Pathophysiology of ischaemia reperfusion injury: Central role of the neutrophil

Welbourn, C R B; Goldman, G; Paterson, I S; Valeri, C R; Shepro, D; Hechtman, H B

doi:10.1002/bjs.1800780607

Cited by 501Neutrophil, Myeloperoxidase and Oxidative MechanismsCardiac Ischemia and ReperfusionInflammation biomarkers and pathways

Pathophysiology of ischaemia reperfusion injury: Central role of the neutrophil

Welbourn, C R B, Goldman, G, Paterson, I S, Valeri, C R, Shepro, D, Hechtman, H B·1991·Journal of British Surgery

DOI 10.1002/bjs.1800780607

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Abstract

Ischaemia is a common clinical event leading to local and remote injury. Evidence indicates that tissue damage is largely caused by activated neutrophils which accumulate when the tissue is reperfused. If the area of ischaemic tissue is large, neutrophils also sequester in the lungs, inducing non-cardiogenic pulmonary oedema. Ischaemia reperfusion injury is initiated by production of reactive oxygen species which initially appear responsible for the generation of chemotactic activity for neutrophils. Later, once adherent to endothelium, neutrophils mediate damage by secretion of additional reactive oxygen species as well as proteolytic enzymes, in particular elastase. Therapeutic options for limiting ischaemia reperfusion injury include inhibition of oxygen radical formation, pharmacological prevention of neutrophil activation and chemotaxis, and also the use of monoclonal antibodies which prevent neutrophil-endothelial adhesion, a prerequisite for injury.

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An excessive PMN response has previously been implicated in the pathogenesis of capillary leak syndromes resulting in decreased perfusion and end-organ damage, including acute respiratory distress syndrome and MOF.
“whereas an excessive PMN response has previously been implicated in the pathogenesis of capillary leak syndromes resulting in decreased perfusion and end-organ damage, including acute respiratory distress syndrome and MOF [22-24].”
From Oral neutrophils are an independent marker of the systemic inflammatory response after cardiac bypass (2014) · cites this paper as [24]

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Authors: Welbourn, C. R. B., Goldman, G., Paterson, I. S., Valeri, C. R., Shepro, D., & Hechtman, H. B.
Affiliations: Brigham and Women's Hospital (US)
Boston University (US)
Naval Blood Research Laboratory, Boston University , Boston MA,
Corresponding author: Hechtman, H B
Venue: Journal of British Surgery
Publisher: Oxford University Press (OUP)
Published: 1991-06-01
Volume: 78
Issue: 6
Pages: 651-655
ISSN: 0007-1323 (ISSN-L)
1365-2168
DOI: 10.1002/bjs.1800780607
OpenAlex: W1971917696
Cited by: 501
References: 52
Citations by year: 2025: 1 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 7 · 2020: 13 · 2019: 8 · 2018: 8 · 2017: 4 · 2016: 6 · 2015: 10 · 2014: 7 · 2013: 11 · 2012: 11
FWCI: 2.53
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
Locations: British journal of surgery (publishedVersion)
PubMed (publishedVersion)
Funders: The National Institute of Health (GM24891-11, GM35141-04, HL16714-13)
The Brigham Surgical Group Inc. and the Trauma Research Foundation
Topics: Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords: ischemia-reperfusion injury, neutrophils, reactive oxygen species, neutrophil chemotaxis, neutrophil-endothelial adhesion, elastase, non-cardiogenic pulmonary edema, neutrophil activation, monoclonal antibodies, tissue damage
MeSH terms: Arachidonic Acids, Cell Adhesion, Humans, Neutrophils, Reperfusion Injury

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Pathophysiology of ischaemia reperfusion injury: Central role of the neutrophil

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