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Oxidative Stress During Platelet‐Activating Factor‐Induced Microvascular Dysfunction
Author(s) -
Kurose Iwao,
Argenbright Lawrence W.,
Wolf Robert,
Granger D. Neil
Publication year - 1996
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.3109/10739689609148313
Subject(s) - platelet activating factor , fluorescein isothiocyanate , extravasation , albumin , oxidative stress , endothelial stem cell , chemistry , platelet , vascular permeability , biochemistry , cd18 , pharmacology , immunology , integrin alpha m , medicine , cell , endocrinology , in vitro , physics , quantum mechanics , fluorescence
Objective : To assess the potential contribution of hydrogen peroxide (H 2 O 2 ) 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 H 2 O 2 in mesenteric tissue was monitored using the H 2 O 2 ‐sensitive fluorochrome, dihydrorhodamine 123 (DHR). PAF elicited a rapid increase in both the rate of 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 cell 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.