RENAL TUBULAR NECROSIS following prolonged infrarenal aortic cross-clamping has been reported clinically and experimentally. There is disagreement as to the etiology of these renal changes. Canine experimental studies have yielded conflicting results.<sup>1-7</sup>In 1957 Powers, Boba, and Stein reported distal renal tubular necrosis following varying periods of infrarenal aortic cross-clamping in dogs.<sup>7</sup>Following cross-clamping, renal-blood flow (direct measurement) was observed to decrease an average of 32%, and oliguria ensued. If the kidney was protected by denervation of the pedicle or administration of a ganglionic blocking agent trimethaphan (Arfonad) camphorsulfonate, renal-blood flow and urine formation remained normal, and tubular necrosis did not occur. They concluded that in the unprotected animal reflex changes secondary to aortic cross-clamping led to increased renal vascular resistance which in turn resulted in ischemia and tubular necrosis. In 1959 Nanson and Noble reported similar findings in dogs.<sup>6</sup>They found that infrarenal aortic cross-clamping for