On leukocyte stasis in hepatic sinusoids.
Vollmar, Brigitte, Sven Richter, Michael D. Menger.
Institute for Clinical & Experimental Surgery, University of
Saarland, D-66421 Homburg/Saar, Germany
APStracts 2:0255G, 1995.
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 following 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 non-ischemic and
postischemic livers, the major fraction of sinusoids presenting with
stagnant leukocytes were found perfused (97+/-1% and 73+/-5%,
respectively), while 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 non-ischemic and postischemic livers when compared to 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 more than 70% of the sinusoids accomodating stagnant
leukocytes are still perfused, indicate that sinusoidal leukostasis
per se does not necessarily determine perfusion failure ("no
-reflow") following I/R of the liver.
Received 14 August 1995; accepted in final form 29 November 1995.
APS Manuscript Number G352-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95