Abstract
Renal artery occlusion was extensively used in animal models to cause acute renal failure. The present isolated tubule microperfusion studies were designed to examine the transport characteristics of multiple nephron segments of the rabbit after 60 min of total renal ischemia. This maneuver produced significant and persistent elevations of serum creatinine. The tubules were perfused and bathed with artificial solutions simulating ultrafiltrate and studied at 37.degree. C. Four nephron segments were examined. Ischemia reduced proximal convoluted tubule fluid reabsorption 77% (0.72 .+-. 0.11 vs. 0.14 .+-. 0.06 nm/mm per min, P < 0.01) and cortical proximal straight tubule fluid reabsorption 88% (0.54 .+-. 0.10 vs. 0.06 .+-. 0.03 nl/mm-1 per min-1, P < 0.005). Ischemia reduced the ability of the thick ascending limb of Henle''s loop to lower perfusate chloride ion concentration 60% (-47 .+-. 9 vs. -19 .+-. 3 meq/liter, P < 0.02) and its diluting ability 49% (-87 .+-. 15 vs. -44 .+-. 7 mosmol/kg H2O, P < 0.01). Ischemia reduced the antidiuretic hormone-dependent osmotic water permeability of the cortical collecting tubule 59% (0.0203 .+-. 0.0023 vs. 0.0083 .+-. 0.0020 cm/s, P < 0.01). Morphologic alterations were noted in the proximal segments but not in the distal segments of the nephron. The current studies demonstrate that 60 min of renal ischemia impairs the transport capability of all proximal and distal nephron segments studied.