J Korean Pediatr Soc.  2001 Nov;44(11):1278-1288.

Effect of Resuscitation with High Concentration Oxygen on a Rat Model of Neonatal Hypoxic-Ischemic Brain Injury

Affiliations
  • 1Department of Pediatrics, College of Medicine, College of Medicine, Kyungpook University, Taegu, Korea. hmkim@knu.ac.kr
  • 2Dongguk University, Kyongju, Department of Pediatrics, College of Medicine, Kyungpook University, Taegu, Korea.
  • 3Department of Pathology, College of Medicine, Kyungpook University, Taegu, Korea.

Abstract

PURPOSE: This study was undertaken to determine whether any features of apoptosis would occur in the established model of cerebral hypoxia-ischemia in neonatal rats. It was also undertaken to evaluate the effect of post-insult hyperoxia on hypoxic ischemic cerebral injury.
METHODS
Seven-day-old neonatal rats underwent unilateral carotid artery dissection followed by 2 hours of hypoxia. To this end rat pups, allocated into 2 groups, were resuscitated with high concentration O2(>FiO2 95%) or room air for a 1-hour period. All of them were killed at 3 days after the above procedures. Their brains were perfusion fixed and removed to examine tissue damage by light microscope and apoptosis by terminal deoxynucleotidyl transferase mediated dUTP- biotin nick end labeling(TUNEL) reactivity.
RESULTS
The result demonstrates that hypoxia-ischemia model induces tissue damage and TUNEL. Post-insult exposure to high reactivity concentration O2 does not aggravate hypoxic-ischemic cerebral injury 3 days after the insult but increases TUNEL reactivity in injured tissue.
CONCLUSIONS
These findings suggest that many cells die by apoptosis following hypoxia-ischemia in neonatal brain and resuscitation with high concentration O2 seems to provide an adverse effect over a brain injury by induction of apoptosis.

Keyword

Hypoxia; Ischemia; Newborn rat; TUNEL; Hyperoxia; Resuscitation

MeSH Terms

Animals
Anoxia
Apoptosis
Biotin
Brain Injuries*
Brain*
Carotid Arteries
DNA Nucleotidylexotransferase
Hyperoxia
Hypoxia-Ischemia, Brain
In Situ Nick-End Labeling
Ischemia
Models, Animal*
Oxygen*
Perfusion
Rats*
Resuscitation*
Biotin
DNA Nucleotidylexotransferase
Oxygen
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