LEUKOCYTE ACTIVATION DOES NOT MEDIATE MYOCARDIAL LEUKOCYTE RETENTION DURING ENDOTOXEMIA IN RABBITS

Our goal was to determine whether coronary leukocyte retention after e ndotoxin infusion was due primarily to leukocyte activation. Leukocyte s were activated by infusion of endotoxin into 12 blood donor rabbits. Separately, 12 isolated rabbit hearts were perfused with blood from a n endotoxemic support rabbit to expose coronary endothelium to an infl ammatory stimulus. During an infusion of 20 mi of donor blood into the isolated heart, the coronary transit time of leukocytes was determine d by deconvolution of multiple measurements of injectate and collected leukocyte concentrations. With no leukocyte activation or inflammator y stimulation of endothelium, leukocyte transit time was 9.2 +/- 3.5 s , and 11.6 +/- 4.1 x 10(6) leukocytes were retained in the coronary ci rculation. Leukocyte activation alone did not alter transit time (9.8 +/- 3.2 s) or retention(9.3 +/- 4.6 x 10(6) leukocytes). Inflammatory stimulation of endothelium with and without leukocyte activation incre ased transit time (18.0 +/- 3.6 and 18.9 +/- 3.8 s, respectively; P < 0.05) and retention (24.8 +/- 8.4 and 25.3 +/- 6.8 x 10(6) leukocytes, respectively; P < 0.05) to the same extent. Differential counts showe d that neutrophils (but not lymphocytes) were slowed and retained. inf lammatory stimulation of endothelium caused coronary capillary endothe lial swelling and pseudopod formation. Thus increased coronary neutrop hil transit time and retention are due to structural changes of corona ry endothelial cells or other effects of the inflammatory response occ urring within coronary capillaries, not only due to activation of leuk ocytes.