K. Ichikawa, S. Tazawa, S. Hamano
Oct 8, 1999
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Quality indicators
Journal
Pharmacology
Abstract
The effect of ozagrel, a selective thromboxane A2 (TXA2) synthetase inhibitor, on the obstruction after cerebral ischemia-reperfusion was studied in experimental animal models. The reduced spontaneously locomotor activity and the obstruction of motor coordination were improved by the administration of ozagrel in the conscious cerebral ischemia-reperfusion mouse model. Ozagrel suppressed the decrease in specific gravity of the brain tissue induced by the occlusion-reperfusion in the conscious cerebral ischemia-reperfusion SHR model, and recovered the postischemic decrease in cortical PO2 after middle cerebral artery occlusion-reperfusion in cats. The level of TXB2, a metabolite of TXA2, in the brain increased after the cerebral ischemia-reperfusion, and ozagrel prevented this increase. Additionally, ozagrel also increased the level of 6-keto-PGF1α, a metabolite of prostaglandin I2 (PGI2), in the brain tissue after cerebral ischemia-reperfusion, and the administration of PGI2 improved the reduced spontaneous locomotor activity in the conscious cerebral ischemia-reperfusion mouse model. Our data suggest that ozagrel suppressed the obstruction following cerebral ischemia-reperfusion by preserving the cerebral blood flow via preventing the increase in TXA2 and causing an increase in the PGI2 level.