Increased fetal colonic muscle contractility following glucocorticoid and thyroxine therapy: implications for meconium passage.

Abstract

The incidence of meconium-stained amniotic fluid increases with advanced gestational age and fetal stress, and meconium passage is likely dependent on fetal colonic muscle function. Antenatal hormone exposure improves fetal pulmonary and cardiovascular function. We hypothesized that in utero exposure to steroid or thyroid hormones effect an increase in fetal distal colonic muscle contractility. In a randomized controlled study 126-day (term 145 days) ovine fetuses were treated with a single ultrasound-guided intramuscular injection of 0.5 mg/kg betamethasone (n = 5), betamethasone plus 60 micrograms/kg thyroxine (n = 5), or saline (n = 7). After 48 h, fetuses (128 days) were delivered, distal colon segments were removed, and peak tension responses to bethanechol (10(-8) to 10(-3) M) characterized in vitro. Peak muscle tensions were significantly greater in fetuses exposed to combined betamethasone and thyroxine therapy (989 +/- 190 g/cm2) than in saline-treated animals (509 +/- 91 g/cm2). There was difference in the maximum tension response between betamethasone alone (559 +/- 75 g/cm2) and the saline animals. The bethanechol ED50 values (2.1 +/- 0.5 x 10(-5) M) were not different among the three groups. Antenatal fetal betamethasone and thyroid hormone treatment increases fetal colonic muscle contractility. We speculate that endogenous or exogenous fetal maturational agents may facilitate the passage of meconium.