ArticleAnnals of surgery2000
Group IIA phospholipase A2 mediates lung injury in intestinal ischemia-reperfusion.
Article in Annals of surgery, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 63 citations in OpenAlex.
- Refining the value of secretory phospholipase A2 as a predictor of acute chest syndrome in sickle cell disease: results of a feasibility study (PROACTIVE).British journal of haematology · 2012Trial
- Analysis of polyunsaturated fatty acids and the omega-6 inflammatory pathway in hepatic ischemia/re-perfusion injury.Molecular medicine reports · 2015Article
- Inhibition of neutral sphingomyelinase decreases arachidonic acid mediated inflammation in liver ischemia-reperfusion injury.International journal of clinical and experimental pathology · 2014Article
- Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.PloS one · 2013Article
- Claude H. Organ, Jr. memorial lecture: splanchnic hypoperfusion provokes acute lung injury via a 5-lipoxygenase-dependent mechanism.American journal of surgery · 2010Article
- Intestinal lipid alterations occur prior to antibody-induced prostaglandin E2 production in a mouse model of ischemia/reperfusion.Biochimica et biophysica acta · 2010Article
- Trans-Serosal Leakage of Proinflammatory Mediators during Abdominal Aortic Aneurysm Repair: Role of Phospholipase A2 in Activating Leukocytes.Annals of vascular diseases · 2010Article
- The synergistic inhibition of atherogenesis in apoE-/- mice between pravastatin and the sPLA2 inhibitor varespladib (A-002).Journal of lipid research · 2009Article
- Surgical manipulation of the intestine results in quantitative and qualitative alterations in luminal Escherichia coli.Annals of surgery · 2004Article
- Comparative protection against rat intestinal reperfusion injury by a new inhibitor of sPLA2, COX-1 and COX-2 selective inhibitors, and an LTC4 receptor antagonist.British journal of pharmacology · 2003Article
- Enteral nutrition prevents remote organ injury and death after a gut ischemic insult.Annals of surgery · 2001Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo assess the mechanistic role of group IIA phospholipase A2 (PLA2) in the process of local and distant organ injury after intestinal ischemia-reperfusion. SUMMARY BACKGROUND DATA: Intestinal ischemia-reperfusion produces lung injury by a mechanism that involves PLA2 activation, but it is unclear which isozyme is responsible for this phenomenon. Group IIA PLA2, one of the secreted forms of PLA2, is known to play a pivotal role in a variety of inflammatory reactions.
methodsRats underwent 45 minutes of superior mesenteric artery occlusion in the presence and absence of pretreatment with group IIA PLA2 inhibitor, S-5920/LY315920Na (20 mg/kg, subcutaneously, 30 minutes before clamping). At 2 hours of reperfusion, intestinal and lung leak was assessed by 125I-albumin tissue/blood ratio, and liver injury was estimated by serum alanine aminotransferase. PLA2 activities in tissues and sera were quantitated by phosphatidyl-glycerol/sodium cholate mixed micelle assay. PLA2 activities in tissues were also measured after in vitro preincubation with EDTA, S-5920/LY315920Na, or antirat group IIA PLA2 antibody.
resultsIntestinal ischemia-reperfusion provoked intestinal leak, liver injury, and lung leak, whereas tissue PLA2 activity was decreased in the intestine, unchanged in the liver, and increased in the lung. Serum PLA2 activities were increased in the portal and systemic circulation during ischemia. Pretreatment with S-5920/LY315920Na eliminated PLA2 activities in all tissues and sera and only abolished lung leak. The in vitro experiment revealed that most of the intestinal and lung PLA2 activities were inhibited by EDTA, S-5920/LY315920Na, and antirat group IIA PLA2 antibody, but hepatic PLA2 activity was not.
conclusionIntestinal ischemia-reperfusion appears to produce lung injury by a mechanism that involves group IIA PLA2 activation. Intestinal ischemia-reperfusion is likely to promote intestinal and hepatic injury independent of group IIA PLA2.
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