Background and Purpose: We tested the hypothesis that intravenous administration of the potent σ-receptor ligand 4-phenyl-1-(4-phenylbutyl) piperidine (PPBP) during transient focal ischemia would decrease postischemic brain infarction volume in rats. Methods: Rats underwent intravascular focal ischemia for 2 hours followed by 22 hours of reperfusion. Halothane anesthesia was used only during initiation and cessation of ischemia. Rats received saline (n=10) or 1 μmol/kg per hour PPBP (n=10) by continuous intravenous infusion starting 1 hour after the initiation of ischemia and continuing through 22 hours of reperfusion. Results: There was no difference between groups in blood pressure, arterial blood gas values, and body temperature. Triphenyltetrazolium-determined infarction volume of ipsilateral cerebral cortex (saline, 39±6%; PPBP, 21±7% of ipsilateral hemisphere; mean±SEM) and striatum (saline, 68±6% PPBP, 33±8% of ipsilateral striatum) was smaller in rats treated with PPBP than in rats treated with saline. Conclusions: These data indicate that σ-receptors may play an important role in the mechanism of injury both in cortex and striatum after 2 hours of transient focal ischemia in rats. Because PPBP afforded protection when administered at the end of ischemia and during reperfusion, σ-receptors may influence the progression of injury in ischemic border regions.
- cerebral ischemia, focal
- neuronal damage
- receptors, sigma
ASJC Scopus subject areas
- Clinical Neurology
- Cardiology and Cardiovascular Medicine
- Advanced and Specialized Nursing