PRESSURE-RELATED CAPILLARY LEUKOSTASIS FOLLOWING ISCHEMIA-REPERFUSIONAND HEMORRHAGIC-SHOCK

Although the receptor-dependent venular adhesion of leukocyte adherenc e has been relatively well characterized, less is known about capillar y leukostasis. With the use of fluorescence intravital microscopy, leu kocyte behavior in the capillaries of rabbit tenuissimus muscle was ev aluated after ischemia-reperfusion or hemorrhage. After fixed volume h emorrhage or 4 h of total ischemia, inflammatory injury was manifest b y broken fibrils, edema, leukocyte infiltration, and margination along the postcapillary venular walls. Nevertheless, as long as arterial pe rfusion pressure was between 27 and 72 mmHg, the frequency of capillar y leukostasis was low (4-8 cells/mm2) and similar in all groups, inclu ding animals treated with the antiadhesion antibody IB4. In contrast, when perfusion pressure decreased to 20 mmHg, capillary leukostasis in creased similarly (to 16-21 cells/mm2) in controls (with or without IB 4) and in those subjected to ischemia. Furthermore, when perfusion pre ssure was increased to more than 27 mmHg, (27-72 mmHg) stationary leuk ocytes returned to the original low level (4-5 cells/mm2). These resul ts are consistent with the conclusion that during some inflammatory in juries, capillary leukostasis is a pressure-related phenomena that is not receptor dependent and is freely reversible with the early restora tion of perfusion pressure.