Kocaman U.Demirçivi Özer F.Oran I.Mete M.Burak-Atci I.Turhan T.Demirtaş E.2024-07-222024-07-22201213001817http://akademikarsiv.cbu.edu.tr:4000/handle/123456789/17796Aim: Thrombocyte activation is one of the mechanisms blamed for emerging of early brain injury(EBI) soon after subarachnoid hemorrhage(SAH). It is wondered by researching to what extend neuron injury is prevented by making thrombocyte inhibition in SAH model. It shows that the role of trombocyte activation on EBI. Material and Method: 21 rabbits weighting 3-5 kg are divided in 3 groups 7 each. After ether anesthesia, 0.2 cc arterial blood taking from group 1 and 2 was injected into cysterna magna and created SAH. After SAH, at regular intervals antithrombocyte drug (tirofiban) was given to group 2 intraperitoneally; no treatment was carried on group 1. 0.2 cc SF was injected into cysterna magna in group 3. Decapitation was done in 72nd hour and then ischemic brain map was done at hippocampus level. The amount of ischemic neuron was scored and statistically analyzed. Results: SAH was detected in all rabbits of group 1 and 2. There are meaningful difference between the group 1 and group 3 of scoring ischemic neuron of hippocampus's CA-3 and CA-4 areas. Whereas in group 2, which is a ischemic neuron treatment group, there is a decline in each area, this decline has reached to a statistical means only in CA-4 area. Conclusion: There can be neuronal loss due to EBI even in the area which is free from blood in experimental SAH. Decreasing the injury of neuron with an antithrombocyte medicine shows that thrombocyte activation plays a great role in pathogenesis of EBI.Englishtirofibananimal experimentanimal modelanimal tissuearticlebrain injurybrain ischemiacisterna magnacontrolled studyhippocampal CA3 regionhistologyhistopathologynonhumanrabbitscoring systemsubarachnoid hemorrhagethrombocyte activationArticle