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  Role of nitric oxide synthase inhibition in leukocyte-endothelium interaction in the rat pial microvasculature

Lindauer, U., Dreier, J., Angstwurm, K., Villringer, A., Einhaeupl, K. M., & Dirnagl, U. (1996). Role of nitric oxide synthase inhibition in leukocyte-endothelium interaction in the rat pial microvasculature. Journal of Cerebral Blood Flow & Metabolism, 16(6), 1143-1152. doi:10.1097/00004647-199611000-00008.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-D6A3-C Version Permalink: http://hdl.handle.net/21.11116/0000-0002-D588-4
Genre: Journal Article

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Lindauer, U., Author
Dreier, J., Author
Angstwurm, K., Author
Villringer, Arno1, Author              
Einhaeupl, K. M., Author
Dirnagl, U., Author
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1External Organizations, ou_persistent22              

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Free keywords: Blood-brain barrier; Cranial window; Laser Dopple;, Confocal microscopy; Fluorescence; Chemiluminescence
 Abstract: We investigated the role of nitric oxide (NO) in leukocyte-endothelium interaction, blood-brain barrier (BBB) function and oxygen free-radical production in the rat pial microcirculation. In a closed cranial window preparation (dura removed) over the parietal cortex of pentobarbital-anesthetized Wistar rats, NO synthase (NOS) was inhibited by systemic and/or topical application of Nω-nitro-l-arginine (l-NNA) under physiological conditions and during leukotriene B4 (LTB4) activation. Circulating leukocytes were labeled by intravenous injection of rhodamine 6G. We used a confocal laser scanning microscope (CLSM) and studied leukocyte rolling and sticking in pial veins and arteries before and after NOS inhibition. At the end of the experiments, sodium-fluorescein was injected intravenously to test BBB integrity. Brain cortex oxygen free-radical production was investigated in the cranial window preparation using lucigenin-enhanced chemiluminescence (CL). l-NNA application did not lead to significant changes in leukocyte-endothelium interaction, BBB function, and oxygen free-radical production under physiological conditions [leukocyte-endothelium interaction: control (n = 5), l-NNA systemically (n = 5), l-NNA topically (n = 5): at baseline rollers/100 μm: 0.76 ± 0.55, 0.64 ± 0.94, 0.44 ± 0.55 and stickers/100 μm: 0.90 ± 0.28, 0.76 ± 0.24, 0.84 ± 0.42; at 60 min rollers/100 μm: 1.49 ± 0.66, 1.21 ± 0.99, 0.67 ± 0.66 and stickers/100 μm: 1.04 ± 0.20, 1.19 ± 0.23, 1.21 ± 0.54; oxygen free-radical production (n = 4): CL count before l-NNA application 35 ± 17 cps, after 1 h of topical superfusion of l-NNA 38 ± 14 cps; p < 0.05]. In contrast to the results achieved under physiological conditions, a significant further increase of rolling leukocytes and BBB permeability occurred due to NOS inhibition under LTB4-activated conditions [76 ± 47% significant (p ≤ 0.01, n = 7) further increase of rollers/100 μm due to 60 min l-NNA application following the activation period of 120 min LTB4 superfusion]. Our results support a modulatory role for NO in leukocyte-endothelium interaction and BBB permeability in the pial microcirculation when this interaction is increased.

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 Dates: 1995-12-281996-05-021996-11-01
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: eDoc: 511563
Other: P9130
DOI: 10.1097/00004647-199611000-00008
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Title: Journal of Cerebral Blood Flow & Metabolism
Source Genre: Journal
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Pages: - Volume / Issue: 16 (6) Sequence Number: - Start / End Page: 1143 - 1152 Identifier: -