Protective effect of triflusal and acetylsalicylic acid against arachidonic acid induced cerebrovascular occlusion in anesthetized rats.
Within 60 sec after intracarotid injection of 0.33 mg/kg arachidonic acid, a pronounced attenuation of electrocortical activity, approaching electrocerebral silence, was induced in the ipsilateral hemisphere of anesthetized and heparinized rats. This effect was a consequence of the cerebrovascular occlusion due to platelet aggregates induced by arachidonic acid. This model has been used to evaluate the protective effect of acetylsalicylic acid (ASA) and of triflusal 2 hr after a single oral dose of 50 mg/kg or after 50 mg/kg, for 5 days. Pentylenetetrazol at 10 mg/kg, i.v. exerts a stimulant effect on CNS, and was used as a positive control. ASA and triflusal exhibit a protective effect in about 35% of animals when acutely administered. After chronic treatments (5 days), the effect of triflusal (60% protection) was superior to that of ASA (27% protection) (p less than 0.01).
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids; D001241:Aspirin / Q000627:therapeutic use*; D002561:Cerebrovascular Disorders / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D004569:Electroencephalography; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012459:Salicylates / Q000627:therapeutic use*
D001095:Arachidonic Acids; D012459:Salicylates; C016167:triflusal; D016718:Arachidonic Acid; D001241:Aspirin