Cited by 293Nitric Oxide and Endothelin EffectsNeutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stress

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Modulation of leukocyte–endothelial interactions by reactive metabolites of oxygen and nitrogen: relevance to ischemic heart disease

Grisham, Matthew B., Granger, D.Neil, Lefer, David J.·1998·Free Radical Biology and Medicine

DOI 10.1016/s0891-5849(98)00094-x

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Abstract

Ischemia and reperfusion (I/R) are thought to play an important role in the pathophysiology of ischemic diseases of the heart. It is now well appreciated that leukocyte-endothelial cell interactions are important determinants for I/R-induced microvascular injury and dysfunction. There is a growing body of experimental data to suggest that reactive metabolites of oxygen and nitrogen are important physiological modulators of leukocyte-endothelial cell interactions. A number of investigators have demonstrated that I/R enhances oxidant production within the microcirculation resulting in increases in leukocyte adhesion and transendothelial cell migration. Several other studies have shown that exogenous nitric oxide (NO) donors may attenuate leukocyte and platelet adhesion and/or aggregation in a number of different inflammatory conditions including I/R. The objective of this review is to discuss the physiological chemistry of reactive metabolites of oxygen and nitrogen with special attention given to those interactions that may modulate leukocyte-endothelial cell interactions, provide an overview of the evidence implicating reactive metabolites of oxygen and nitrogen as modulators of leukocyte-endothelial cell interactions in vivo, and discuss how these mechanisms may be involved in the pathophysiology of ischemic heart disease.

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Effects of jejunum ATPase activity and antioxidant function on the growth performance, feed conversion efficiency, and intestinal flora of Hu sheep (Ovis aries)Preprint
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Self-citation
Additional file 1 of Relationship between jejunum ATPase activity and antioxidant function on the growth performance, feed conversion efficiency, and jejunum microbiota in Hu sheep (Ovis aries)
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Untitled work
(1999) · doi:10.1002/(sici)1096-9926(199909)60:3

Authors: Grisham, M. B., Granger, D. N., & Lefer, D. J.
Affiliations: Louisiana State University (US)
Corresponding author: Grisham, Matthew B.
ORCID: Grisham, Matthew B.
Lefer, David J.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 1998-09
Volume: 25
Issue: 4-5
Pages: 404-433
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/s0891-5849(98)00094-x
OpenAlex: W2094525668
Cited by: 293
References: 211
Citations by year: 2025: 5 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 11 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 6 · 2012: 11
FWCI: 3.21
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01dk047663-06)
National Institute of Diabetes and Digestive and Kidney Diseases (P01 DK-43785, DK-47663, P01DK043785)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: reactive oxygen species, reactive nitrogen species, leukocyte-endothelium interaction, ischemia-reperfusion injury, ischemic heart disease, nitric oxide donors, leukocyte adhesion, transendothelial migration, platelet aggregation, microvascular damage, oxidative stress
MeSH terms: Animals, Cell Adhesion, Endothelium, Vascular, Humans, Iron, Leukocytes, Nitric Oxide, Oxidation-Reduction, Myocardial Reperfusion Injury, Myocardial Ischemia, Reactive Oxygen Species

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Modulation of leukocyte–endothelial interactions by reactive metabolites of oxygen and nitrogen: relevance to ischemic heart disease

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