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Thermotolerance induces heat shock protein 72 expression and protects against ischaemia-reperfusion-induced lung injury

Background Ischaemia–reperfusion injury is mediated by neutrophil–endothelial interaction. Induction of heat shock proteins attenuates neutrophil–endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neutrophil‐mediated lun...

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Published in:British journal of surgery 1998-07, Vol.85 (7), p.943-946
Main Authors: Javadpour, M., Kelly, C. J., Chen, G., Stokes, K., Leahy, A., Bouchier-Hayes, D. J.
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container_end_page 946
container_issue 7
container_start_page 943
container_title British journal of surgery
container_volume 85
creator Javadpour, M.
Kelly, C. J.
Chen, G.
Stokes, K.
Leahy, A.
Bouchier-Hayes, D. J.
description Background Ischaemia–reperfusion injury is mediated by neutrophil–endothelial interaction. Induction of heat shock proteins attenuates neutrophil–endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neutrophil‐mediated lung injury in an animal model of lower torso ischaemia–reperfusion. Methods Sprague‐Dawley rats were randomized into: control, ischaemia–reperfusion, and ischaemia–reperfusion preconditioned with hyperthermia groups. Ischaemia–reperfusion injury was induced by infrarenal aortic clamping for 30 min and reperfusion for 120 min. Thermotolerance was induced by raising the core body temperature to 40·5–41·5°C for 15 min, 18 h before ischaemia–reperfusion. Wet:dry lung (W:D) weight ratio, bronchoalveolar lavage protein (BALprot) concentration, tissue myeloperoxidase (MPO) activity and bronchoalveolar lavage polymorphonuclear neutrophil (BAL PMN) count were measured. Heat shock protein 72 (hsp72) expression in lung, intestine and mesentery was measured using Western immunoblotting. Results Ischaemia–reperfusion resulted in a significant increase in tissue oedema (W:D weight ratio) and BALprot concentration. In addition there was a marked increase in tissue neutrophil infiltration (MPO activity, BAL PMN concentration). Preconditioning with hyperthemia resulted in increased expression of hsp72 and significantly reduced tissue oedema and neutrophil infiltration. Conclusion Thermal preconditioning protects against neutrophil‐mediated ischaemia–reperfusion‐induced lung injury, possibly by increasing the expression of heat shock proteins. © 1998 British Journal of Surgery Society Ltd
doi_str_mv 10.1046/j.1365-2168.1998.00722.x
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J. ; Chen, G. ; Stokes, K. ; Leahy, A. ; Bouchier-Hayes, D. J.</creator><creatorcontrib>Javadpour, M. ; Kelly, C. J. ; Chen, G. ; Stokes, K. ; Leahy, A. ; Bouchier-Hayes, D. J.</creatorcontrib><description>Background Ischaemia–reperfusion injury is mediated by neutrophil–endothelial interaction. Induction of heat shock proteins attenuates neutrophil–endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neutrophil‐mediated lung injury in an animal model of lower torso ischaemia–reperfusion. Methods Sprague‐Dawley rats were randomized into: control, ischaemia–reperfusion, and ischaemia–reperfusion preconditioned with hyperthermia groups. Ischaemia–reperfusion injury was induced by infrarenal aortic clamping for 30 min and reperfusion for 120 min. Thermotolerance was induced by raising the core body temperature to 40·5–41·5°C for 15 min, 18 h before ischaemia–reperfusion. Wet:dry lung (W:D) weight ratio, bronchoalveolar lavage protein (BALprot) concentration, tissue myeloperoxidase (MPO) activity and bronchoalveolar lavage polymorphonuclear neutrophil (BAL PMN) count were measured. Heat shock protein 72 (hsp72) expression in lung, intestine and mesentery was measured using Western immunoblotting. Results Ischaemia–reperfusion resulted in a significant increase in tissue oedema (W:D weight ratio) and BALprot concentration. In addition there was a marked increase in tissue neutrophil infiltration (MPO activity, BAL PMN concentration). Preconditioning with hyperthemia resulted in increased expression of hsp72 and significantly reduced tissue oedema and neutrophil infiltration. Conclusion Thermal preconditioning