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PubMed · 9086452

Oxidative stress during platelet-activating factor-induced microvascular dysfunction.

I Kurose·L W Argenbright·R Wolf·D N Granger
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Abstract

OBJECTIVE: To assess the potential contribution of hydrogen peroxide (H2O2) to the leukocyte-endothelial cell adhesion and increased microvascular permeability (to fluorescein isothiocyanate [FITC]-albumin) observed in rat mesenteric venules exposed to platelet-activating factor (PAF). METHODS: The production of oxidants derived from H2O2 in mesenteric tissue was monitored using the H2O2-sensitive fluorochrome, dihydrorhodamine 123 (DHR). PAF elicited a rapid increase in both the albumin extravasation and oxidation of DHR, which was followed by an increased adherence and emigration of leukocytes in postcapillary venules. RESULTS: The PAF-induced oxidation of DHR, leukocyte-endothelial cells interactions, and albumin leakage were attenuated by treatment with either catalase or dimethylthiourea. Treatment with monoclonal antibody directed against either CD11b/CD18 on leukocytes or ICAM-1 on endothelial cells attenuated the PAF-induced oxidative stress, albumin leakage, and leukocyte-endothelial cell adhesion. CONCLUSIONS: These findings indicate that most of the oxidants generated in mesenteric tissue exposed to PAF results from the accumulation of activated leukocytes.

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AnimalsAntibodies, MonoclonalCapillary PermeabilityCatalaseCell AdhesionCell Adhesion MoleculesFluorescein-5-isothiocyanateHydrogen PeroxideLeukocytesMaleMesenteryMicrocirculationMicroscopy, VideoOxidation-ReductionOxidative StressPlatelet Activating FactorRatsRats, Sprague-DawleyRhodaminesSerum Albumin, BovineThioureaJournal ArticleResearch Support, U.S. Gov't, P.H.S.

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I Kurose, L W Argenbright, R Wolf, D N Granger. 1996. Oxidative stress during platelet-activating factor-induced microvascular dysfunction.. https://doi.org/10.3109/10739689609148313

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