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The Effect of Hypoxia on Traumatic Head Injury in Rats: Alterations in Neurologic Function, Brain Edema, and Cerebral Blood Flow
Author(s) -
Naoki Ishige,
Lawrence H. Pitts,
I. Berry,
Sara Carlson,
Merry Nishimura,
Michael E. Moseley,
Philip R. Weinstein
Publication year - 1987
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.1987.131
Subject(s) - hypoxia (environmental) , medicine , cerebral blood flow , traumatic brain injury , anesthesia , edema , head injury , pathology , magnetic resonance imaging , cerebral edema , brain damage , cerebral hypoxia , cerebral perfusion pressure , perfusion , ischemia , surgery , radiology , chemistry , organic chemistry , psychiatry , oxygen
We evaluated the effects of early posttraumatic hypoxia on neurologic function, magnetic resonance images (MRI), brain tissue specific gravities, and cerebral blood flow (CBF) in head-injured rats. By itself, an hypoxic insult (P a O 2 40 mm Hg for 30 min) had little effect on any measure of cerebral function. After temporal fluid-percussion impact injury, however, hypoxia significantly increased morbidity. Of rats subjected to impact (4.9 ± 0.3 atm) plus hypoxia, 71% had motor weakness contralateral to the impact side 24 h after injury, while only 29% of rats subjected to impact alone had demonstrable weakness (p < 0.05). Lesions observed on MR images 24 h after injury were restricted to the impact site in rats with impact injury alone, but extensive areas with longer T1 relaxation times were observed throughout the ipsilateral cortex in rats with impact injury and hypoxic insult. Brain tissue specific gravity measurements indicated that much more widespread and severe edema developed in rats with impact injury and hypoxia. [ 14 C]Iodoantipyrine autoradiography performed 24 h after injury showed that there was extensive hypoperfusion of the entire ipsilateral cortex in rats with impact injury and hypoxia. These results show that large areas of impact-injured brain are extremely vulnerable to secondary insults that can irreparably damage neural tissue, and provide experimental evidence for the observed adverse effects of hypoxia on outcome after human head injury.

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