protects against neutrophil‐mediated ischaemia–reperfusion‐induced lung injury, possibly by increasing the expression of heat shock proteins. © 1998 British Journal of Surgery Society Ltd</description><identifier>ISSN: 0007-1323</identifier><identifier>EISSN: 1365-2168</identifier><identifier>DOI: 10.1046/j.1365-2168.1998.00722.x</identifier><identifier>PMID: 9692569</identifier><identifier>CODEN: BJSUAM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Bronchoalveolar Lavage Fluid - chemistry ; Constriction ; Heat-Shock Proteins - metabolism ; HSP72 Heat-Shock Proteins ; Hyperthermia, Induced - methods ; Intestines - metabolism ; Lung - blood supply ; Lung - metabolism ; Lung Injury ; Male ; Medical sciences ; Mesentery - metabolism ; Microcirculation ; Neutrophils - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - prevention &amp; control ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart</subject><ispartof>British journal of surgery, 1998-07, Vol.85 (7), p.943-946</ispartof><rights>1998 British Journal of Surgery Society Ltd</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4470-b8d664be826bce18bd6a0d5060e79256e7eda461e2853b6a8140ac851adac3f33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=2301987$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9692569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Javadpour, M.</creatorcontrib><creatorcontrib>Kelly, C. J.</creatorcontrib><creatorcontrib>Chen, G.</creatorcontrib><creatorcontrib>Stokes, K.</creatorcontrib><creatorcontrib>Leahy, A.</creatorcontrib><creatorcontrib>Bouchier-Hayes, D. J.</creatorcontrib><title>Thermotolerance induces heat shock protein 72 expression and protects against ischaemia-reperfusion-induced lung injury</title><title>British journal of surgery</title><addtitle>Br J Surg</addtitle><description>Background Ischaemia–reperfusion injury is mediated by neutrophil–endothelial interaction. Induction of heat shock proteins attenuates neutrophil–endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neutrophil‐mediated lung injury in an animal model of lower torso ischaemia–reperfusion. Methods Sprague‐Dawley rats were randomized into: control, ischaemia–reperfusion, and ischaemia–reperfusion preconditioned with hyperthermia groups. Ischaemia–reperfusion injury was induced by infrarenal aortic clamping for 30 min and reperfusion for 120 min. Thermotolerance was induced by raising the core body temperature to 40·5–41·5°C for 15 min, 18 h before ischaemia–reperfusion. Wet:dry lung (W:D) weight ratio, bronchoalveolar lavage protein (BALprot) concentration, tissue myeloperoxidase (MPO) activity and bronchoalveolar lavage polymorphonuclear neutrophil (BAL PMN) count were measured. Heat shock protein 72 (hsp72) expression in lung, intestine and mesentery was measured using Western immunoblotting. Results Ischaemia–reperfusion resulted in a significant increase in tissue oedema (W:D weight ratio) and BALprot concentration. In addition there was a marked increase in tissue neutrophil infiltration (MPO activity, BAL PMN concentration). Preconditioning with hyperthemia resulted in increased expression of hsp72 and significantly reduced tissue oedema and neutrophil infiltration. Conclusion Thermal preconditioning protects against neutrophil‐mediated ischaemia–reperfusion‐induced lung injury, possibly by increasing the expression of heat shock proteins. © 1998 British Journal of Surgery Society Ltd</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Constriction</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>HSP72 Heat-Shock Proteins</subject><subject>Hyperthermia, Induced - methods</subject><subject>Intestines - metabolism</subject><subject>Lung - blood supply</subject><subject>Lung - metabolism</subject><subject>Lung Injury</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesentery - metabolism</subject><subject>Microcirculation</subject><subject>Neutrophils - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - prevention &amp; control</subject><subject>Surgery (general aspects). 