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Hypoxia reoxygenation‐induced injury of cultured pulmonary microvessel endothelial cells
Author(s) -
Wiles Marc E.,
Hechtman Herbert B.,
Morel Nicole M.L.,
Shepro David
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.53.5.490
Subject(s) - hypoxia (environmental) , microvessel , reactive oxygen species , superoxide dismutase , reperfusion injury , immunology , superoxide , biology , ischemia , pharmacology , andrology , angiogenesis , oxygen , chemistry , endocrinology , medicine , biochemistry , cancer research , oxidative stress , enzyme , organic chemistry
Polymorphonuclear leukocyte (PMN) sequestration within the pulmonary microvasculature is known to occur in association with ischemia/reoxygenation (I/R). This sequestration is dependent on eicosanoids and reactive oxygen species. PMN sequestration within the lungs suggests that pulmonary microvascular endothelial cells (MECs) may in part regulate the I/R response. Simulating I/R, we examined the effect of hypoxia/reoxy‐ genation (H/R) on pulmonary MECs in vitro, with and without PMNs. Significant cellular injury, assessed by 51 Cr release, occurred upon reoxygenation of MECs (P < .01). Addition of PMNs to the H/R‐injured monolayers did not increase MEC injury. Reoxygenation of MECs also resulted in increased thromboxane (Tx) B2 production compared to controls (P < .01). Inhibition of Tx secretion by aspirin reduced H/R‐induced PMN adhesion to MECs (P< .01). Furthermore, H/R‐induced increases in PMN‐MEC adhesion were prevented by al‐ lopurinol and superoxide dismutase (P< .01). These data suggest that the pulmonary response to H/R is mediated by MEC generation of reactive oxygen radical species and Tx, which promotes increased PMN adhesion.