Meeting Abstract
Glucocorticoids are commonly delivered to women who are at risk of premature birth in order to stimulate lung development in their infants. Although studies have shown an increase in lung development in steroid-treated babies, effects of glucocorticoids on ventilatory muscle development are not widely known. Previous studies in our laboratory found no change in the activity of an oxidative enzyme, citrate synthase (CS), in prenatal steroid-treated fetal guinea pig diaphragms. However, we found a decrease in the myoglobin concentration and fatigue resistance of these muscles in comparison to control fetal diaphragms. In order to determine if these changes in the morphology of the fetal diaphragm (DIA) represent acceleration of muscle development due to prenatal steroid exposure, a morphological profile of the neonatal muscle must be developed for comparison. The activity of CS was determined with enzyme kinetic assays on DIA samples of one-day-old guinea pigs. In addition, the fatigue resistance of neonatal diaphragms was measured using a standard two-minute fatigue test. Finally, SDS-PAGE was performed on neonatal DIA samples to determine the myoglobin concentration. The neonatal CS activity, fatigue resistance, and myoglobin concentration will be compared to prenatal steroid-treated fetal DIA characteristics using ANOVAs. If the steroid-treated fetal DIAs are found to not differ significantly from the neonatal DIAs in these characteristics, then the hypothesis that prenatal steroids accelerate breathing muscle development will be supported. And, if it is supported, treated babies would be better able to withstand ventilatory challenges when compared to their untreated counterparts due to an increase in oxidative capacity.
