Related Experiment Videos
Opioids accelerate fetal rat lung maturation in vitro
I H Gewolb1, J O'Brien, R E Slavin
1University of Maryland School of Medicine, Department of Pediatrics, Division of Neonatology, Baltimore, Maryland 21201, USA. igewolb@peds05.ab.umd.edu
American Journal of Respiratory Cell and Molecular Biology
|February 25, 1999
Summary
High-dose opioids accelerate fetal rat lung maturation in vitro, indicated by increased phosphatidylcholine production and cell development. Cocaine did not show similar effects, suggesting indirect mechanisms for reduced respiratory distress syndrome in exposed infants.
Area of Science:
- Perinatology
- Pharmacology
- Developmental Biology
Background:
- Neonatal respiratory distress syndrome (RDS) incidence is lower in infants exposed to maternal heroin and cocaine addiction.
- The direct drug-mediated effects on fetal lung development remain unclear.
Purpose of the Study:
- To investigate the in vitro effects of opioids (heroin, morphine, methadone) and cocaine on fetal rat lung maturation.
Main Methods:
- Fetal rat lung explants (18-20 days) and type II cells were exposed to varying drug concentrations.
- Choline incorporation into phosphatidylcholine (PC) and disaturated PC was measured.
- Morphological analysis of lung explants was performed.
Main Results:
- High-dose opioids (heroin, morphine, methadone) significantly increased choline incorporation into PC.
- Opioid exposure led to a significant increase in type II pneumocytes and lamellar bodies.
- Cocaine did not demonstrate an acceleratory effect on fetal lung maturation parameters in vitro.
Conclusions:
- High-dose opioids accelerate biochemical and morphologic parameters of fetal lung maturation in vitro.
- The lack of in vitro acceleration by cocaine suggests that observed reductions in RDS incidence are likely secondary effects.