Normal renocortical blood flow in experimental acute renal failure.

Renal cortical blood flow of rats with postischemic, myohemoglobinuric, and mercury-induced acute renal failure was measured by the hydrogen washout technique using implanted platinum electrodes. Total renal blood flow was determined by venous cannulation in separate series of rats. The values obtained with the two methods were in excellent qualitative agreement (r=0.99, P less than 0.001), although venous cannulation gave values that were constantly lower than those calculated for whole kidney from the cortical flow rate and assumed cortical mass. Myohemoglobinuria produced by glycerol injection caused cortical blood flow to fall from a control value of 7.37+/-0.23 (SEM) ml/min X g of cortex to approximately one-half that value for four hours after injection (P less than 0.001). Flow rates 12 and 24 hr after glycerol injection were 85% (P less than 0.001) and 90% (P less than 0.05) of control, respectively. Cortical flow was reduced to 5.49+/-0.39 (SEM) ml/min X g of cortex four hours after release of one hour's total bilateral renal arterial occlusion (P less than 0.001), but rose to normal within 24 hr. Poisoning with 4.7 mg/kg of body wt of mercuric chloride produced a cortical blood flow value that was 30% higher than control 24 hr after injection (P less than 0.01), while a 12 mg/kg of body wt dose gave a normal flow value. Inulin clearance was severely depressed in all models at all study times. Thus, in contrast to human acute renal failure, marked renal cortical ischemia is not an essential feature of these different forms of murine acute renal failure.