title: Changes in Brain Swelling and Infarction Volume over Four Days After Hypoxia Ischemia in Neonatal Rats.
abstract: The leading cause of morbidity and mortality in infants is hypoxia-ischemia (HI). The current therapies for HI have limited success, in part due to a lack of understanding of HI pathophysiology and underlying mechanisms. Herein, a neonatal rat model of HI was used to examine the changes in brain swelling and infarct volume over 4 days after HI. Forty-four P10 rat pups were sacrificed at 2, 3, or 4 days post-HI. After sacrifice, the brains were removed, sliced, and stained with TTC (2,3,5-triphenyl-2H-tetrazolium chloride). Images of TTC-stained brains were used for measurement of the ipsilateral hemisphere brain volumes and infarct volumes, calculated using standard equations. The hemispheric brain volumes of HI animals in all groups was lower than that of sham animals and decreased as the post-HI sacrifice time increased. The infarct volume of HI animals was larger than that of sham animals. Infarct volumes tended to decrease over the days post-HI. The change in infarct volume is likely the result of a combination of brain growth and repair mechanisms. However, changes in the hemispheric brain volume may include tissue growth and repair mechanism, so also may be a limitation of the current algorithm used for calculating ipsilateral hemisphere brain volume.
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Devin W
authors.initials: DW
authors.lastname: McBride
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Christine
authors.initials: C
authors.lastname: Jacob
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Desislava
authors.initials: D
authors.lastname: Doycheva
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Brandon J
authors.initials: BJ
authors.lastname: Dixon
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Jay
authors.initials: J
authors.lastname: Malaguit
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Tim
authors.initials: T
authors.lastname: Lekic
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Jiping
authors.initials: J
authors.lastname: Tang
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA. jhzhang@llu.edu.|Department of Neurosurgery, Loma Linda University School of Medicine, Loma Linda, CA, USA. jhzhang@llu.edu.
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000473:pathology*; D001929:Brain Edema / Q000473:pathology*; D020520:Brain Infarction / Q000473:pathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology*; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
keywords: Brain swelling; HI; Hypoxia ischemia; Infarct; Stroke