Abstract

A colloid (Hespan) fluid regimen in a 4 h rat model of endotoxaemia was used to prevent the development of the early hypodynamic phase of shock. Groups (N = 10 each) of isoflurane-anaesthetized, male Sprague-Dawley rats received either 1) E. coli endotoxin (E, 20 mg.kg-1 BW, i.v.), 2) 0.9% saline (S), 3) endotoxin + Hespan (E + H), or 4) saline + Hespan (S + H). After a 30 min baseline, 15 ml of 6% hetastarch (Hespan) were infused over 1 h beginning 1 min after endotoxin or saline. Pulmonary artery wedge pressures suggested no fluid overload in the E + H or S + H groups. By the end of the study, there were six spontaneous deaths in the E group vs. no deaths in the other groups. However, despite successful prevention of the early hypodynamic response together with increased cardiac output, increased oxygen delivery, decreased oxygen extraction, and sustained normal oxygen consumption in the E + H group, this fluid regimen failed to prevent significant and progressive acidaemia and hyperlactataemia. Also, by 4 h the E + H group exhibited declining blood pressures, marked hypoglycaemia, and significant small intestinal damage. Our results indicate that the early hypotensive, hypodynamic period is not crucial for the development of significant pathology in endotoxaemia, and that early flow-dependency of whole body oxygen uptake is not inherent to the early response to endotoxin in this model.

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