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Permanent link (DOI): https://doi.org/10.7939/R3VX4F

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The Effect of Hypoglycemia on the Functional and Pathological Outcome of the Newborn Rat Open Access

Descriptions

Other title
Subject/Keyword
Hypoglycemia
Newborn
Neurology
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Karimi Pour, Alireza
Supervisor and department
Yager, Jerome Y. (Pediatrics)
Examining committee member and department
Hanstock, Chris (Biomedical Engineering)
Thébaud, Bernard (Pediatrics)
Cheung, Po-Yin (Pediatrics)
Department
Centre for Neuroscience
Specialization

Date accepted
2010-01-05T17:25:58Z
Graduation date
2010-06
Degree
MASTER OF SCIENCE
Degree level
Master's
Abstract
Controversy remains about the contribution of hypoglycemia to brain damage in the newborn. Therefore, the objective of this study was to determine the effects of isolated hypoglycemia on damage to the immature rat brain. Seven-day-old rats, equivalent to a late preterm human newborn, were placed in either Sham or hypoglycemic groups. Hypoglycemia was induced by insulin infusion for variable periods of time. Outcomes were assessed by behavioral, neurochemical and neuropathologic determination. Rats were categorized as having mild, moderate, or severe hypoglycemia. Behavioral tests revealed no abnormality in hypoglycemic animals. Floro-JadeB showed significant damage in the thalamic reticular nucleus (TRN) of the severe hypoglycemic animals at PD9. However, neuronal (Neu-N), astrocytic (GFAP), and myelin (MBP) staining at PD21 showed no brain injury. There was a significant rise in aspartate and arginine, and drop in glutamine and alanine of hypoglycemic brains. Oxidative stress markers were also increased in hypoglycemic brains. We conclude that isolated prolonged severe hypoglycemia caused a transient, region specific increase in neuronal cell death within the TRN. Though transient in nature, the associated neurochemical alterations warrant further research to determine if more subtle long-term effects may result.
Language
English
DOI
doi:10.7939/R3VX4F
Rights
License granted by Alireza Karimi Pour (alireza.karimipour@gmail.com) on 2009-12-22T01:50:06Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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