| ICP is endemic in pregnancy complications, later to clinical characteristic of itching and jaundice. It mainly damages fetal, making wai births increased morbidity and mortality. The etiology is unclear, possibly with female, progesterone, genetic, immune and environmental factors.The toxicity of hydrochloric acid is the hotspot in recent years. The ICP wombs when the fetus premature rupture of membrane, premature birth or intrauterine distress, spontaneous pregnancy amniotic fluid tire dung pollution. Especially it is limited with a fetal growth, unpredictable fetal sudden death, the newborn babies, intracerebral haemorrhage neural system sequela etc. Among them, the unpredictable fetal sudden death having become a clinical doctor’s tricky question and giving huge economic losses to social and personal family. ICP pregnant women in the serum bile acid with bravery, m.p. (cA) increased levels of primarily. Therefore bile acid may be ICP resulting in the fetus and neonatal death culprit. High-dose oral bile acid can make the animals die, and quickly with high bile acid are long-term heart function suppression, lower blood pressure, immune function inhibition and carcinogenic chronic toxicity. This study by detecting ICP neonatal myocardial enzymes CK, calcium protein levels and muscular LDH, and constructs the ICP pregnant mouse model to investigate the fetal rats further research on the mechanism of myocardial injury. This experiment is divided into two parts:Part 1. Gestational intrahepatic cholestasis disorder newborn level compares myocardial enzyme Choose between January 2009 and January 2011 in our antenatal examination and inpatient delivery pregnant women diagnosed with ICP (mild, severe) and normal pregnant women, the various 50 cases of newborns creatine kinase (CK) and lactate dehydrogenase (LDH) two myocardial enzymes to determine. Results: ICP severe group of CK, LDH calcium protein levels and muscular than the control group and mild group increased significantly (P<0.05). Conclusion: ICP patients serum high concentrations of bile acid cause fetal progressive aggravating arrhythmia and sudden death one reason inside the womb.Part 2. Pregnant mice myocardial cell pathological changes to its structure and mitochondrial oxidatie stress mechanism .Experiment with clean level SD rats with male queens female SD rats 1:1 close cage breeding, every day without loss of observation dung disc, Yin Yin bolt wax block off as pregnancy, tethered to the first days, points raised to use. Take progesterone 14 days, SD rats, only 30 high and low estrogen were randomly divided into trial group and control group, each group respectively in hind, only 10 medial subcutaneous injection dose 5.0 (high doses) 2.5 mg/(Kg. d) (low dose) benzoic acid estradiol and 2 ml/(Kg. d) physiological saline, 1 times/d, continuous 5 d, cervical vertebra, taking the death rats dislocated myocardial tissue fetal rats were observed pathological structure change HE dyeing and extraction mitochondrial determination ROS and membrane potential level. Results:①High concentrations of group of fetal rats lower doses groups and normal controls MingXiu since myocardial cell atrophy.②Mitochondria high level on clusters of reactive groups and low concentration is significantly higher than normal control group. And membrane potential level was significantly lower after both. Conclusion: high concentrations of bile acid may occur by inducing myocardial tissue mitochondrial oxidatie stress, so bring into play its promote myocardial cell damage, apoptosis broadened ischemia toxic sex role and speculating that this might be the reason caused by sudden fetal palace. |
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