Partial aortic ligation: a hypoperfusion model of ischemic acute renal failure and a comparison with renal artery occlusion.

Ischemic acute renal failure (ARF) in humans typically results from hypoperfusion, not total blood flow interruption. However, experimental studies of ischemic ARF have relied on total blood flow cessation models because no reliable hypoperfusion model has been described. Therefore, the goal of this study was to develop a hypoperfusion model of ischemic ARF and then to contrast it to a blood flow cessation model (renal artery occlusion). Rats were uninephrectomized, and then temporary (30 or 45 minute) partial aortic ligation (PAL) was created just above the left renal artery, yielding a renal perfusion pressure of 15 to 20 mm Hg and a renal blood flow of 0.1 to 0.2 ml/min. The severity of renal injury was assessed 24 hours later. Azotemia (30-minute PAL: BUN 47 +/- 5 mg/dl; 45-minute PAL: 118 +/- 11 mg/dl), depressed inulin clearances, and extensive pars recta proximal tubular necrosis resulted. Comparing 30 minutes of PAL with 30 minutes of renal artery occlusion revealed far less severe ischemic adenosine triphosphate depletion (P less than 0.001), less azotemia (P less than 0.05), less medullary vascular congestion (P less than 0.05), and less cast formation (P less than 0.05) with PAL. However, both models induced comparable degrees of tubular necrosis, oxidant tissue stress (as assessed by oxidized-reduced glutathione tissue assay), and post-ischemic adenosine triphosphate depletion. Both similarities and differences exist between hypoperfusion and blood flow cessation-induced experimental ARF. The difference indicate that blood flow cessation models may not closely simulate clinical ischemic renal injury.