ABSTRACf. Developmental changes in the myocardial contractile system were evaluated in the fetus at 18, 21, and 28 days of gestation (full term 31 days) and in 3-to 5-day-old newborn rabbits. Mechanical function was studied using the isolated arterially perfused heart. Perfusion with ryanodine (10-5 M), an inhibitor of Ca release from the sarcoplasmic reticulum, decreased contractile force and increased the time to peak tension in the 28-day fetus and newborn but these changes were minimal in the 18-and 21-day fetus. Postextrasystolic potentiation, which is thought to be caused by Ca release from the sarcoplasmic reticulum, was observed in the 28-day fetus and the newborn, but was not significant in the 18-and 2l-day fetus . An ultrastructural study showed poorly developed sarcoplasmic reticulum and myofibrils in the 18-and 21-day fetus. Although the maximum developed tension observed at high extracellular calcium increased with development, the relative value of developed tension at various extracellular calcium was similar in the three fetal groups and only in the newborn the extracellular calcium-developed tension curve shifted to the right. Myofibrillar yield increased with development but sensitivity of myofibrillar ATPase activity to Ca was similar in the fetus and newborn. These data suggest that 1) the sarcoplasmic reticulum does not function significantly in the 18-and 21-day fetus, 2) although sarcoplasmic reticulum starts to function at late gestation, it does not cause significant changes in intracellular calcium in the fetal period, 3) myocardial contractility remains similar in the fetus from the 18th to 28th day of gestation and major changes in contractility occur after birth. tPediatr Res 22: 201-207, 1987) Abbreviations DT, developed tension +dT/dt(max), maximal rate of tension development TPT, time to peak tension IhRT, half relaxation time PES, paired electric stimulation RT, resting tension ICa)o, extracellular calciumIn the adult myocardium, a relatively small Ca influ x across the sarcolemma induces the subsequent release of greater Received November 3,1986; accepted March 27, 1987. Correspondence Toshio Nakanishi, M.D., Pediatric Cardiology, Heart Institut e of Japan , Tokyo Women's Medical College, 10 Kawadacho, Shinjuku , Tokyo, Japan .Supported by Research Grant 59480241 and 59570411 from the Japan ese Ministry of Education, Science, and Culture and by a grant-in-aid from the Japan Research Promotion Society for Cardiovascular Diseases. amounts of Ca from the sarcoplasmic reticulum, which then activates the myofilaments (I ). The study of Nakanishi and Jarmakani (2) suggeststhat the role of the sarcoplasmic reticulum in cardiac contraction in the newborn and near-term fetus is less than in the adult. Furthermore, several investigators (3-10) have shown that the neonatal myocardium develops less force than the adult myocardium and myofibrillar and sarcoplasmic reticulum contents increase with development. However, these studies were performed using neonatal or near-term fetal an imal...