Abstract
The ability of the nonglucocorticoid 21-aminosteroid U74006F, a potent inhibitor of iron-dependent lipid peroxidation, to antagonize acute progressive cerebral hypoperfusion following experimental subarachnoid hemorrhage (SAH) was examined in chloralose-anesthetized cats. The SAH was produced by injection of 0.5 ml/kg of unheparinized autologous blood into the cisterna magna after prior withdrawal of an equivalent volume of cerebrospinal fluid. In untreated animals the SAH caused a progressive decline in caudate nuclear blood flow (CNBF) (-51.4% by 3 h) and an increase in intracranial pressure (ICP) (+18.5 mm Hg by 3 h). In comparison, in cats that received a 1 mg/kg iv dose of U74006F at 30 min after SAH, there was a complete prevention of the fall in CNBF and a significant attenuation of the rise in ICP. Furthermore, the drug reduced a concomitant fall in the mean arterial blood pressure and cerebral perfusion pressure. While not as effective as the 1 mg/kg dose, a 0.1 mg/kg dose also significantly attenuated the post-SAH fall in CNBF. These results supporte a role of lipid peroxidation in the acute pathophysiology of SAH and suggest that U74006F may be useful in the early treatment of this disorder.
Original language | English |
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Pages (from-to) | 244-248 |
Number of pages | 5 |
Journal | Experimental Neurology |
Volume | 102 |
Issue number | 2 |
DOIs | |
State | Published - Nov 1988 |
Bibliographical note
Copyright:Copyright 2014 Elsevier B.V., All rights reserved.
ASJC Scopus subject areas
- Neurology
- Developmental Neuroscience