妊娠肝内胆汁淤积症胎兔心肌细胞损伤的研究被引量：5

Cardiac myocyte damage in fetus of rabbits with intrahepatic cholestasis pregnant

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摘要目的观察妊娠肝内胆汁淤积症(intrahepatic cholestasis of pregnancy,ICP)胎兔心肌细胞超微结构及细胞凋亡率,检测心肌腺苷三磷酸(ATP)、超氧化物歧化酶(SOD)、丙二醛(MDA)含量。方法16只孕兔,分为ICP组和对照组。ICP组自妊娠第22天,颈后皮下注射苯甲酸雌二醇0.1mg.kg-1.d-1,对照组颈后皮下注射0.9%生理盐水,直至分娩。观察ICP组和对照组胎兔心肌细胞超微结构,检测心肌细胞ATP、SOD、MDA含量及细胞凋亡指数。结果电镜观察见ICP胎兔心肌细胞线粒体轻度肿胀、髓鞘样结构形成,细胞质内糖原颗粒分布减少,对照组超微结构无明显改变。ICP组胎心组织ATP、SOD含量减少,MDA含量和细胞凋亡数明显增多,与对照组相比差异均有统计学意义(P<0.05)。结论ICP胎兔存在心肌细胞损伤。 Objective To investigate ultrastructure and apoptotic rate of fetal cardiac myocytes of rabbits with intrahepatic cholestasis of pregnancy （ICP） and the levels of adenosine triphosphate （ ATP）, superoxide dismutase （SOD） and malondialdehyde （MDA） in the myocardial tissues. Methods Sixteen pregnant rabbits were randomly divided into control group and ICP group. Rabbits in ICP group were subcutaneously injected with benzestrofol at a dose of 0.1 mg · kg^-1· d^-1 and control group with 0.9% saline solution from the 22nd gestation day to delivery day. The levels of ATP, SOD and MDA in myocardial tissues of ICP rabbit fetuses and control fetuses were determined. Ultrastructure and number of apoptosis ceils were observed. Results Compared with controls, the levels of ATP and SOD in ICP rabbit fetuses＇ cardiac myocytes significantly decreased （ P 〈 0.05 ）, while the levels of MDA and the number of apoptosis cells in ICP rabbit fetuses＇ cardiac myocytes significantly increased. Slight swelling, vacuolation and myelinoclasis in mitochondria, and decreased glycogen granules in cytoplasm were observed in ICP rabbit fetuses＇ cardiac myocytes under electron microscope. However, these ultrastructural alteration was not observed in controls. Conclusion The damage of cardiac myocytes does exist in fetuses of rabbits with ICP.

作者冯丽霞李力俞丽丽郑英如郭建新易萍颜耀华

机构地区第三军医大学大坪医院野战外科研究所妇产科

出处《第三军医大学学报》 CAS CSCD 北大核心 2009年第4期334-337,共4页 Journal of Third Military Medical University

关键词肝内胆汁淤积妊娠胎儿心肌细胞 intrahepatic cholestasis pregnancy fetus cardiac myocyte

分类号 R-332 [医药卫生] R542.2 [医药卫生—心血管疾病]

