We studied ischemic acute renal failure in 28 dogs by micropuncture, microsphere, morphologic, and whole kidney hemodynamic techniques, 18 to 24 hours after the renal artery was clamped (clamping time, 60 to 90 min). Before the artery was clamped, renal blood flow (RBF) averaged 3.49 ± (SEM) 0.23 ml/min x g and was not significantly different (3.70 ± 0.34 ml/min x g) 18 hours after the ischemic episode. RBF autoregulatory capability was, however, significantly reduced. Fractional outer cortical blood flow decreased slightly from 41 ± 2 to 36 ± 3% (P < 0.05) postischemia. Single nephron glomerular filtration rate (SNGFR) was highly variable from one animal to the next and ranged from 0 to 87 nl/min (mean, 36 ± [SEM] 7 nl/min) in a manner similar to whole kidney inulin clearance, which ranged from 0 to 0.56 ml/min x g (mean, 0.30 ± 0.05 ml/min x g). The correlation coefficient between SNGFR and inulin clearance was highly significant, indicating an association between SNGFR and whole kidney GFR. Proximal tubule pressure (PTP) averaged 20 ± (SEM) 1 mm Hg. In 6 dogs, the glomerular filtration coefficient (K(f)) was determined by measurements of stop-flow pressure, colloid osmotic pressure, SNGFR, PTP, and single nephron filtrating fraction. K(f) was below that obtained for control animals. Scanning electron microscopy (SEM) studies indicated that the endothelial fenestrations were reduced in number and size. These studies suggest that one major characteristic of ischemic nephropathy in the dog is a derangement in the filtration process. The maintenance of RBF in the postischemic phase may occur by utilization of the autoregulatory reserve of the renal vasculature.
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