Background. Investigations have shown an increase of leukocyte-endothelium-
interaction in a variety of organs following an ischaemic insult. To elucid
ate the role of leukocyte-endothelium-interaction following global, cerebra
l ischaemia the present study was performed.
Methods. Global, cerebral ischaemia was induced for twenty minutes by four-
vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studie
d in the cerebral microcirculation using a rat closed cranial window and in
travital microscopy. Leukocytes were stained intravenously using rhodamine
6G. Diameters of pial vessels, leukocyte centreline velocity and number of
rolling or adhering leukocytes were determined off-line up to 2 h following
global cerebral ischaemia. To confirm these results immunohistochemistry o
f the brain was performed.
Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis
and minimal rest flow in arterioles. Reperfusion yielded a significant inc
rease of the arteriolar (p < 0.001) and a smaller increase of the venular d
iameters (p < 0.01). Up to 2 h after ischaemia no significant increase of t
he number of rolling or adhering leukocytes was measured which was confirme
d by immunohistochemistry.
Interpretation. In contrast to other studies, in particular regarding focal
cerebral ischaemia, an increase of leukocyte-endothelium-interaction in ra
t brain following 20 min of global cerebral ischaemia was not observed desp
ite histological evidence of ischaemic damage. Thus in our model leukocytes
seem not to contribute to the brain damage following global ischaemia.