EFFECTS OF FUROSEMIDE ON RENAL OXYGEN-CONSUMPTION AFTER ISCHEMIA IN NORMAL AND STREPTOZOTOCIN-DIABETIC RATS

Normal and streptozotocin diabetic rats were subjected to ischemic injury by unilateral renal artery occlusion for 60 min. The cortical and the medullary oxygen consumption (QO2) in the postischemic and the control, contralateral nonischemic, kidneys were measured 1 h, 1 day, and 1, 2 and 4 weeks for normal rats and 1 day, and 1 and 4 weeks for diabetic rats after ischemia. The effects of furosemide on QO2 of the cortex and the medulla of normal and diabetic rats were studied. The diabetic kidney was more vulnerable to ischemic injury than the normal kidney. Furosemide-sensitive active transport function in the medulla of the diabetic kidney was higher than that of the normal kidney. Furosemide did not decrease the cortical QO2 significantly in the control and the postischemic kidneys of normal and diabetic rats. In contrats, the medullary QO2 of the control kidney in both rats was significantly reduced by furosemide at every period after ischemia. In the medullary QO2 of the postischemic kidney, there were no significant decreases at any period after ischemia in the diabetic rats and only after a 1-hour period for normal rats. However, 4 weeks after ischemia, there was no statistically significant difference in the medullary QO2 inhibition by furosemide between the control and the postischemic kidneys in both normal and diabetic rats. We conclude that the furosemide-sensitive active transport function in the medulla recovers by the 4th week after ischemia in normal and diabetic rats.