Role of the leukocyte in endotoxin-induced alterations of the red cell membrane. Second place winner of the Conrad Jobst Award in the Gold Medal paper competition.

Sepsis and endotoxemia are known to be associated with alterations in the red cell membrane that result in diminished flexibility. This decreased flexibility may be responsible, in part, for the microcirculatory abnormalities accompanying sepsis. The etiology of these sepsis-associated changes remains unclear. This study evaluates the role of the white blood cell in these abnormalities. Specimens were obtained from 44 volunteers and divided into two treatment groups. Group I specimens were incubated with Escherichia coli endotoxin (2 micrograms/ml) followed by removal of the white blood cells. The white blood cells were removed from group II specimens before endotoxin incubation. Paired, saline-incubated samples served as controls. After incubation, washed erythrocytes were evaluated for deformability and membrane viscosity. Deformability was assessed by filtration through 4.7-microns membranes. Red cell deformability was expressed as filtration rate (volume of cells per second per square centimeter). Membrane viscosity was assessed by fluorescent spectroscopy of cells into which the membrane probe 1(4-(trimethylamino)-phenyl)-6-phenyl-1,3,5-hexatriene had been incorporated. Results were expressed as anisotropy. Endotoxin resulted in a significant increase in erythrocyte membrane viscosity (experimental, 0.296 +/- 0.002 vs. control, 0.284 +/- 0.002, P < 0.001). This was reflected by a significant decrease in cellular deformability (experimental, 142.55 +/- 6.55 vs. control, 157.86 +/- 8.63, P < 0.01). However, these alterations are not a direct effect of endotoxin, but require the presence and participation of the white blood cell and/or its mediators (experimental, 0.301 +/- 0.002 vs. control, 0.300 +/- 0.001, P = NS).