Methods: The experiments were performed 24 Wistar albino rats divided into three groups: sham-operated control, ischemia-created control and tirofiban-treatment groups. Temporary cerebral ischemia was created by the occlusion of bilateral carotid communis arteries for 10 minutes. In the treatment group, a tirofiban infusion (I.V. 0.4 µg /kg /minute) for 30 minutes was given by the femoral vein. The rats were sacrificed at the 3'd hour af ter ischemia and their brains were removed. The effects of ischemia and the efficacy of tirofiban were investigated by the assessment of the tissue lipid peroxidation, nitric oxide (NO), superoxide dismutase (SOD) and ATP levels.

Results: The average lipid peroxidation levels were 129,12 ± 2,69 in group I, 233 ± 3,25 in group II, and 163,62 ± 3,96 nmo]/ g wet tissue in group III. The mean tissue NO levels were 0,51 ± 0,02 in the first group, 0,73 ± 0,02 in the ischemic group, and it was 0,58 ±0,02 µmol/mg in the treatment group. In other words, the levels of lipid peroxidation and NO statistically decreased after the tirofiban treatment (p<0,001). The average tissue SOD level in the control group was 11,20 ± 0,25 U/mg protein whereas it was 12,57 ± 0,19 U/mg protein in the treatment group. The mean level of tissue A TP in ischemia group was 65,97 ± 12,25 nmol/ g wet tissue while it was 125,83 ± 16,46 nmol/ g wet tissue in treatment group.

Conclusion: In the ischemia group, a significant deerease in SOD and ATP levels was seen. After the tirofiban treatment, the deereased SOD and ATP tissue levels increased (p<0,001)A. ll these findings have revealed that tirofiban used immediately after ischemia way have a potential role in the treatment of acute cerebral ischemia and that it may be an alternative agent in these cases. Anahtar Kelimeler : Brain ischemia, neuroprotective agents, rat, thrombocyte aggregation inhibitors, thrombocyte glycoprotein GP ITh/Illa complex