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1 Departments of Pharmacology and Medicine, Schools of Medicine, University of Pennsylvania, and Edward B. Robinette Foundation, Medical Clinic, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Cardiac output, and renal and femoral venous outflows were measured simultaneously and continuously by rotameters during hemorrhage and inferior vena caval obstruction. Acute reductions in cardiac output resulted in an immediate increased femoral and renal fraction of the cardiac output, the femoral increasing more than the renal. Further augmentation of the femoral flow fraction with reduction of the renal flow fraction was accomplished by baroreceptor area denervation or guanethidine. Following guanethidine-induced reduction of sympathetic vasoconstrictor activity of the femoral bed, the femoral flow pattern was converted to a renal flow pattern. The partition of cardiac output during acute hypotensive procedures in this experimental setting was determined by differential vasoconstrictor activity, possibly by neurohumoral agents which selectively influence certain vascular beds, and by an intrinsic property of the blood vessel wall which determines in part its response to acute reduction in flow.
Note:
With the Technical Assistance of Mark K. Saperstein
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