Effect of Resuscitation with High Concentration Oxygen on a Rat Model of Neonatal Hypoxic-Ischemic Brain Injury.
- Author:
Dong Seok LEE
1
;
Su Hee KWAK
;
Heng Mi KIM
;
Yoon Kyung SOHN
Author Information
1. Department of Pediatrics, College of Medicine, College of Medicine, Kyungpook University, Taegu, Korea. hmkim@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Hypoxia;
Ischemia;
Newborn rat;
TUNEL;
Hyperoxia;
Resuscitation
- MeSH:
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*
- From:Journal of the Korean Pediatric Society
2001;44(11):1278-1288
- CountryRepublic of Korea
- Language:Korean
-
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.
