Prior mannitol and furosemide infusion in a model of ischemic acute renal failure

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Abstract
Tubular transport abnormalities were recently characterized in a rabbit model of ischemic acute renal failure (ARF). Previously severe observable morphologic and functional changes in the proximal nephron together with functional changes in the distal nephron were demonstrated. Tubular debris was often produced by perfusion of proximal nephron segments. Presently, agents used to prevent ARF were tested in this rabbit model of ARF. Rabbits were infused with either 5% body wt 5% mannitol or 20 .mu.g.cntdot.kg-1.cntdot.min-1 furosmide in 5% body wt normal saline for the 60 min preceding 60 min of total renal ischemia. Mannitol prevented the development of ARF, maintained fluid reabsorption in the proximal convoluted tubule (PCT) (0.59 .+-. 0.03 vs. 0.52 .+-. 0.1 nl.cntdot.mm-1.cntdot.min-1) and proximal straight tubule (PST) (0.34 .+-. 0.05 vs. 0.39 .+-. 0.07 nl.cntdot.mm-1.cntdot.min-1), depressed NaCl reabsorption in the cortical thick ascending limb of Henle''s loop (TALH), and did not prevent a decrease in ADH[antidiuretic hormone]-mediated osmotic water flow in the cortical collecting tubule (CCT). Furosemide partially preserved renal function, partially protected the PCT (0.63 .+-. 0.05 vs. 0.38 .+-. 0.04 nl.cntdot.mm-1.cntdot.min-1) and PST (0.32 .+-. 0.04 vs. 0.022 .+-. 0.02 nl.cntdot.mm-1.cntdot.min-1), and did not change the transport capacity of the TALH or the ADH response of the CCT. Preservation of proximal nephron integrity was also reflected by the absence of debris formation. There is a direct relation between an agent''s ability to protect the functional integrity of the cells of the proximal nephron and its ability to preserve renal function.