Flow redistribution in a hyperdynamic small animal burn: Comparison to patterns in sepsis

Abstract

Visceral hypoperfusion with local accumulation of lactate in the ischemic tissues has been reported in a septic rat model despite a hyperdynamic systemic circulation. This visceral ischemia is felt to contribute to the multiple system organ failure (MSOF) syndrome associated with sepsis. The purpose of this study was to determine whether a similar redistribution of blood flow existed in rats after a severe thermal injury as it too is associated with MSOF. Twenty-four hours after animals were subjected to either a resuscitated 50% scald burn (BURN) or sham treatment (SHAM), thermodilution cardiac output (CO), effective hepatic blood flow (EHBF) by galactose clearance at low concentrations, effective renal plasma flow (ERPF) by para-aminohippurate clearance, and blood, liver, and skeletal muscle pyruvate (P), and lactate (L) concentrations were determined. CO increased 52% in BURN (46.5 ± 2.8 ml/min/100 g, n = 21) versus SHAM (30.7 ± 1.0 ml/min/100 g, n = 22; P < 0.001) while EHBF increased only 18% (BURN: 6.81 ± 0.36 ml/min/100 g, n = 8 vs SHAM: 5.77 ± 0.29 ml/min/100 g, n = 8; P < 0.025) and ERPF showed an insignificant 24% increase (BURN: 2.98 ± 0.32 ml/min/100 g, n = 6 vs SHAM: 2.40 ± 0.40 ml/min/100 g, n = 6; P < 0.10), demonstrating a redistribution of flow. There was no local accumulation of lactate in blood, liver, or skeletal muscle and no derangement in P L ratios. This study when compared to previous observations in sepsis suggests that (1) the flow redistribution of sepsis has features differentiating it from solely a “stress response;” (2) the mechanism and/or mediators of the flow redistribution in acute burn injury differ from those in hyperdynamic sepsis; and (3) infection may be the final common mediator leading to MSOF.