The effects of increasing renal perfusion pressure on renal hemodynamics, microcirculation，and oxygen metabolism in a septic shock model

Abstract

BackgroundThe optimal target for mean arterial pressure (MAP) during clinical management of septic shock remains a topic of debate. This study investigates how elevating MAP, and thereby increasing renal perfusion pressure (RPP, defined as MAP-CVP), influences renal hemodynamics, microcirculation, and oxygen metabolism in a septic shock model. MethodsSixteen New Zealand rabbits of either sex and similar weight were randomly assigned to sham group (n=8) and septic shock group (n=8). Renal blood flow (RBF), microcirculatory blood flow and velocity in the kidney, as well as tissue oxygen pressure in the renal cortex and medulla, were assessed at four distinct time points: baseline (T0), model establishment (T1), restoration of MAP to baseline levels (T2), and an increase in MAP by more than 15% above baseline (T3). ResultsWithin the septic shock group, although MAP and consequent RPP were increased, RBF markedly decreased from 17.63{+/-}2.50 to 8.50{+/-}1.93 ml/min (p < 0.05). No significant changes in microcirculation blood flow or flow velocity were observed between T2 and T3. Tissue oxygen pressure in the renal cortex and medulla declined significantly from 21.20{+/-}1.80 to 17.14{+/-}1.72 (p < 0.05) and from37.74{+/-}4.85 to 24.34{+/-}3.74 (p < 0.05), respectively. ConclusionElevating RPP does not improve RBF, renal microcirculation, or tissue oxygen pressure in the renal cortex or medulla in septic shock. Elevating RPP does not improve RBF, renal microcirculation, or tissue oxygen pressure in the renal cortex or medulla in septic shock. We advocate restoring MAP to the baseline level rather than increasing it further to enhance renal perfusion pressure.