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Published on: November 20, 2015
Prenatal dexamethasone treatment improves survival of newborn rats during prolonged high O2 exposure
1Pulmonary Research Center, University of Miami School of Medicine, Florida 33101.
Insights
Prenatal dexamethasone (DEX) treatment enhances newborn rat survival in high oxygen by boosting lung antioxidant enzymes (AOE). This prenatal DEX exposure improved tolerance to hyperoxia, reducing lung injury and increasing survival rates.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Pharmacology
Background:
- Prenatal dexamethasone (DEX) accelerates fetal lung maturation, including surfactant and antioxidant enzyme (AOE) systems.
- AOE systems are crucial for defending the lungs against hyperoxia (high oxygen).
Purpose of the Study:
- To investigate if prenatal DEX treatment improves the ability of newborn rats to tolerate prolonged exposure to hyperoxia.
- To assess the impact of prenatal DEX on lung injury markers and AOE activity under hyperoxic conditions.
Main Methods:
- Term newborn rats were exposed to hyperoxia (>95% O2) for up to 14 days.
- Survival rates, lung wet/dry weight ratios, pulmonary edema, and lung conjugated dienes were compared between prenatal DEX-treated and control groups.
- Pulmonary AOE activities (superoxide dismutase, catalase, glutathione peroxidase) were measured at various time points.
Main Results:
- Prenatal DEX significantly increased survival rates in hyperoxia at both 7 and 14 days compared to controls (97% vs 71% at 7d; 55% vs 31% at 14d).
- DEX-treated pups showed reduced lung wet/dry weight ratios, less pulmonary edema, and lower conjugated dienes.
- Prenatal DEX led to significantly elevated AOE activities by day 2 of hyperoxia, with consistently higher levels observed throughout the 7-day period.
Conclusions:
- Prenatal DEX treatment offers a protective effect against hyperoxia-induced lung injury in newborn rats.
- This protection is associated with enhanced pulmonary antioxidant enzyme activity, suggesting a strategy to improve neonatal lung defense.
- The findings support the role of prenatal DEX in bolstering the lung's capacity to handle oxidative stress in the neonatal period.
Abstract:
Prenatal dexamethasone (DEX) treatment is known to accelerate the maturation of both the surfactant system and the fetal lung antioxidant enzyme (AOE) system (Frank L, Lewis P, Sosenko IRS: Pediatrics 75:569-574, 1985). Because of this stimulatory effect of prenatal DEX on the normal late gestational development of the AOE system, we questioned whether this treatment might have a salutary effect on the ability of the newborn rat to tolerate early and prolonged exposure to hyperoxia, inasmuch as the AOE are the primary lung defensive system against high O2 challenge. In nine experiments with term newborn rats in greater than 95% O2, the composite percentage of survival was significantly greater in the prenatal DEX pups at all time periods in hyperoxia from 7 d [control pups, 67 of 94 (71%); prenatal DEX, 96 of 99 (97%)] to 14 d [controls, 10 of 32 (31%); prenatal DEX, 18 of 33 (55%)] (p less than 0.01). In addition to survival per se, the prenatal DEX pups showed significantly decreased lung wet weight/dry weight ratios, pathologic evidence of pulmonary edema, and lung conjugated dienes versus the O2 control newborn group. Of the many comparative parameters examined, the major difference found between the two groups was in the pulmonary AOE responses to hyperoxia. By 2 d in hyperoxia, the prenatal DEX rat pups showed significantly elevated superoxide dismutase, catalase, and glutathione peroxidase activities compared to air control pups, and at 4 and 7 d in O2 the AOE levels were consistently greater in the DEX group than the AOE responses in the control O2 pups.(ABSTRACT TRUNCATED AT 250 WORDS)