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J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4470-b8d664be826bce18bd6a0d5060e79256e7eda461e2853b6a8140ac851adac3f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Constriction</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>HSP72 Heat-Shock Proteins</topic><topic>Hyperthermia, Induced - methods</topic><topic>Intestines - metabolism</topic><topic>Lung - blood supply</topic><topic>Lung - metabolism</topic><topic>Lung Injury</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesentery - metabolism</topic><topic>Microcirculation</topic><topic>Neutrophils - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - prevention &amp; control</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Javadpour, M.</creatorcontrib><creatorcontrib>Kelly, C. J.</creatorcontrib><creatorcontrib>Chen, G.</creatorcontrib><creatorcontrib>Stokes, K.</creatorcontrib><creatorcontrib>Leahy, A.</creatorcontrib><creatorcontrib>Bouchier-Hayes, D. J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Javadpour, M.</au><au>Kelly, C. J.</au><au>Chen, G.</au><au>Stokes, K.</au><au>Leahy, A.</au><au>Bouchier-Hayes, D. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thermotolerance induces heat shock protein 72 expression and protects against ischaemia-reperfusion-induced lung injury</atitle><jtitle>British journal of surgery</jtitle><addtitle>Br J Surg</addtitle><date>1998-07</date><risdate>1998</risdate><volume>85</volume><issue>7</issue><spage>943</spage><epage>946</epage><pages>943-946</pages><issn>0007-1323</issn><eissn>1365-2168</eissn><coden>BJSUAM</coden><abstract>Background Ischaemia–reperfusion injury is mediated by neutrophil–endothelial interaction. Induction of heat shock proteins attenuates neutrophil–endothelial interactions. The aim of this study was to determine whether thermal preconditioning could have a protective effect on neutrophil‐mediated lung injury in an animal model of lower torso ischaemia–reperfusion. Methods Sprague‐Dawley rats were randomized into: control, ischaemia–reperfusion, and ischaemia–reperfusion preconditioned with hyperthermia groups. Ischaemia–reperfusion injury was induced by infrarenal aortic clamping for 30 min and reperfusion for 120 min. Thermotolerance was induced by raising the core body temperature to 40·5–41·5°C for 15 min, 18 h before ischaemia–reperfusion. Wet:dry lung (W:D) weight ratio, bronchoalveolar lavage protein (BALprot) concentration, tissue myeloperoxidase (MPO) activity and bronchoalveolar lavage polymorphonuclear neutrophil (BAL PMN) count were measured. Heat shock protein 72 (hsp72) expression in lung, intestine and mesentery was measured using Western immunoblotting. Results Ischaemia–reperfusion resulted in a significant increase in tissue oedema (W:D weight ratio) and BALprot concentration. In addition there was a marked increase in tissue neutrophil infiltration (MPO activity, BAL PMN concentration). Preconditioning with hyperthemia resulted in increased expression of hsp72 and significantly reduced tissue oedema and neutrophil infiltration. Conclusion Thermal preconditioning protects against neutrophil‐mediated ischaemia–reperfusion‐induced lung injury, possibly by increasing the expression of heat shock proteins. © 1998 British Journal of Surgery Society Ltd</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>9692569</pmid><doi>10.1046/j.1365-2168.1998.00722.x</doi><tpages>4</tpages></addata></record>
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ispartof British journal of surgery, 1998-07, Vol.85 (7), p.943-946
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1365-2168
language eng
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source Oxford Journals Online
subjects Animals
Biological and medical sciences
Blotting, Western
Bronchoalveolar Lavage Fluid - chemistry
Constriction
Heat-Shock Proteins - metabolism
HSP72 Heat-Shock Proteins
Hyperthermia, Induced - methods
Intestines - metabolism
Lung - blood supply
Lung - metabolism
Lung Injury
Male
Medical sciences
Mesentery - metabolism
Microcirculation
Neutrophils - metabolism
Rats
Rats, Sprague-Dawley
Reperfusion Injury - prevention & control
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Surgery of the heart
title Thermotolerance induces heat shock protein 72 expression and protects against ischaemia-reperfusion-induced lung injury
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