Leukocyte-endothelium-interaction in pial vessels following global, cerebral ischaemia

Citation
C. Abels et al., Leukocyte-endothelium-interaction in pial vessels following global, cerebral ischaemia, ACT NEUROCH, 142(3), 2000, pp. 333-339
Citations number
37
Categorie Soggetti
Neurology
Journal title
ACTA NEUROCHIRURGICA
ISSN journal
00016268 → ACNP
Volume
142
Issue
3
Year of publication
2000
Pages
333 - 339
Database
ISI
SICI code
0001-6268(2000)142:3<333:LIPVFG>2.0.ZU;2-P
Abstract
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.