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Oxidative stress during platelet-activating factor-induced microvascular dysfunction
I Kurose1, L W Argenbright, R Wolf
1Department of Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
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.