Effects of norepinephrine on the renal vasculature in normal and endotoxemic dogs

Septic shock is often complicated by systemic hypotension despite normal or increased cardiac output. Restoration of arterial pressure usually require s the administration of systemic vasopressor agents, such as norepinephrine . However, because norepinephrine induces vasoconstriction in other vascula r beds, it may decrease visceral blood flow, impairing visceral organ funct ion. Because sepsis is often associated with impaired peripheral vascular r esponsiveness, we hypothesized that unlike in normal circulatory conditions , norepinephrine would improve visceral organ blood flow in sepsis by selec tively increasing organ perfusion pressure. Thus, in nine pentobarbital-ane sthetized, mechanically ventilated dogs, we measured the effect of norepine phrine infusion (0.3 mu g/kg/min) on renal, hepatic, and portal steady-stat e pressure-flow relations (P/(Q) over dot) and the dynamic vascular P/(Q) o ver dot, created by transient, inferior vena caval occlusion, under basal a nd endotoxic conditions. Norepinephrine increased organ perfusion pressures during both control and endotoxemic conditions. However, even after contro lling for the pressure effect using a general linear model, NE was associat ed with an increase in renal blood flow both before and after endotoxin adm inistration. We conclude that unlike the effects of administering norepinep hrine under baseline conditions, norepinephrine infusion during endotoxic s hock actually increases renal blood Flow and that this effect is not: the r esult: of an increase in perfusion pressure alone.