INFLUENCE OF AMINOPHYLLINE AND CYCLIC-AMP ON GLYCOGEN-METABOLISM IN FETAL RAT LUNG IN ORGAN-CULTURE

The glycogen content of fetal rat lung declines coincident with increased pulmonary phospholipid synthesis. Aminophylline, a methylxanthine cyclic adenosine 3ʹ,5ʹ monophosphate (AMP) phosphodiesterase inhibitor, and cyclic AMP augment fetal lung phospholipid synthesis. Because lung glycogen breakdown may contribute to pulmonary phospholipid synthesis, the effects of aminophylline and cyclic AMP on glycogen metabolism were studied in explants of 19 day fetal rat lung in organ culture. Treatment with aminophylline or dibutyryl cyclic AMP for 24 hr, resulted in a 25% (P < 0.025) and 75% (P < 0.001) decrease, respectively, in the glycogen conent of the explants. Glycogen synthase I activity was reduced by 32% in aminophylline treated cultures (P < 0.025) and 25% in cyclic AMP treated cultures (P < 0.025). The percent of total synthase in the active form was significantly reduced in all treated cultures. Neither aminophylline nor cyclic AMP treatment resulted in significant changes in glycogen phosphorylase a or total phosphorylase activity. Speculation: The enhancement of fetal pulmonary surfactant by cyclic AMP and aminophylline may be due, in part, to the effects of these agents on lung carbohydrate metabolism. © 1979 International Pediatric Research Foundation, Inc.