Glucocorticoids, hyperinsulinemia, and fetal lung maturation
| Autor: | Jeanne C. Beck, Wayne Mitzner, Peter A. Lee, William T. London, John W.C. Johnson, D. L. Sly |
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| Rok vydání: | 1981 |
| Předmět: |
Male
medicine.medical_specialty Amniotic fluid medicine.medical_treatment Betamethasone chemistry.chemical_compound Fetal Organ Maturity Pregnancy Internal medicine Phosphatidylcholine Hyperinsulinemia Medicine Animals Insulin Lung volumes Lung Fetus business.industry Obstetrics and Gynecology respiratory system medicine.disease Amniotic Fluid Fetal Blood Macaca mulatta respiratory tract diseases Sphingomyelins Pulmonary Alveoli Endocrinology medicine.anatomical_structure Glucose chemistry Phosphatidylcholines Female business medicine.drug |
| Zdroj: | American journal of obstetrics and gynecology. 139(4) |
| ISSN: | 0002-9378 |
| Popis: | Glucocorticoids are reported to accelerate fetal lung development, whereas insulin is alleged to interfere with this effect of glucocorticoids. A paradox exists, however, in that glucocorticoids also induce hyperinsulinemia. The purpose of this study was to explore the interrelationships of betamethasone, hyperinsulinemia, and hyperglycemia to fetal lung maturation. In this rhesus preparation, maternal betamethasone administration produced an alarming increase in maternal and fetal plasma insulin values. A significant increase in total lung volumes also occurred, but lung surfactant properties (as measured by amniotic fluid lecithin/sphingomyelin concentrations, lung alveolar deflation stability, and lung phosphatidylcholine concentrations) remained unchanged. These findings are consistent with the following hypotheses: (1) Betamethasone-induced hyperinsulinemia impairs acceleration of surfactant production but does not negate increases in maximum lung volume; (2) betamethasone-induced increases in maximum lung volume occur through mechanisms other than alveolar surfactant alterations. |
| Databáze: | OpenAIRE |
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