Abstract
Introduction: High oxygen concentrations have been identified as one factor contributing to the pathogenesis of the retinopathia of prematurity, chronic lung disease of the preterm infant and preterm brain injury. Preterm infants also show short- and long-term alterations of the endocrine system. If hyperoxia is one pathogenetic factor has not been investigated yet. With regard to the high prevalence of neurodevelopmental impairments in preterm infants, the hypothalamus-pituitary-thyroid (HPT) axis, the hypothalamus-pituitary-adrenal (HPA) axis and the hypothalamus-pituitary-somatotropic (HPS) axis are of special interest due to their important role in neurodevelopment.Objective: The aim of this study was to investigate the effect of hyperoxia on the endocrine system in the neonatal rat by analyzing the activities of the HPT, HPA and HPS axes, respectively.Methods: Three-days old Wistar rats were exposed to hyperoxia (oxygen 80%, 48 h). On postnatal day 5 (P5) and P11, transcript levels of thyroid-stimulating hormone (TSH), proopiomelanocortin and growth hormone (GH) were analyzed in pituitary sections by in situ hybridization. Serologic quantification of TSH and thyroxine (T4), adrenocorticotropic hormone and GH were performed by Multiplex analysis and Enzyme-linked Immunosorbent Assay.Results: At P5, significantly lower GH levels were observed in pituitaries (mRNA) and in sera of rats exposed to hyperoxia. Serum TSH was significantly elevated without changes in T4.Conclusion: This is the first study demonstrating transient endocrine alterations following hyperoxia in the neonatal rat making oxygen a possible contributor to the pathogenesis of endocrine alterations seen in preterm infants. Considering the detrimental multi-organ effects of hyperoxia on the immature organism, a rational use of therapeutic oxygen in the treatrnent of preterm infants is of utmost importance.
Highlights
High oxygen concentrations have been identified as one factor contributing to the pathogenesis of the retinopathia of prematurity, chronic lung disease of the preterm infant and preterm brain injury
3-days old Wistar rat pups were exposed to 48 h hyperoxia (HO, oxygen 80% from postnatal day 3 (P3)-P5), while the control group was under normoxic conditions (NO, oxygen 21%)
To investigate the effect of hyperoxia on the activity of the HPT, hypothalamus-pituitary adrenal (HPA) and HPS axes, mRNA expression of thyroid-stimulating hormone (TSH), POMC and Growth hormone (GH) was analyzed in pituitary sections of 5- and 11-days old Wistar rat pups by in situ hybridization (ISH) using digoxigenin-labeled cRNA probes for TSH, POMC and GH (Figure 2A)
Summary
High oxygen concentrations have been identified as one factor contributing to the pathogenesis of the retinopathia of prematurity, chronic lung disease of the preterm infant and preterm brain injury. The transition to the relative hyperoxic extra-uterine environment (PaO2 of 70 mm Hg) exposes a preterm born infant to oxidative stress in a period when the antioxidant system is still immature [1, 2] with detrimental effects on the developing child. Understanding its effects on the immature infant is indispensable It is well-established that high levels of oxygen contribute to the development of the retinopathia of prematurity and chronic lung disease of the preterm infant [4, 5]. In a rat model of hyperoxia-induced brain injury, our study group could repeatedly show that the exposition of rat pups to 2-48 h of hyperoxia (FiO2 80%) leads to transient hypomyelination and long-term cognitive deficits by cellular degeneration, oxidative stress and inflammation [7,8,9,10,11,12,13]
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