Hüsnü KÜRŞAD, Cemal GÜNDOĞDU, Mahmut ARIK, Tülay ONAY, Hakan Hadi KADIOĞLU

Limited protective effects of hyperglycemia on cerebral ischemic damage in rabbits

Bu çalışmada hipergliseminin tavşanlarda a. Carotis Communis'in tek taraflı ligasyonu ile oluşturulan hemisferal serebral iskemi üzerine olan etkisi incelenmiştir. Çalışmada, 20 tanesi kontrol, 20 tanesi de çalışma grubu olmak üzere toplam 40 adet tavşan kullanıldı. Her iki grupta da halothan inhalasyonu ile anesteziyi takiben sağ a. carotis Communis ligature edildi. Çalışma grubuna ligasyon öncesi 5 mg/kg 'dan % 30luk dekstroz intravenöz olarak verilirken kontrol grubuna aynı dozda % 0.45'lik NaCI verildi. Bağlamadan 6 saat sonra her iki gruptaki denekler intrakardiak KCI enjeksiyonu ile sakrifiye edilerek beyinleri çıkarıldı. Çıkarılan beyinler % 10 formaldehit içerisinde tesbit edildikten sonra coronal kesitler alındı. Her beyin için alınan kesitler ışık mikroskopu ile incelenerek iskeminin en yoğun olduğu alanlar saptandı ve her iki gruptaki iskemik nöronal değişiklikler değerlendirildi. Sonuçta, hiperglisemi ile sağaltılan grupta gözlenen iskemik nöronal değişikliklerin kontrol grubuna göre oransal olarak daha az olduğu görülerek hipergliseminin iskemik nöronal yaralanmada sınırlı koruyucu bir etkisi olabileceği kanısına varıldı.

Tavşanlarda serebral iskemik yıkım üzerine hafif hipergliseminin sınırlı koruyucu etkisi

In this study, we attempted to research experimentally the effect of hyperglycemia on the cerebral ischemia induced by unilateral carotid ligation. In our experiments 40 rabbits were used, 20 of which were control group and the others 20 were study group. Right a. Carotis Communis was ligated in both groups following anaesthesia with halothan inhalation. In the study group, 30 % dextrose was infused with a dose 2.5 gr/kg before carotid ligation, while the same dose of 0.45 % NaCI was being infused in control group. At the end of 6 hours after ligation, all the rabbits in both groups were sacrified, and the brains were removed. Coronal sections were made after the brains had been fixated in buffered 10 % formol solution. Each slice of brain was examined carefully under light microscope to establish the most intensive ischémie areas. Then, ischémie neuronal alterations in both group were evaluated by light microscope. We observed that neuronal ischemie changes were less in the study group than the control one. We therefore, concluded that hyperglycemia may have a limited protective effect in ischémie neuronal injury.

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