were associated with Doppler ultrasound signs of increased resistance to arterial blood flow, both on the fetal and maternal sides of the placenta. No significant relation to the uterine venous flow velocities was found.     

Israeli and British women's wellbeing and eating behaviours in pregnancy and postpartum

Objectives: The study had two main objectives: (a) track changes in self-esteem, eating behaviours and body satisfaction from early pregnancy to 24 months postpartum and (b) to compare changes by context (Israel vs. UK) and maternal body mass index (BMI).

Background: High maternal BMI is associated with negative body image and restrained eating, which are experienced differently across cultures.

Methods: 156 pregnant women were recruited from Israel and the UK. Seventy-three women were followed up every six months from early postpartum and until 24 months following birth. Women completed questionnaires assessing self-esteem (RSEQ), body image (BIS/BIDQ) and eating behaviours (DEBQ) and self-reported weights and heights so that BMI could be calculated.

Results: Women with higher BMI had higher levels of self-esteem and were less satisfied with their body. Healthy-weight women were more likely to lose all of their retained pregnancy weight compared to overweight and obese women. Self-esteem, body image and eating behaviours remained stable from pregnancy until 24 months postpartum. No significant differences were found for any measure by context.

Conclusion: BMI was the strongest predictor of self-esteem and body dissatisfaction and a higher BMI predicted less weight loss postpartum.     

Prostacyclin and thromboxane in gynecology and obstetrics

The gynecologic and obstetric implications of the smooth muscle-relaxing, antiaggregatory prostacyclin and its endogenous antagonist, thromboxane A2, are reviewed. In addition to the vascular wall and circulating platelets, which are primary sources for prostacyclin and thromboxane A2, respectively, reproductive tissues produce great amounts of these prostanoids, evidently for the regulation of the vascular tone and/or vascular platelet interaction. Several gynecologic and obstetric disorders are characterized by abnormalities in prostacyclin and/or thromboxane A2. In primary menorrhagia the uterine release of prostacyclin is increased, and consequently menstrual blood loss can be reduced with various prostaglandin synthesis inhibitors. Prostacyclin relaxes the nonpregnant myometrium in vitro and may also do so in vivo, although intravenous infusion of prostacyclin has no effect upon the uterine contractility in nonpregnant or pregnant subjects. Patients with pelvic endometriosis may have increased levels of prostacyclin and thromboxane A2 metabolites in the peritoneal fluid. The prostacyclin/thromboxane A2 balance shifts to thromboxane A2 dominance in patients with gynecologic cancer. During pregnancy the production of prostacyclin and thromboxane A2 increases in the mother and fetoplacental tissue. Preeclampsia and other chronic placental insufficiency syndromes are accompanied by prostacyclin deficiency in the mother and in fetomaternal tissues and by an overproduction of thromboxane A2, at least in the placenta. These changes may account for the vasoconstriction and platelet hyperactivity, which are pathognomonic for hypertensive pregnancies. By directing the prostacyclin/thromboxane A2 balance to prostacyclin dominance (by dietary manipulation, administration of prostacyclin and/or its analogues, drugs with prostacyclin-stimulating and/or thromboxane A2-inhibiting action), it may be possible to prevent and/or treat hypertensive pregnancy complications in the future.