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

Normal and streptozotocin diabetic rats were subjected to ischemic inj ury by unilateral renal artery occlusion for 60 min. The cortical and the medullary oxygen consumption (QO2) in the postischemic and the con trol, 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 dia betic rats after ischemia. The effects of furosemide on QO2 of the cor tex and the medulla of normal and diabetic rats were studied. The diab etic kidney was more vulnerable to ischemic injury than the normal kid ney. Furosemide-sensitive active transport function in the medulla of the diabetic kidney was higher than that of the normal kidney. Furosem ide did not decrease the cortical QO2 significantly in the control and the postischemic kidneys of normal and diabetic rats. In contrats, th e medullary QO2 of the control kidney in both rats was significantly r educed 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-hou r period for normal rats. However, 4 weeks after ischemia, there was n o statistically significant difference in the medullary QO2 inhibition by furosemide between the control and the postischemic kidneys in bot h normal and diabetic rats. We conclude that the furosemide-sensitive active transport function in the medulla recovers by the 4th week afte r ischemia in normal and diabetic rats.