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1Lammert F, Marschall H U, Glantz A, et al. lntrahepatic cholestasis of pregnancy: molecular pathogenesis, diagnosis and management [ J ]. J Hepatol, 2000, 33(6) : 1012 -1021.
2冯丽霞,李力,胡珊,郑英如.孕兔妊娠肝内胆汁淤积症模型的构建[J].第三军医大学学报,2005,27(10):994-996. 被引量：1
3Glantz A, Marschall H U, Mattsson L A. Intrahepatic cholestasis of pregnancy: relationships between bile acid levels and fetal complication rates[J]. Hepatology, 2004, 40(2): 467-474.
4Lee R H, Kwok K M, Ingles S, et al. Pregnancy outcomes during an era of aggressive management for intrahepatic cholestasis of pregnancy [J]. Am J Perinatol, 2008, 25(6) : 341 -345.
5Fickert P, Trauner M, Fuchsbichler A, et al. Cytokeratins as targets for bile acid-induced toxicity[J]. Am J Pathol, 2002, 106(2) : 491 - 499.
6Gumpricht E, Dahl R, Devereaux M W, et al. Beta-carotene prevents bile acid-induced cytotoxicity in the rat hepatocyte : Evidence for an antioxidant and anti-apoptotic role of beta-carotene in vitro [ J ]. Pediatr Res, 2004, 55(5) : 814 -821.
7Palmeira C M, Rolo A P. Mitochondrially-mediated toxicity of bile acids[J]. Toxicology, 2004, 203(1-3): 1 -15.
8Perez M J, Macias R I, Duran C, et al. Oxidative stress and apoptosis in fetal rat liver induced by maternal cholestasis. Protective effect of ursodeoxycholic acid [J]. J Hepatol, 2005, 43 (2) : 324 - 332.
9Perez M J, Macias R I, Matin J J. Maternal cholestasis induces placental oxidative stress and apoptosis. Protective effect of ursodeoxycholic acid[J]. Placenta, 2006, 27( 1 ): 34-41.
10邵勇,姚珍薇,陆杰,李红霞,吴味辛,丁敏.肝内胆汁淤积症孕鼠的胎鼠心率功率谱变化与猝死的关系[J].生物医学工程学杂志,2007,24(6):1215-1219. 被引量：3

二级参考文献19

1常青,王静波,陈勇,史常旭.熊脱氧胆酸、地塞米松、思美泰对抗孕大鼠肝内胆汁淤积症的比较研究[J].第三军医大学学报,2004,26(12):1091-1093. 被引量：10
2王智彪,顾美礼,凌萝达,管必隆,王芷龙,王志刚,熊正爱,冯若.超声波抗早孕的动物实验研究——Ⅲ.超声波对妊娠第7天小鼠的抗孕研究[J].中国超声医学杂志,1995,11(3):201-206. 被引量：10
3Leslie K K,Reznikov L,Simon F R,et al.Estrogens in intrahepatic cholestasis of pregnancy[J].Obstet Gynecol,2000,95(3):372-376.
4Geier A,Dietrich C G,Gerloff T,et al.Regulation of basolateral organic anion transporters in ethinylestradiol-induced cholestasis in the rat[J].Biochim Biophys Acta,2003,1609(1):87-94.
5Zimmermann P,Koskinen J,Vaalamo P,et al.Doppler umbilical artery velocimetry in pregnancies complicated by intrahepatic cholestasis[J].J Parinat Med,1991,19(5):351-355.
6Williamson C,Gorelik J,Eaton B M,et al.The bile acid taurocholate impairs rat cardiomyocyte function:a proposed mechanism for intra-uterine fetal death in obstetric cholestasis[J].Clin Sci (Lond),2001,100(4):363-369.
7Gorelik J,Shevchuk A,de Swiet M,et al.Comparison of the arrhythmogenic effects of tauro- and glycoconjugates of cholic acid in an in vitro study of rat cardiomyocytes[J].BJOG,2004,111(8):867-870.
8Williamson C, Gorelik J, Eaton BM, et al. The bile acid taurochlate impairs rat cardiomyocyte function: a proposed mechanism for intra-uterine fetal death in obstetric cholestasis. Clin Sci, 2001,100(4) : 363.
9Gorelik J, Shevehuk AI, Diakonov I, et al. Dexamethasone and ursodeoxyeholie acid protect against the arrhythmogenie effect of tauroeholate in an in vitro study of rat eardiomyoeytes. Br JObs Gyn, 2003,110 (5) : 467.
10Lehnart SE, Wehrens XH, Laitinen PJ, et al. Sudden death in familial polymorphic ventricular tachycardia associated with calcium release channel (ryanodine receptor) leak. Circulation, 2004,109(25) : 3208.