نقش کانالهای پتاسیم حساس به ATP (KATP) در آسیب ناشی از ایسکمی و برقراری مجدد جریان خون در کلیه موش صحرایی

The precise mechanism of ischemia reperfusion (IR) injury is not fully understood. Recent studies on Rat myocardium revealed that activation of the K ATP channels inhibits this process. The goal of this study is finding the same effect of K ATP channels on IR injury, in rat kidney. In this study the effects of K ATP agonist (Diazoxide) and K ATP antagonist (Glibenclamide) plus a K ATP independent vasodilator (Hydralazin) on ischemia reperfusion injury examined. Female rats of 200-250 g were anesthesized and used for study. Different doses of Diazoxide (1, 5, 15mg/kg) and Glibenclamid (1, 5, 10mg/kg) and hydralazin (1, 3, 15mg/kg) were used (SC) 120 minutes prior to the initiation of IR. Kidneys were removed and checked histologically for the grading of injury. Diazoxide (5mg/kg) prevented these lesions. Different doses of Glibenclamide and hydralazine failed to prevent IR injury. Diazoxide is also a vasodilator agent but failure of hydralazine to prevent the injury revealed that vasodilation was not the exact mechanism of action of Diazoxide.