title: Leukocyte-endothelium interactions in pial venules during the early and late reperfusion period after global cerebral ischemia in gerbils.
abstract: The contribution of leukocytes to secondary brain damage after cerebral ischemia is still under discussion. The purpose of the present study was to examine the pial microcirculation after global cerebral ischemia while focusing on leukocyte-endothelium interactions during the early and late reperfusion period of up to 4 days. A closed cranial window technique that leaves the dura mater intact was used. Global cerebral ischemia of 15 minutes' duration was induced in male Mongolian gerbils (n = 91). Pial microcirculation was observed by intravital fluorescence microscopy. Leukocyte-endothelium interactions (LEIs) in pial venules, vessel diameters, capillary density, and regional microvascular blood flow measured by laser Doppler flowmetry were quantified during 3 hours of reperfusion and in intervals up to 4 days after ischemia. Within 3 hours of reperfusion, the number of leukocytes (cells/100 microm x minute) rolling along or adhering to the venular endothelium increased from 0.1 +/- 0.2 to 28.4 +/- 17.4 (P < 0.01 vs. control) and from 0.2 +/- 0.2 to 4.0 +/- 3.8 (P < 0.05), respectively. There was no capillary plugging by leukocytes; capillary density remained unchanged. In the late reperfusion period, at 7 hours after ischemia, LEIs had returned to baseline values. Furthermore, from 12 hours to 4 days after ischemia, no LEIs were observed. Changes in regional microvascular blood flow did not correlate with LEIs. Global cerebral ischemia of 15 minutes' duration induces transient LEIs that reach a maximum within 3 hours of reperfusion and return to baseline at 7 hours after ischemia. LEIs are not related to changes in microvascular perfusion, which suggests mainly that the expression of adhesion receptors is necessary to induce LEIs rather than rheologic factors. It seems unlikely that this short-lasting activation of leukocytes can play a role in the development of secondary brain damage.
authors.affiliation: Department of Neurosurgery, Grosshadern University Hospital, Ludwig-Maximilians-University, Munich, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Uhl
authors.forename: J
authors.initials: J
authors.lastname: Beck
authors.forename: W
authors.initials: W
authors.lastname: Stummer
authors.forename: J
authors.initials: J
authors.lastname: Lehmberg
authors.forename: A
authors.initials: A
authors.lastname: Baethmann
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001812:Blood-Brain Barrier / Q000276:immunology*; D002196:Capillaries / Q000276:immunology; D002450:Cell Communication / Q000276:immunology; D004730:Endothelium, Vascular / Q000166:cytology* / Q000276:immunology; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000276:immunology / Q000473:pathology*; D007962:Leukocytes / Q000166:cytology* / Q000276:immunology; D008297:Male; D010841:Pia Mater / Q000098:blood supply*; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology*; D013997:Time Factors; D014699:Venules / Q000166:cytology