Direct Measurement of LDL Cholesterol

able amounts of radiolabeled dextran in the plasma protein fraction [15]. Consequently, we do not think this mechanism plays a substantial role in producing the lower than expected dextran concentrations seen in the present study. The dextran we used had a mean molecular mass of 70 000 Da. Thus, some quantity of lower-molecular-mass dextran could have leaked out of the vascular space and distributed into the interstitial fluid, accounting for the increase in distribution volume. The decrease in dexiran concentration could also be the product of hemodilution caused by the large quantities of fluids administered after the HSD. Hemnatocrit values agreed closely with the volume of fluid infused (r = 0.60, n = 13, P <0.05) but not with the dextran concentrations (r = 0.22, n = 13, P = 0.46). Factors other than hemodilution from the administration of additional fluids must further decrease dextran. Thus, the lower concentrations of plasma dextran observed in trauma patients could be the product of a variety of factors and warrant further study to possibly improve the efficacy of HSD. Importantly, the dextran concentrations observed in these trauma patients are much lower than those previously observed to adversely affect blood typing or coagulation [19, 20]. In vitro, a 1:5 ratio of HSD to erythrocytes did not affect blood typing but did slightly increase prothrombin time and decrease platelet aggregation. This ratio is about twice the concentration expected if an adult lost half of his or her blood volume and received 250 mL of HSD. Generally, prolonged bleeding or clotting times or adverse effects on blood typing have been associated with dextrans of average molecular masses >150 000 Da or after administration of large doses (>1.5 g/kg) of dextrans of >60 000 Da [19,20]. No adverse effects on blood typing or coagulation were observed in the large clinical trials [3, 10]. Consequently, therapeutic use of HSD should carry minimal risk.