胎儿宫内发育迟缓的预防

胎儿宫内发育迟缓 (IUGR)是指胎儿出生体重低于相应孕周的第 10百分位数。导致其发生的原因较多 ,主要有遗传因素、胎儿畸形和宫内感染 ,与胎儿生长相关因子或激素分泌异常以及胎儿宫内营养不良等有关。近年研究表明 :I UGR除围生期并发症如胎儿窘迫、新生儿窒息、胎粪吸入、新生儿低血糖和红细胞增多症增加外 ,成年期一些疾病发生率也明显升高 ,主要包括有冠心病、脑卒中、慢性高血压及 1型糖尿病。另外肺部疾患、肾病的发生与IUGR低出生体重也存在一定的相关性[1] 。因此 ,预防和减少IUGR的发生对改善围生儿质量 ,提高人口素质具有…     

胎儿宫内发育迟缓时孕妇及胎儿心钠素的变化及意义

目的 探讨胎儿宫内发育迟缓的孕妇血清、脐血和羊水中心钠素水平的变化.方法 采用放射免疫法测定正常足月妊娠62例(正常组)和足月妊娠IUGR 38例(IUGR组)孕妇血清、脐血和羊水中心钠素的水平.结果 IUGR组孕妇脐血中心钠素水平显著下降(P<0.05),血清和羊水中心钠素水平与正常组比较无统计学差异(P>0.05).结论 心钠素分泌不足可能是IUGR发病原因之一,它对维持胎儿内环境平衡产生重要作用.     

川芎嗪对孕鼠宫内发育迟缓的防治作用

目的观察川芎嗪对宫内发育迟缓(I UGR)孕鼠及胎仔发育的影响,探讨川芎嗪的作用机理。方法利用被动吸烟法建立大鼠I UGR模型。36只孕鼠随机分为对照组、模型组、小剂量和大剂量川芎嗪防治组。孕21d剖宫取胎,测量胎仔体重及胎盘重,检测孕鼠血清及胎盘组织中一氧化氮(NO)含量及丙二醛(MDA)、超氧化物歧化酶(SOD)活性。结果模型组I UGR发生率为54·95%,比对照组明显增高(P<0·01);胎仔重及胎盘重分别为(3·067±0·334)g和(0·390±0·065)g,比对照组明显降低(P<0·01);血清及胎盘组织中NO含量及SOD活性降低,MDA水平增高(P<0·01)。小剂量、大剂量川芎嗪防治组与模型组比较,I UGR发生率明显降低,胎仔体重及胎盘重增加,NO含量和SOD活性增高,MDA水平降低(P<0·01)。结论孕中晚期应用适量川芎嗪可有效防治被动吸烟孕鼠I UGR的发生,提示川芎嗪可调节机体的氧化与抗氧化平衡失调,改善胎盘的血管功能,保证胎仔发育。     

妊高征伴胎儿宫内发育迟缓的胎儿血流波形变化

胎儿血流速度波形 (ＦＦＶＷｓ)的改变与围产儿预后有关。然而 ,反映ＦＦＶＷｓ的各项指标 ,各家报道不一。关于其对高危胎儿的预测价值仍有待于进一步研究。特别是ＦＦＶＷｓ对妊高征 (ＰＩＨ)胎儿宫内发育迟缓 (ＩＵＧＲ)的临床价值 ,国内尚未见报道。本研究通过检测妊高征患者胎儿的脐动脉 (ＵＡ)、大脑中动脉 (ＭＣＡ)的ＦＦＶＷｓ ,以评价彩色多普勒超声检测ＦＦＶＷｓ作为妊高征胎儿ＩＵＧＲ监护方法的临床价值。对象与方法一、研究对象1999年 1月～ 12月在山东医科大学附属医院门诊和住院病人中随机选择孕 2 9～ 36周妇女 74例 ,其中…     

