[Study on the functional development of the sympathetic nervous system of fetal heart in rats]

The drugs acting on the autonomic nervous system were administered intravenously to dams or intraperitoneally to the 20-day-old fetuses maintained by umbilical and placental circulation. The fetal heart rates were accelerated by the administration of isoproterenol, epinephrine, norepinephrine, tyramine and dopamine to fetuses, and they were decelecated by the injection of propranolol and methacholine to fetuses. However, the tachycardia caused by the fetal injection of isoproterenol and the bradycardia by methacholine were inhibited by the pretreatment of propranolol and atropine. The fetal bradycardia and hypoxia caused by the administration of epinephrine under the pretreatment of propranolol to fetuses were inhibited by the injection of alpha-adrenergic receptor blockers such as phentolamine and yohimbine. Furthermore, the tyramine treatment to fetuses produced significant acceleration of the fetal heart rate on day 19-20 of gestation, but not on day 18. These findings suggest that fetal cardiac beta-adrenergic, muscarine-cholinergic receptors and vascular postsynaptic alpha-adrenergic receptor may be sensitive enough to respond to sympathomimetic and sympatholytic drugs, and the fetal cardiac sympathetic innervation between the adrenergic nerve terminal and synapse effector cells may be developed on day 18-19 of gestation.