Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intrahepatic cholestasis of pregnancy (ICP) is a rare complication of late pregnancy associated with a high rate of premature delivery, antepartum fetal death and fetal hypoxia. Since the principal biochemical feature of ICP is a marked elevation of maternal serum bile acid levels, a role of these substances in the pathophysiology of fetal complications has been suggested. In this study, the effect of bile acids on isolated human placental chorionic veins is described. High concentrations of bile acids, especially cholic acid, have a dose-dependent vasoconstrictive effect, which suggests that these substances could exert a detrimental effect on the fetus by increasing the resistance in chorionic veins through a vasospasm of the placental chorionic surface. An abrupt reduction of the oxygenated blood flow at the level of the placental chorionic plate may cause an acute impairment of the fetal perfusion and oxygenation, leading to fetal asphyxia. This is the first report that provides experimental evidence of the possible role of bile acids in those mechanisms that trigger fetal asphyxia in pregnancies complicated by ICP.
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PMID:Vasoconstrictive effect of bile acids on isolated human placental chorionic veins. 177 76

Intrahepatic cholestasis of pregnancy(ICP) is complicated by acute placental-fetal hypoxia. Corticotropin-releasing hormone(CRH) and urocortin(UCN) are vasodilatory regulators of blood flow in the placenta. An ethinylestradiol(EE)-induced cholestasis rat model was reproduced and serum/placental CRH/UCN were detected during 14-21days of gestation(DG). Maternal serum or placental CRH/UCN levels in the control rats were relatively consistent during 14-21DG. Serum CRH was reduced in the EE-treated rats compared with the control rats at 21DG. Regarding serum UCN, we observed a decrease at 17DG as well as an increase at 21DG in the EE-treated rats compared with the controls. Moreover, we observed a noticeable reduction of placental CRH/UCN expression at 17 or 19DG in the EE-treated rats compared with the control rats. The serum bile acids levels exhibited an inverse correlation with placental CRH/UCN expression. EE-induced cholestasis rats might serve as a good model to further investigate the pathological mechanism underlying CRH/UCN dysregulation in ICP.
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PMID:Dynamic expression of corticotropin-releasing hormone and urocortin in estrogen induced-cholestasis pregnant rat. 2749 20