Effects of tirilazad mesylate on postischemic brain lipid peroxidation and recovery of extracellular calcium in gerbils
| Autor: | Edward D. Hall, K E Pazara, Braughler Jm |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
Lipid Peroxides medicine.medical_specialty medicine.medical_treatment Ischemia chemistry.chemical_element Calcium Gerbil Calcium in biology Lipid peroxidation chemistry.chemical_compound Internal medicine medicine Extracellular Animals Vitamin E Pregnatrienes Advanced and Specialized Nursing business.industry Brain medicine.disease Kinetics Endocrinology Blood pressure chemistry Ischemic Attack Transient Anesthesia Reperfusion Lipid Peroxidation Neurology (clinical) Gerbillinae Cardiology and Cardiovascular Medicine business |
| Zdroj: | Stroke. 22:361-366 |
| ISSN: | 1524-4628 0039-2499 |
| DOI: | 10.1161/01.str.22.3.361 |
| Popis: | We describe the effects of the 21-aminosteroid tirilazad mesylate (U-74006F) on postischemic lipid peroxidation (depletion of brain vitamin E) and cortical extracellular calcium recovery in gerbils subjected to 3 hours of unilateral carotid artery occlusion. Male gerbils were treated with either 0.2 ml vehicle (0.05N HCl) or 10 mg/kg i.p. U-74006F 10 minutes before the induction of ischemia and again immediately after the initiation of reperfusion. In the first series of experiments, the brain concentration of vitamin E, which was unaffected by ischemia without reperfusion, was decreased after 2 hours of reperfusion by an average of 60% in vehicle-treated animals compared with sham-operated animals; in the U-74006F-treated gerbils, the 2-hour postischemic vitamin E loss was only 27% (p less than 0.002 different from vehicle-treated animals). In the second series, unilateral carotid artery occlusion produced a decrease in the cortical extracellular calcium concentration from 1.05 mM before ischemia to 0.11 mM by the end of the ischemic episode in both vehicle- and U-74006F-treated gerbils. After 2 hours of reperfusion, the calcium concentration had recovered to only 0.22 mM in the vehicle-treated animals compared with 0.56 mM in the U-74006F-treated group (p less than 0.01). Cortical blood flow, mean arterial blood pressure, and blood gases did not differ significantly between the two treatment groups. Administration of only the immediate postreperfusion dose (i.e., no pretreatment) also significantly improved the recovery of cortical extracellular calcium. The results indicate that U-74006F inhibits postischemic lipid peroxidation as assessed by the preservation of brain vitamin E and that, secondary to this membrane-protective effect, the processes responsible for the reversal of ischemia-triggered intracellular calcium accumulation are preserved. |
| Databáze: | OpenAIRE |
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