Abstract

Objective. To determine the correlation between maternal bile acid (BA) level and fetal pulmonary surfactant in rats and study the effects of BA on fetal lung in rat model of intrahepatic cholestasis of pregnancy. Methods. Forty pregnant rats were treated with (A) 5.5 mg/kg BA, (B) 1.4 mg/kg BA, and (C) 1 ml physiological saline. Levels of total bile acid (TBA), ALT, AST, TBIL, DBIL, and SP-A were determined and the lungs of fetal rats were analyzed for pathological changes. Results. Groups A and B intervened with BA showed significant higher level of TBA in both maternal and fetal serum, more mortality rate of fetal rats, more concentration of SP-A in fetal serum, and wider alveolus mesenchyme of fetal rats than the control Group C. Higher level of BA associated with increased fetal risk and lower numerical density of mitochondria in type II alveolar epithelial cells. The levels of TBA in maternal serum were found to have significant positive correlation with those in fetal serum and SP-A level but negatively with the area of alveolus and the numerical density of lamellar body. Conclusions. The TBA level in maternal serum showed significant association with lung pathological changes in fetal rats.

Highlights

  • Intrahepatic cholestasis of pregnancy (ICP) is liver disease which could lead to premature birth, fetal distress and neonatal asphyxia, and increasing risk of fetal morbidity and mortality [1]

  • Our animal studies showed that there is no significant difference in the concentration of total bile acid (TBA), ALT, AST, total bilirubin (TBIL), and direct bilirubin (DBIL)

  • Previous studies have showed that high concentration of bile acid gathered in alveolus cleaning solution in ICP neonates [22], but the incidence of ICP in neonatus had no direct correlation with bile acid concentration in amniotic fluid, while it had close relationship with high bile acid level in fetal blood [2, 23]

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Summary

Introduction

Intrahepatic cholestasis of pregnancy (ICP) is liver disease which could lead to premature birth, fetal distress and neonatal asphyxia, and increasing risk of fetal morbidity and mortality [1]. The best biomarker for diagnosis and follow-up of ICP is up to knowing percentage levels of bile acids (taurocholic and glycocholic acids) over 40% with TBA ≥14 mmol/L. Howard and Murphy found that fetal serum TBA was higher than that of the maternal level during late stage of normal pregnancy [4]. Bile acid is transferred from fetus to mother through fetus circulation, and mother exhausted the exceeding bile acid out of the body with normal liver and gall system. While ICP occurs, high bile acid level in maternal blood made damage to placental transport, leading to bile acid deposition in fetal body [5]

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