ÝNCE BARSAKLARDA MEZENTER ARTER ÝSKEMÝSÝNE BAÐLI ÝSKEMÝ REPERFÜZYON HASARI ÜZERÝNE PROSTAGLANDÝN E2'NÝN ETKÝSÝ

Ýnce barsaklarda mezenter arter iskemisine baðlý iskemi-reperfüzyon hasarýný ve PGE2'nin etkisini gözlemek için 40 sýçanda eksperimental çalýþma yapýldý. Sham, ligasyon, deney ve ligasyon + prostaglandin E2 guruplarý yapýldý. Superior mezenterik arter aortadan çýkýþ yerinden atravmatik mikrovasküler klemplerle tutularak bir saatlik iskemi ve iki saatlik reperfüzyon saðlandý. 1 ve 3. saatlerde CPK, LDH, AST ve ALT analizi için kan örnekleri, malondialdehit ve redükte glutatyon saptanmasý ve histopatolojik inceleme amacýyla intestinal doku örnekleri alýndý. CPK, LDH, AST ve ALT deðerleri SMA ligasyonunu takiben yükseldi ve PGE2 verilen gurupta anlamlý düþme saptandý. Glutatyon seviyesi ligasyon gurubunda oldukça düþük, PGE2 verilen gurupta lipit peroksidasyonun ürünü olan malondialdehit anlamlý olarak düþük saptandý. Sonuç olarak histopatolojik bulgularýn biyokimyasal bulgularla paralellik gösterdiði ve PGE2'nin barsaklardaki, iskemik hasarý anlamlý olarak azalttýðý, daha da önemlisi iskemik hasarýn irreversible safhaya gelmesini önlediði gözlendi.

THE EFFECTS OF PROSTAGLANDIN E2 ON ISCHEMIA-REPERFUSION DAMAGE, RESULTING FROM MESENTER ARTERIAL ISCHEMIA IN SMALL INTESTINES

To observed the ischemia reperfusion damage and the effect of PGE2 resulting from mezenter arterial ischemia on 40 rats an experimental study is carried out. One-hour ischemia and two hour reperfusion model is applied by clemping the superior mesenteric artery at bifurcation site from aorta abdominal with atravmatic microvasculer in sham, ligation, experiment and ligation + PGE2 (n=10) groups. The blood samples were taken for alanine transaminase (ALT), aspartate transaminase (AST), lactic dehydrogenase (LDH), creatinin phosphokinase (CPK) analysis at 1st and 3rd hours. Intestinal tissue samples were removed for malonyldialdehyde and reduced glutathione determinations and histopathologic examination. CPK, LDH, AST and ALT values increased after the SMA ligation and there was a meaningful decrease in the group that was given PGE2. Glutation levels were rather low in the ligation group and malonyldialdehyde, the product of lipid peroxidatiton decreased in the PGE2 group. Finally; it is observed that histopathologic findings were in concordance with biochemical results and it is also found out that PGE2 lessens the ischemic damage in small intestines, furthermore, PGE2 enhances the ischemic damage to reach irreversible phase.