Akademik Veri Yönetim Sistemi
Anestezi Dergisi, cilt.33, sa.2, ss.142-147, 2025 (Scopus)
Objective: Global cerebral ischemia occurs due to interruption of cerebral blood flow during cardiac arrest and major vascular surgeries. Brain damage occurring in global cerebral ischemia is secondary to ischemia and reperfusion; It develops as a result of complex pathophysiological processes including N-methyl-D-aspartate (NMDA) receptor activation, disruption of intracellular Ca+2 homeostasis, and oxidative stress. Memantine, an extrasynaptic NMDA receptor inhibitor, is a molecule that can be used in the treatment of neurodegenerative diseases in humans due to its low side effects. The aim of this study is to investigate the effects of memantine on cerebral ischemia reperfusion injury. Methods: In this study, 24 male Wistar-Albino rats were randomly divided into 4 groups; control group (G C), ischemia group (G I), ischemia-reperfusion group (G IR), memantine group (G M). Cerebral ischemia model in rats other than the control group was performed using the 4-vessel occlusion model described by Pulsinelli et al. Serum neuron specific enolase (NSE) and S-100 calcium binding protein B (S-100 β) and antioxidant parameters superoxide dismutase (SOD), catalase (CAT), malonyl dialdehyde (MDA) and glutathione S transferase (GST) levels were studied in four groups. Results: Compared to G C, S-100 β and NSE levels were found to be statistically significantly higher in G I and G IR. S-100 β and NSE levels were found to be statistically significantly lower in GM than in G IR. Statistically significantly lower levels of antioxidant parameters SOD, CAT, and MDA were detected in G M than in G IR. Conclusion: As a result, we think that memantine administration may be protective against ischemia reperfusion injury in global cerebral ischemia.