Türk Nöroşirürji Dergisi 2002 , Vol 12 , Num 3
Birol YANIK1, Aşkın GÖRGÜLÜ1, Talat KIRIŞ2, Sabahattin ÇOBANOĞLU1
1Trakya Üniversitesi Tıp Fakültesi Nöroşirürji, Anabilim Dalı, Edirne,
2Istanbul Üniversitesi İstanbul Tıp Fakültesi Nöroşirürji, Anabilim Dalı, İstanbul
Purpose: In experimental cerebral ischemia, the progress of secondary damage after primary insult is considered as the major cause of definitive neurological deficit. In the process of secondary damage, the influx of calcium has an important role. In this study in the ischemia-reperfusion model in rat hindarance of Ca entry into the cell is aimed by blocking both voltage and agonist operated Ca channels.

Materials and Methods: The effects of memantine, a N-methyl-D-aspartat blocker; and nimodipine, a voltage sensitive calcium canal blocker were examined in 48 female Wistar rats that underwent right middle cerebra! artery infarction by endovascular suture technique. Rats were equally divided into three therapy and one control groups. In therapy groups, memantine (LO mg/kg, ip) and nimodipine (0.1 mg/kg, ip) were administered alone or in combination 15 minutes before ischemia. Three hours after ischemia, brains were reperfused. Neurological evaluation was performed at six hours after ischemia, then rats were sacrified. The brains were sectioned coronally, and stained with tripheniltetrazolium chloride. The percentage of areas of infarction were evaluated in brain specimens.

Results: The results showed that the use of memantin alone or in combination with nimodipine improves neurological autcome and decreases the size of infarction (p<0.005). The use of nimodipine alone slightly decreased the size of infarction in some slices (6, 7, 8, 9 mm).

Conclusion: This study demonstrated in cerebral ischemia-reperfusion model in rat memantin was effective in decreasing of infaret size alone and in combination with nimodipine whereas the use of nimodipine alone was not effective. Anahtar Kelimeler : Cerebral ischemia, excitatory aminoacid, memantine, reperfusion