CAN VASCULAR SHUNTING BE INDUCED IN THE KIDNEY BY VASOACTIVE DRUGS? 1

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Abstract
Expts. involving detns. of PAH, mannitol, O2 content and hematocrit in renal venous and peripheral (or renal) arterial blood before and after injn. of epinephrine, histamine or pentothal were performed in 8 hypertensive and 6 normoten-sive patients, and in 15 dogs. In patients, renal venous blood was collected by catheterization of the right renal vein. The maximal decrease in the extraction of PAH by the kidneys of patients after subcut. injn. of epinephrine or histamine was 11.4%; dog expts. were inconclusive. In dogs, there was a consistent difference in the O2 capacity, hematocrit, and plasma protein content between renal arterial and renal venous blood, the latter being more concd. This difference was increased by epinephrine. It is suggested that this loss of fluid from the renal blood may have occurred through renal lymphatic vessels or other vascular channels by-passing the renal vein. In human subjects arterio-venous oxygen differences were sometimes increased and sometimes decreased by epinephrine. Large intermittent renal shunts were therefore not elicited by doses of epinephrine or histamine large enough to cause systemic reactions in man or by larger doses of epinephrine in dogs. Even in subjects with essential hypertension, relatively small and inconsistent changes which could be ascribed to the presence of shunts were seen.