Leukocyte stasis in hepatic sinusoids

There is ongoing debate on the significance of capillary leukostasis for the manifestation of ischemia-reperfusion (I/R)-induced capillary ''no-reflow.'' Using intravital fluorescence microscopy, we studied leukocyte trafficking through the hepatic microvasculature and the relevance of sinusoidal leukostasis for nutritive perfusion failure in rats after hepatic I/R (n = 8). Sham-operated animals (n = 8) served as controls. Hepatic reperfusion was characterized by perfusion failure of individual sinusoids and a significant increase of sinusoidal leukostasis. However, in both nonischemic and postischemic livers, the major fraction of sinusoids presenting with stagnant leukocytes were found perfused (97 +/- 1 and 73 +/- 5%, respectively), whereas only 3 +/- 1 and 27 +/- 5% failed to conduct flow. Analysis of leukocyte trafficking in sinusoids with leukostasis revealed a marked reduction of leukocyte velocity and leukocyte flux in nonischemic and postischemic livers compared with sinusoids without leukostasis. Thus stagnant leukocytes retard cellular passage through hepatic sinusoids, probably due to an increase of flow resistance. However the fact that during postischemic reperfusion >70% of the sinusoids accommodating stagnant leukocytes are still perfused indicates that sinusoidal leukostasis per se does not necessarily determine perfusion failure (''no-reflow'') after I/R of the liver.