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  • 1
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    Online Resource
    The cerebral microcirculation in focal ischemia and reperfusion
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Stroke Vol. 32, No. suppl_1 ( 2001-01), p. 359-359
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. suppl_1 ( 2001-01), p. 359-359
    Abstract: P111 The role of the microcirculation and of the inflammatory response in secondary brain damage from cerebral ischemia is hardly understood. Objective of the study was to assess leukocyte-endothelium interactions (LEI), functional capillary density (FCD), and the microvascular patency in the reperfusion period after an acute ischemic insult. Focal ischemia was induced in gerbils by transient (2 h) ligation of the left CCA. Only animals with a reduction of rCBF to 〈 10 % baseline (n=8) were studied in comparison with sham operated controls (n=7) as determined by laser-doppler flowmetry. A transdural window was implanted for observation of the brain surface by intravital microscopy before, during and up to 3 h following ischemia. FITC-Dextran and Rhodamine 6G were i.v. administered as fluorescence dyes for contrast enhacement of blood vessels and labeling of leukocytes. A brief but significant increase in the number of rolling leukocytes (rollers) was found at 5 (7.7 ± 4.2) and 30 min (6.4 ± 2.4 / 100 μm x min) of postischemic reperfusion. Subsequently, however, the number of rollers declined reaching the control level. Leukocytes firmly attached to the endothelium of postcapillary venules were also shortly increased after ischemia, albeit without reaching statistical significance. The number of perfused postcapillary venules (8–20 μm) was decreased to 44 ± 18 % at 2 h of ischemia. The recovery of the venular patency and, thus, perfusion was significantly delayed, i.e. until 1h of reperfusion. With onset of ischemia FCD decreased from 168 ± 10 cm -1 to 7 ± 5 cm -1 (p 〈 0.05) and did not recover with the ongoing reperfusion during the whole postischemic observation period (3 h). Activation of LEI as inflammatory response was limited to the immediate reperfusion period (5–30 min) only, rendering its pathophysiological significance questionable. On the other side FCD was drastically reduced and did not recover in animals with dense focal ischemia ( 〈 10%), with a delay of reperfusion of small venules for 1h or more. The marked disturbances of the microcirculation are most likley involved in the maturation of ischemic brain damage and may, thus, represent a promising target for therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.32.suppl_1.359-b
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1467823-8
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  • 2
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    Online Resource
    Intraoperative Detection of Early Microvasospasm in Patients with Subarachnoid Hemorrhage by Using Orthogonal Polarization Spectral Imaging
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Neurosurgery Vol. 52, No. 6 ( 2003-06), p. 1307-1317
    Details
    In: Neurosurgery, Ovid Technologies (Wolters Kluwer Health), Vol. 52, No. 6 ( 2003-06), p. 1307-1317
    Type of Medium: Online Resource
    ISSN: 0148-396X
    URL: Article
    DOI: 10.1227/01.NEU.0000065154.04824.9E
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1491894-8
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  • 3
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    Impact of the endothelin-A receptor antagonist BQ 610 on microcirculation in global cerebral ischemia and reperfusion
    Elsevier BV ; 2003
    In:  Brain Research Vol. 961, No. 2 ( 2003-01), p. 277-286
    Details
    In: Brain Research, Elsevier BV, Vol. 961, No. 2 ( 2003-01), p. 277-286
    Type of Medium: Online Resource
    ISSN: 0006-8993
    URL: Article
    DOI: 10.1016/S0006-8993(02)03974-4
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2003
    detail.hit.zdb_id: 1462674-3
    SSG: 12
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  • 4
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    Bradykinin Antagonists Reduce Leukocyte–Endothelium Interactions after Global Cerebral Ischemia
    SAGE Publications ; 2003
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 23, No. 4 ( 2003-04), p. 441-448
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 23, No. 4 ( 2003-04), p. 441-448
    Abstract: The aim of the present study was to evaluate the influence of bradykinin on microcirculatory changes and outcome after global cerebral ischemia (15 minute) in Mongolian gerbils. The cerebral microcirculation was investigated by fluorescent intravital microscopy. Survival and functional outcome was evaluated up to 4 d after ischemia. Animals were treated with the selective B 1 and B 2 receptor antagonists B 9858 and CP 0597, respectively, and the nonselective B 1 /B 2 receptor antagonist B 9430. Leukocyte activation was significantly reduced by all antagonists as indicated by a significant decrease in the number of rolling (33 ± 20, 6 ± 8, 9 ± 10, and 13 ± 10) and adherent leukocytes (9 ± 7, 3 ± 4, 1 ± 1, and 2 ± 3 · 100 μm –1 · min –1 in controls and in animals treated with B 1 , B 2 , and B 1 /B 2 antagonist, respectively). Arteriolar diameters were significantly reduced during reperfusion (35 ± 11 before and 27 ± 8 μm 40 minutes after ischemia) in animals treated with the B 2 antagonist. The postischemic hypoperfusion, however, was not affected. Mortality was significantly higher in animals treated with the B 1 and the B 1 /B 2 antagonist. The authors concluded that bradykinin is involved in postischemic disturbances of cerebral microcirculation. The therapeutic effect of specific bradykinin receptor antagonists on functional outcome, however, remains unclear.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/01.WCB.0000052280.23292.35
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2003
    detail.hit.zdb_id: 2039456-1
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  • 5
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    Online Resource
    Leukocyte-Endothelium Interactions in Pial Venules during the Early and Late Reperfusion Period after Global Cerebral Ischemia in Gerbils
    SAGE Publications ; 2000
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 20, No. 6 ( 2000-06), p. 979-987
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 20, No. 6 ( 2000-06), p. 979-987
    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 μm × 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.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/00004647-200006000-00010
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2000
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  • 6
    Online Resource
    Online Resource
    Bradykinin Antagonists Reduce Leukocyte???Endothelium Interactions After Global Cerebral Ischemia
    SAGE Publications ; 2003
    In:  Journal of Cerebral Blood Flow & Metabolism
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications
    Type of Medium: Online Resource
    ISSN: 0271-678X
    URL: Article
    DOI: 10.1097/00004647-200304000-00008
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2003
    detail.hit.zdb_id: 2039456-1
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