Comparative Effects Of 7% Naci In 6% Dextran 70 And 0.9% Naci On Oxygen Transport In Endotoxemic Dogs

1994 
ABSTRACT We compared the effects of 7% NaCI in 6% dextran 70 (HSD) and 0.9% NaCI (IS) resuscitation of endotoxic dogs on hemodynamic and cardiorespiratory parameters and the oxygen consumption-delivery relationship. Escherichia coli endotoxin (3 mg.kg-1, intravenously) was infused over 5 min into 13 paralyzed, chloralose-anesthetized, splenectomized dogs. Six additional dogs received a sham endotoxin infusion (saline) and served as controls. After 30 min, the endotoxic animals were resuscitated to 150% of their baseline cardiac output (CO) and maintained at this CO for 30 min using 7% NaCI in 6% dextran 70 (HSD at 1 ml.kg-1. min-1; n = 7) or 0.9% NaCI (IS at 4 ml.kg-1.min-1; n = 6). Oxygen consumption (VO2), measured by indirect calorimetry, hemodynamic parameters, and oxygen delivery (DO2), improved in similar temporal patterns in both groups during resuscitation and VO2 reached steady-state values. Oxygen delivery, VO2, mean arterial pressure, and cardiac output did not significantly differ between groups at the end of resuscitation, but VO2 increased significantly from baseline values only in the HSD group. The total volume of HSD administered averaged 10.0 ± 0.2 ml.kg-1 which was significantly less than the volume of IS, which averaged 67.2 ± 9.3 ml.kg-1. Incremental hemorrhages (2–5 ml.kg-1) were then performed in all dogs to determine the oxygen consumption-delivery relationship and the critical level of oxygen delivery (DO2Crit). The average DO2Crit values of the HSD, IS, and control groups were 9.42, 9.15, and 6.82 ml.min-1.kg-1, respectively. The DO2Crit values for the HSD and IS groups were not significantly different, but both were significantly greater than the control group value. Our results demonstrate that HSD provides no measurable advantages over IS in the early resuscitation period in terms of cardiorespiratory or hemodynamic parameters. Further, the DO2Crit values suggest that HSD provides no benefit over IS in terms of improving endotoxin-induced pathologic oxygen supply dependence.
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