硫酸镁治疗胎儿宫内发育迟缓疗效的研究分析

目的观察分析应用硫酸镁治疗胎儿宫内发育迟缓效果。方法将227例胎儿宫内发育迟缓(IUGR)孕妇随机分为观察组和对照组。对照组112例,用10%葡萄糖500ml 复方丹参液14ml 低分子右旋糖酐500ml 5%复方氨基酸500ml静脉滴注;观察组115例,在对照组相同的处方上,再加用5%葡萄糖500ml 25%硫酸镁20ml静脉滴注,10天1个疗程,两组每天都间断吸氧。治疗后复查B超,观察胎头双顶径的增加情况,出生后测量新生儿体重及胎盘重量。全部孕妇均于42周前分娩。结果观察组宫内胎头双顶径的增加情况及新生儿出生体重和胎盘重量明显优于对照组,有显著性差异(P<0.05或P<0.01);而生产分娩周数无显著性差异(P>0.05)。结论应用硫酸镁治疗胎儿宫内发育迟缓安全有效。     

3组治疗胎儿宫内生长迟缓的药物经济学分析

目的：运用药物经济学分析方法比较3组治疗胎儿宫内发育迟缓（IUGR）的药物,为有限的医疗费用分配提供依据。方法：60例患IUGR孕妇分3组治疗：能量合剂十三方氨基酸胶囊组（A组）、能量合剂+复方氨基酸注射液组（B组）、能量合剂+复方氨基酸胶囊+10％脂肪乳剂组（C组）,分别进行药物经济学及敏感度分析。结果：A、B、C3组费用-效果比（元）分别为156．85、253．93、257．82。由敏感度分析费用-效果比（元）分别为154．05、240．15、234．13。结论：A组治疗方案最经济有效。     

氨苯碱治疗胎儿宫内发育迟缓的疗效观察

目的：探讨氨茶碱对胎儿宫内发育迟缓的疗效及其机制。方法：随机给予５７例ＩＵＧＲ孕妇（观察组）每日静滴氨茶碱０．２５ｇ,连续１０ｄ;５４例ＩＵＧＲ孕妇（对照组）给予维生素Ｃ２．０ｇ,静滴１０ｄ,两组其余治疗相同。结果：观察组的胎儿双顶径在治疗后两周增长２．２５±０．０７ｍｍ,其新生儿的出生体重为３．２５±０．０７ｍｍ,其新生儿的出生体重为３．２５±０．１３ｋｇ,显著高于对照组。结论：静滴氨茶碱治疗胎     

胎儿宫内发育迟缓病因与防治

胎儿宫内发育迟缓 (ｉｎｔｒａｕｔｅｒｉｎｅｇｒｏｗｔｈｒｅｔａｒｄａｔｉｏｎ ,ＩＵＧＲ)是指胎儿体重低于该孕龄正常体重的第 10百分位 ,或低于平均值的两个标准差。ＩＵＧＲ为产科重要并发症 ,占围生儿死亡的第二位 ,其围生儿病死率为正常发育儿的 6～ 10倍 ,在死胎死产中约占 30 % ,产时宫内缺氧中 5 0 %为ＩＵＧＲ儿。1　病因通常将ＩＵＧＲ的病因分为母体因素、胎儿因素、胎盘因素、脐带因素。1 1　母体因素1 1 1　营养因素 :孕妇是胎儿营养物质的基本来源 ,孕妇营养不良 ,尤其是蛋白质和能量供用不足即会影响胎儿的生长发育。另…     

咖啡因致胎儿宫内发育迟缓机制的研究进展

宫内发育迟缓(IUGR)是最常见的发育毒性之一,不仅可造成围产儿发病和死亡,而且其不良影响还可延续至成年,严重影响了人口生存质量。咖啡因广泛存在于多种日常饮料和某些药物中,其全球消耗量正逐年增加,妊娠妇女摄入含咖啡因的食品和药物也越来越多见。研究已证实,妊娠期摄入咖啡因是引起IUGR的危险因素之一,然而目前咖啡因引起胎儿不良反应的机制尚无定论。本文从母体(肾素-血管紧张素系统)、胎盘(细胞增殖/凋亡)和胎儿(神经内分泌干扰)3方面,综述了咖啡因致IUGR的发生机制。     

