Abstract
Neutrophils may contribute to the pathogenesis of ischemia-reperfusion injury by impairing microcirculatory flow and causing tissue damage. In this study neutrophil deformability and activation were studied after acute ischemia and reperfusion of the rat hindlimb. A cell transit analyzer with 8 μm pore filters was used to measure the flow resistance of individual neutrophils isolated from arterial blood drawn 30 seconds and 5 minutes after reperfusion, after 2 hours of femoral or iliac artery occlusion, in anesthetized rats. Femoral occlusion followed by 30 seconds of reperfusion resulted in a 16% rise in mean pore transit time, and iliac occlusion caused a 31% increase. Neutrophil activation (percentage of cells with nonspherical shape) rose from 6% to 23% (femoral occlusion) or from 7% to 29% (iliac occlusion). By 5 minutes of reperfusion, transit times, but not shape change, had almost returned to preischemic levels. Sham-occluded rats had no significant change in neutrophil behavior. Plasma isolated from rats after 30 seconds of reperfusion after 2 hours of iliac occlusion caused a 27% increase in mean transit time when incubated with nonautologous neutrophils, while activation rose from 32% to 55%. Thus plasma factor(s) released after ischemia and reperfusion of rat hindlimb caused transient rheologic alteration of circulating neutrophils, which may contribute to local or disseminated vascular occlusion and tissue injury.
Published Version
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