Key result
Treatment with acetylsalicylic acid significantly reduced brain perfusion deficits 1 hour, but not 3 hours, after middle cerebral artery occlusion in an embolic stroke model in rats.
Why the study?
Does acetylsalicylic acid reduce perfusion deficits in a rat embolic model of stroke?
Does acetylsalicylic acid reduce perfusion deficits in a rat embolic model of stroke?
Acetylsalicylic acid reduces early perfusion deficits in a rat model of embolic stroke, suggesting its mechanism involves reopening cerebral microvessels.
ASA may confer time-sensitive microvascular benefit in rodent embolic stroke; leaves open translation to human therapy.
Acetylsalicylic acid (ASA) is an antiplatelet agent which has been used in treatment and prevention of stroke in humans. In the present study, the effects of ASA on perfusion deficits in the brain have been studied in an embolic model of stroke. Data showed that perfusion deficits were observed in all rats sacrificed immediately after middle cerebral artery (MCA) occlusion. Treatment with ASA significantly reduced perfusion deficits 1 h but not 3 h after the MCA occlusion. These findings thus support that ASA is useful agent in treatment and prevention of stroke, and show that its mechanism of action is likely through the reopening of cerebral microvessels.
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Uddin et al. (2003) studied Embolic model of stroke. Acetylsalicylic acid (ASA) was evaluated on Perfusion deficits in the brain. Treatment with acetylsalicylic acid significantly reduced brain perfusion deficits 1 hour, but not 3 hours, after middle cerebral artery occlusion in an embolic stroke model in rats.
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