Giris ve amaç: Akut gastrik mukozal lezyonlarin patofizyolojisini belirlemeyi amaçlayan bir çok çalisma yapilmis olmasina ragmen, patogenezi hala net olarak ortaya konulamamistir. Bunlarda mide mukozasinin iskemisi ve mukus salgisindaki azalmanin ana rolü oynadigi düsünülmektedir. Antitrombin III (ATIII)’ün iskemi-reperfüzyon modellerinde nötrofil infiltrasyonunu baskiladigi ve prostocyclin I2 ( PGI2 )’nin sekresyonunu artirdigi gösterilmistir. Bundan yola çikarak yanik olusturulan ratlarda ATIII'ün gastrik mukozal lezyonlar üzerine etkisinin arastirilmasi amaçlanmistir. Gereç ve yöntem: Otuz adet Sprague-Dawley cinsi erkek rat çalismaya alindi. Ratlar randomize olarak 3 gruba ayrildi. Grup II ve III ratlarda 95 0C su ile 10 saniye sürede sirt bölgelerinde total vucut yüzeyinin %30’içeren yanik olusturuldu. Sham grubunda (grup 1) ratlar 21 0C suda 10 sn tutuldu. Grup III ratlara yanik olusturulmadan 15dk önce 250U/kg dozunda juguler ven yoluyla ATIII verildi. Grup I ve II ratlara plasebo amaciyla 1ml %0.9 NaCl ayni yol ile verildi. Yanik olusturulmasindan 12 saat sonra tüm ratlar yüksek doz anestetik verilerek öldürüldü ve mideleri alinarak büyük kurvatur boyunca açildi lezyonlar makroskobik olarak incelendi. Bu islemden sonra histolojik degerlendirme yapildi. Bulgular: Grup 1 de makroskobik ve mikroskobik mide lezyonu saptanmadi. Grup II’ de makroskopik olarak 2 ratta hiperemi ve bir ratta erezyon saptandi. Histolojik olarak 5 ratta (%50) akut gastrit saptanirken ATIII verilen (Grup 3) grupta hiçbir ratta akut gastrit bulgusu saptanmadi (p<0.05). Sonuç: Bu sonuçlara göre yanik olusturulan ratlarda gastrik mukozal lezyonlar daha çok nötrofil infiltrasyonu (akut gastrit) seklinde ortaya çikmaktadir. ATIII ile bu lezyonlar önlenebilmektedir. ATIII gastrik mukozal lezyonlarin önlemek amaciyla yaniktan hemen sonra erken dönemde kullanilabilir.
Background and aims: Although many studies have been made to define the pathophysiology of acute gastric mucosal lesion, its pathogenesis is still not clearly defined. The ischemia of gastric mucosa and decrease in mucus secretion are considered the main causes of acute gastric lesions. It has been shown that antithrombin III (ATIII) inhibits neutrophil infiltration in ischemia-reperfusion injury and increases the secretion of PGI2. The aim of this study was to evaluate the effects of ATIII on gastric mucosal lesions in burned rats. Materials and methods: Thirty Sprague- Dawley male rats were used. They were divided into three groups. A sham burn group (Group 1, n:10) was exposed to 21 OC water. A burn group (Group 2, n:10) and burn + ATIII group (Group 3, n:10) were exposed to 95 OC water for 10 sec., producing full-thickness burn in 30% of total body surface. Group 3 rats received 250 U/kg ATIII via right jugular vein, 15 minutes before burn injury. One ml 0.9% NaCl was given as placebo in Group 1 and Group 2 rats by the same route. The rats of all three groups were killed 12 hours after burn injury by an overdose anesthetic. The stomachs of all the rats were removed and opened along great curvature. Specimens were first evaluated macroscopically. A pathologist evaluated the hisopathologic specimens blindly. Results: There was no macroscopic or microscopic gastric lesions in Group 1. In Group 2, hyperemia in two rats, and erosion in one rat were found macroscopically. Histopathologic examinations revealed acute gastritis in 5 rats (50%) of Group 2; however, there was no acute gastritis in rats treated with ATIII (Group 3) (p<0.05). Conclusion: According to these results, gastic lesions of burned rats generally occurs as neutrophil infiltation (acute gastritis). These lesions can be prevented by the administration of ATIII. Antithrombin III may be used effectively to prevent the gastric mucosal lesions in the early period of burn injury.