DENEYSEL AKUT PANKREATİT MODELİNDE GELİŞEN AKCİĞER HASARINA TEMPOL’ÜN ETKİSİ

The Effects of Tempol on Lung Injury in A Model of Experimental Acute Pancreatitis

Özet

Amaç: Akut pankreatitte gelişen akciğer hasarına Tempol’ün etkisi araştırıldı.Yöntem: 30 adet rat üç gruba ayrıldı ( n=10). Grup I (Kontrol grubu): Laparotomi ve bilio-pankreatik kanalhazırlığı yapıldı. Grup II (Akut pankreatit grubu):Bilio-pankreatik kanal bağlanarak akut pankreatit ve akciğerhasarı oluşturuldu. Grup III (Tedavi grubu): Bilio-pankreatik kanal bağlandı ve Tempol verildi. Her üç gruptada akciğer dokusunun ıslak/kuru ağırlık oranı, akciğer dokusu miyeloperoksidaz aktivitesi ve malondialdehitseviyesi ölçüldü.Bulgular: Grup II ve III de ıslak/kuru ağırlık oranında, miyeloperoksidaz aktivitesinde ve malondialdehitmiktarında artış kontrol grubuna göre anlamlı derecede yüksek saptandı (p

Abstract

Background: Acute pancreatitis. especially in the severe form, is a well-known disease causing both local intra- abdominal and remote organ disturbances, including lungs. As a membreane-permeabl radical scavenger,Tempol was previously shown to attenuate the tissue damage after isehemia-reperfusion and sepsis . Here, we examined the effects of Tempol on pulmonary injury in a rat acute pancreatitis model. Methods: Thirty male Wistaı-Albino rats underwent median laparotomy and randomized into three groups: Group I (control) bilio-pancreatic duct was dissected but not ligated (n=10), group II (acute pancreatitis group) bilio-pancreatic duct was ligated (n=10), and group III (Tempol treated group) Tempol 30 mg/kg intravenously was injected following bilio-pancreatic duct ligation (n=10). After observation time (48 hours) animals were killed and level of malondialdehyde ,myeloperoxidase activity together with tissue wet/dry ratio in the lung parenchyma were assessed and compared. Results: There was a statistically significant increase in the quantity of malondialdehyde, myeloperoxidase activity and tissue wet/dry ratio of lungs in the acute pancreatitis group when compared to the control group. Treatment of animals with Tempol partly reduced the pulmonary injury characterized by increased tissse wet/dry ratio, level of malondialdehyde and myeloperoxidase activity. But this reduction was not found to be statistically significant. Conclusion: Beneficial effects of Tempol in preventing pulmonary injury following experimental models of sepsis and isehemia-reperfusion have been reported previously. In our model of experimental acule pancreatitis, Tempol showed some attenuating effect on pulmonary injury despite it was limited when compared to that of ischemia- reperfusion and sepsis models. This result suggests that some other confounding factors may be involved in the mechanisms of pulmonary injury related to acute pancreatitis. We believe that further detailed studies are needed to elucidate the exact mechanisms of that injury.