Role of neutrophils in endotoxin-mediated microvascular injury in hamsters

The purpose of this study was to examine the role of circulating neutrophils in endotoxin-induced increase in microvascular permeability in vivo. Fifteen hamsters were anesthetized, and a plastic chamber was placed in each cheek pouch to observe the microvasculature. Fluorescein-labeled dextran (FITC-D, 150 kDa) was injected intravenously, and changes in leaky sites and FITC-D clearance were measured in three groups: control (saline, n = 4), endotoxin suffusion (n = 6), and endotoxin suffusion after neutropenia induction (n = 5). We found a significant increase in leaky sites and FITC-D clearance with endotoxin (45 ± 18/cm² and 20 ± 6 x 10^-6 ml/min, respectively; mean ± SD, P < 0.05) in comparison to control (7 ± 6/cm² and 7 ± 5 X 10^-6 ml/min) and endotoxin suffusion in neutropenic animals (19 ± 11/cm² and 12 ± 4 x 10^-6 ml/min). There was a significant correlation between the number of leaky sites and FITC-D clearance (r = 0.91, P < 0.01) and between the number of circulating neutrophils and FITC-D clearance (r = 0.87, P < 0.01). We conclude that endotoxin-mediated increase in microvascular permeability in the peripheral circulation is dependent in part on circulating neutrophils.