Effect of zinc on hepatic lipid peroxidation and antioxidative enzymes in ethanol-fed rats

A 3-ml aliquot of 30% ethanol was fed daily to normal as well as zinc-treated (227 mg l(-1)) rats for periods of 2, 4 and 8 weeks. A highly significant increase in the levels of hepatic lipid peroxidation was observed in ethanol-fed rats after 4 and 8 weeks of treatment. On the other hand, the levels of lipid peroxidation came down significantly following ethanol feeding to zinc-treated rats. The activities of glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD) in liver were elevated significantly after ethanol administration to rats for durations of 2, 4 and 8 weeks. Interestingly, zinc treatment to rats given ethanol was able to bring down the elevated levels of SOD, catalase and GPx to within normal limits, However, zinc administration alone did not cause any significant alteration in the activities of these antioxidative enzymes.     

自噬与宫内发育迟缓

宫内发育迟缓(intrauterine growth retardation,IUGR)是最常见的发育毒性结局,可导致子代围产期发病率和死亡率增加,且其危害会延续至出生后引起成年多种慢性疾病易感。自噬,作为胚胎发育的重要调节者,参与了多脏器发育过程。自噬增强或减弱可通过调控细胞增殖、分化等生命活动,参与胎盘及胎儿多种脏器发育,最终导致IUGR。该文主要综述了自噬的发生机制及其与IUGR的关系,为自噬在IUGR相关疾病中的研究提供理论依据。     

Effects of lignans on hepatic drug-metabolizing enzymes

The effects of lignans, related to macelignan, on hepatic microsomal drug-metabolizing enzyme (DME) activity were evaluated to elucidate the structure-activity relationship in mice and rats. The compounds carrying the methylenedioxyphenyl nucleus were found to be the most potent among compounds tested; which not only produced a marked inhibition of DME with a single dose but a significant induction with repeated treatments. Lack of the methylenedioxy group caused marked decrease in the activity, implying that a methylenedioxy group is essential and of major importance eliciting DME modifying activity. Part 15 in the series “Studies on crude drugs action on drug-metabolizing enzymes” For part 14, see ref 1.     

Effects of lemongrass oil and citral on hepatic drug-metabolizing enzymes,oxidative stress,and acetaminophen toxicity in rats

The essential oil from a lemongrass variety of Cymbopogon flexuosus [lemongrass oil (LO)] is used in various food and aroma industry products and exhibits biological activities, such as anticancer and antimicrobial activities. To investigate the effects of 200 LO (200 mg/kg) and 400 LO (400 mg/kg) and its major component, citral (240 mg/kg), on drug-metabolizing enzymes, oxidative stress, and acetaminophen toxicity in the liver, male Sprague-Dawley rats were fed a pelleted diet and administered LO or citral by gavage for 2 weeks. After 2 weeks of feeding, the effects of LO and citral on the metabolism and toxicity of acetaminophen were determined. The results showed that rats treated with 400 LO or citral had significantly reduced hepatic testosterone 6β-hydroxylation and ethoxyresorufin O-deethylation activities. In addition, NAD(P)H:quinone oxidoreductase 1 activity was significantly increased by citral, and Uridine 5′-diphospho (UDP) glucurosyltransferase activity was significantly increased by 400 LO in the rat liver. Treatment with 400 LO or citral reduced lipid peroxidation and reactive oxygen species levels in the liver. After acetaminophen treatment, however, LO and citral treatment resulted in little or no change in plasma alanine aminotransferase activity and acetaminophen-protein adducts content in the liver. Our results indicate that LO and citral may change the activities of drug-metabolizing enzymes and reduce oxidative stress in the liver. However, LO and citral may not affect the detoxification of acetaminophen.     

