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Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures
Published on: November 2, 2015
Multiple-organ effect of normobaric hyperoxia in neonatal rats
Dan Torbati1, Gim H Tan, Stanley Smith
1Division of Critical Care Medicine, Miami Children's Hospital, Miami FL 33155, USA. dan.torbati@mch.com
Journal of Critical Care
|April 18, 2006
Summary
Prolonged exposure to normobaric hyperoxia (NH) in neonatal rats alters blood cell counts and causes lung damage. This oxygen toxicity also affects kidney and intestinal tissues, suggesting systemic effects beyond the lungs.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Toxicology
Background:
- Prolonged normobaric hyperoxia (NH) is known to activate and sequester leukocytes in the lungs.
- The impact of NH on extrapulmonary organs and blood cell profiles remains under-investigated.
Purpose of the Study:
- To investigate simultaneous changes in blood cell profiles and pulmonary, renal, and intestinal histology during NH and after weaning.
- To determine if NH-induced leukocyte changes affect organs beyond the lungs.
Main Methods:
- Neonatal rats were exposed to NH (FiO2 >0.98) or normoxia for 2-4 days.
- Blood was collected for differential white blood cell analysis.
- Lung, ileum, and kidney tissues were evaluated histologically.
Main Results:
- Both NH and weaning increased neutrophil counts; lymphocytes increased post-weaning.
- NH induced mild renal tubular damage and inflammation.
- Intestinal vasodilation and vascularization significantly increased after weaning from NH, coinciding with pulmonary oxygen toxicity.
Conclusions:
- Pulmonary oxygen toxicity in neonatal rats is linked to altered leukocyte counts and kidney/ileum histology.
- NH may impact peripheral organs independently of lung pathology, possibly via leukocyte activation or direct effects.