Abstract
The renal response to sepsis results in increased renal blood flow, decreased renal vascular resistance, polyuric renal failure and a change in intracortical renal blood distribution. Prior reports used whole animal preparations, where the effects of sepsis on other organs may have led to systemic vasoactive changes altering the experimental model. To elucidate the direct effect of gram negative bacteremia on the kidney, intracortical hemodynamics and urinary flow were investigated using isolated canine kidneys perfused with a nonpulsatile pump oxygenator primed with modified dog plasma. Bacteremia was produced by 2.5 x 10(11) live Escherichia coli organisms infused directly into the perfusate. Intracortical blood flow distribution was measured by radioactive microsphere trapping using 15 microns diameter plastic radioactive microspheres. Urine flow increased 157% (p less than 0.05) following E. coli bacteremia while intracortical blood distribution was unchanged. The polyuric renal failure of sepsis is therefore, a direct result of bacteremia and not secondary to a change in intracortical flow as previously reported. The changes in intracortical blood distribution reported previously in sepsis using intact animal models probably reflect the renal response to release of vasoactive compounds originating in other organs rather than an intrinsic renal reaction to bacteremia.