Schmid-Schönbein G W, Simon S I, Newcom D R, Engler R L
Department of Applied Mechanics and Engineering Sciences--Bioengineering, University of California, San Diego, La Jolla 92092.
Eur Heart J. 1987 Dec;8 Suppl L:75-81. doi: 10.1093/eurheartj/8.suppl_l.75.
Recent evidence suggests that granulocytes play a key role in perfusion of the microcirculation. In this regard two phenomena are of specific importance: pseudopod formation and adhesion to the endothelium. Thus we studied the influence of AQA-39 on leukocyte adhesion to the endothelium in rat mesentery venules and on pseudopod formation in human granulocytes. Direct intravital estimates of granulocyte fracture stress were obtained by measurement of the ratio of leukocyte and midstream velocity. The marginating and circulating cell flux and the areal density of stationary granulocytes on the intraluminal side of the endothelium were measured simultaneously in the same venular segments. During administration of 10 mg kg-1 AQA-39 the fracture stress is significantly reduced resulting in decreased areal density of marginating cells and also washout of strongly adhering stationary leukocytes found frequently on the endothelium of such vessels. Furthermore it was observed on single granulocytes that AQA-39 leads to transient obliteration of pseudopod formation. These results suggest that the effect of AQA-39 on flow may be mediated in part by reduction in granulocyte adhesion to the endothelium and suppression of pseudopod formation.
