Meeting Abstract
When a mother is set to give birth prematurely, she is often given glucocorticoids to accelerate the development of her fetus’ lungs. Despite the steroids’ known effect on lung development, little is known about the effects on ventilatory muscles. We hypothesize that exposure to prenatal steroids accelerates the development of these muscles. Thus, the breathing muscles of fetuses exposed to these steroids will have fiber-type profiles and enzyme activities more similar to those of 1-day-old neonatal muscles than the muscles of control fetuses. Pregnant guinea pigs were injected with either betamethasone (0.5 mg/kg body weight – treated) or sterile water (control) at 65%, 75%, and 85% gestation, and samples of the fetal rectus thoracis (RT) muscle were collected. Sections of the treated and control RTs were cut with a cryostat and stained for their reaction to myosin heavy chain antibodies. The antibody A4951 was used to stain for type I, slow-twitch fibers, and the antibody 2F7 was used to stain for type IIA, fast-twitch oxidative glycolytic fibers. Using ImageJ software, the diameter and density of staining for 2F7 was measured for the fast-twitch fibers. To determine the glycolytic and oxidative capacities of fetal, neonatal (1-day-old), and adult RT, lactate dehydrogenase (LDH) and citrate synthase (CS) activities were measured. The LDH and CS data will hopefully allow us to draw a conclusion about enzyme activity throughout development. If the treated fetal and neonatal data are similar, it would support the hypothesis that prenatal steroids accelerate fetal breathing muscle development. Thus, premature infants exposed to prenatal steroids will be able to ventilate their lungs just as well as full term infants.