胎儿宫内生长迟缓的实验动物模型

目的　建立胎儿宫内生长迟缓的实验动物模型及观测指标。方法　妊娠动物被动吸烟、被动吸烟 +饮酒、注射亚硝基左旋精氨酸甲酯、注射更生霉素、维生素B1缺乏饮食+抗硫胺素、结扎子宫动脉等。结果　胎仔体重降低、身长短小 ,幼仔体格及神经系统发育缓慢 ,母体体重降低、血液营养物质和胎盘血流减少 ,胎盘组织细胞结构和功能发等。结论　上述方法可以建立胎儿宫内生长迟缓动物模型     

Comparative incidence of oral ochratoxicosis and aflatoxicosis on the activity of drug-metabolizing enzymes in rat liver

Mycotoxicosis has been produced in the rat by daily oral administrations of ochratoxin A (1.5 mg/kg/day) or aflatoxin B1 (1 mg/kg/day). Hepatic microsomal cytochrome P-450 and b5 contents and many phase I and II biotransformation systems have been measured in the course of ochratoxicosis (4 to 15 dosings) and aflatoxicosis (1 to 8 dosings). In case of ochratoxicosis, decreases in cytochrome P-450 level, aminopyrine demethylase and aniline hydroxylase activities were observed in rats receiving 15 administrations of the toxin. Aflatoxicosis induced more severe decreases in cytochrome P-450, aminopyrine demethylase and ethoxycoumarin deethylase following 8 daily gavages. In the two studies, there was no significant change in activities of liver phase II biotransformation enzymes.     

当归注射液对烟酒所致大鼠宫内发育迟缓的拮抗作用及机制

目的 :了解烟酒所致胎儿宫内发育迟缓 (IU GR)时孕鼠胎盘组织抗氧化功能的改变 ,探讨当归注射液的保护作用及机制。方法 :采用烟酒混合因素建立大鼠IUGR模型 ,部分孕鼠给予当归注射液0 .2 5g·kg-1治疗 ,测定胎盘组织中还原型谷胱甘肽(GSH)和丙二醛 (MDA)的含量及超氧化物歧化酶(SOD)、过氧化氢酶 (Cat)和谷胱甘肽过氧化物酶(GSH Px)的活性。结果 :IUGR孕鼠胎盘组织MDA和GSH含量均明显增加 (P <0 .0 1,P <0 .0 5 ) ,SOD、GSH Px和Cat活性显著下降 (P <0 .0 1,P <0 .0 5 )。经当归注射液治疗后 ,胎儿宫内生长发育接近正常 ,上述指标也得到改善。结论 :胎盘氧化损伤可能是IUGR发病的一个重要机制。当归注射液能提高IUGR孕鼠胎盘的抗氧化能力 ,促进胎儿宫内生长发育。     

肝纤维化状态下小肠药物代谢功能的改变

目的　探讨肝纤维化时小肠药物代谢功能的变化 ,为合理用药提供依据。方法　在大鼠肝纤维化模型上 ,测定小肠粘膜上皮细胞药物代谢酶、抗氧化酶及膜流动性变化 ,并与急性肝损伤、慢性肝硬化大鼠小肠相关指标进行比较。结果　与正常对照组相比 ,肝纤维化大鼠小肠粘膜上皮细胞药物代谢Ⅰ相酶红霉素N 脱甲基酶 (CYP3A)、7 乙氧异口恶唑O 脱乙基酶 (CYP1A1)和苯胺羟化酶 (CYP2E1)活性分别增加 2 .2 ,0 .6和 0 .3倍 ,而Ⅱ相酶葡糖醛酸转移酶 (UDPGT)和α 、π 谷胱甘肽S 转移酶 (GST)活性则分别减少 15 % ,4 3%和 5 7% ,同时膜脂质过氧化产物增加 ,抗氧化酶活性减弱 ,膜流动性降低。急性肝损伤时 ,上述指标无明显变化 ,而肝硬化时上述指标与肝纤维化组变化一致 ,并进一步增强。结论肝纤维化可影响小肠粘膜上皮细胞药物代谢功能 ,使Ⅰ相氧化功能增强 ,Ⅱ相结合反应减弱。小肠抗氧化功能降低可能与Ⅰ相氧化代谢增强有关。