Beneficial effects of dextran 70 versus ringer's acetate on pulmonary function, hemodynamics and survival in a porcine endotoxin shock model

Abstract

The effects of Dextran 70 with NaCl as against Ringer's acetate on hemodynamics, gas exchange, oxygen transport and survival were evaluated in a porcine model of pulmonary and circulatory insufficiency induced by a continuous i.v. endotoxin infusion over 6 h. Dextran and Ringer's acetate were infused continuously to maintain baseline mean left atrial pressure (MLAP) throughout the endotoxin period. Twelve pigs receiving endotoxin + Ringer's acetate displayed a progressive 45% decline in cardiac output (Qt) and a two peaked increase in pulmonary vascular resistance (PVR) with a late increase of 250%. Venous admixture (Qva/Qt) increased progressively more than 6-fold and extravascular lung water (EVLW) increased by 55%. Mean arterial blood pressure (MAP) fell by 25%, oxygen delivery by 40%, base excess (BE) ranged between - 4.5 and - 9 mmol.1(-1) at the end of the endotoxin period and 4 of 12 animals died. Polymorphonuclear cell count (PMNs) fell rapidly by 90% and was severely decreased throughout the endotoxin period. Contrastingly, the 12 pigs that received endotoxin + Dextran maintained Qt near baseline and PVR was significantly lower in this group. Qva/Qt increased progressively more than 4-fold, but was significantly lower than in the Ringer's group as was the increase in EVLW (23%). MAP only decreased by 10%, oxygen delivery only decreased by 20%. BE ranged between - 1.0 and - 3.0 at the end of the endotoxin period and all animals survived. PMNs fell by 90% at 0.5 h but subsequently tended to return towards baseline. PMNs were significantly increased compared with the Ringer's group. The amount of Ringer's acetate necessary to maintain a stable MLAP averaged 4.6 times the Dextran volume. The superiority of Dextran as compared with Ringer's acetate in this endotoxemic shock model seems to be consequent to better rheological effects combined with pharmacological interactions with granulocytes.