The Effect of Tirizad Mesylate on Brain Lipid Peroxidation Following Cerebral Ischemia in Gerbils
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Authors
Hathaway, Darren P.
Issue Date
1991
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
Due to the vast clinical potential of the novel 21-
aminosteroid analogs to reduce cerebral damage following an
ischemIc event, a greater knowledge of their mechanism of action is
desirable. This study was designed to elucidate the role of lipid
peroxidation in the destruction of cerebral tissue and to determine
if the cytoprotective action of the 21-aminosteroids was through
inhibition of lipid peroxidation. Computer assisted image analysis
was used to quantitate the extent of lipid peroxidation and tissue
death following 3 hours of unilateral carotid occlusion (UCO) in
the Mongolian gerbil. A dihydroxydiphenylamine chromogenic
substrate was used in a novel histochemical procedure to stain
lipid peroxides in coronal slices of ischemic brain. At 24 hours
of reperfusion, lipid peroxides were present in 30% of the brain
slice of vehicle treated animals. Peroxides were localized
predominantly in the cerebral cortex of the ischemic hemisphere.
Similarly, 2, 3, 5-triphenyl tetrazolium chloride (TTC)
histochemistry showed that 35% of the coronal section was damaged
by the ischemic event. Treatment with Tirilazad Mesylate (U-
74006F) immediately before and immediately after a 3 hour UCO had
no statistically significant effect on the extent of lipid
peroxidation in the ischemic hemisphere. These data suggest that
the reported cytoprotective potential of U-74006F is mediated
through mechanisms other than via direct chemical inhibition of
lipid peroxidation.
Description
v, 37 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.