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ROLE OF SUPEROXIDE DISMUTASE IN HYPOXIA‐INDUCED MICROVASCULAR INFLAMMATION.
Author(s) -
West Cameron E.,
Gonzalez Norberto C.,
Allen Julie A.,
Casillan Alfred J.,
Wood John G.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1288-b
Subject(s) - superoxide dismutase , intravital microscopy , microcirculation , inflammation , hypoxia (environmental) , vascular permeability , degranulation , chemistry , immunology , medicine , endocrinology , pharmacology , oxidative stress , oxygen , receptor , organic chemistry
Systemic hypoxia (Hx) results in leukocyte‐endothelial adhesive interactions and increased vascular permeability in post‐capillary venules, and elevated ROS levels are an early initiating event. When animals are kept in hypoxia for several weeks, the initial microvascular inflammatory response resolves. Objective: This study evaluated whether inhibition of superoxide dismutase (SOD) promoted Hx‐induced microvascular inflammation in non‐acclimatized rats and in rats acclimatized to 2 weeks of chronic hypoxia. Methods: Intravital microscopy was used to measure leukocyte adherence and mast cell degranulation (MCD) in the mesenteric microcirculation of anesthetized rats. Results: Hx caused rapid MCD and leukocyte adherence to mesenteric venules of non‐acclimatized rats. The SOD inhibitor DDC did not significantly affect the magnitude of these responses. In contrast, there was no microvascular inflammation during Hx in acclimatized rats. However, Hx plus DDC resulted in MCD and leukocyte adherence in acclimatized rats. Conclusion: These results indicate that superoxide dismutase plays a major role in attenuating Hx‐induced microvascular inflammation in acclimatized rats. Supported by HL64195 and HL39443.