Induction of heat-shock protein 72 protects against ischemia/reperfusion in rat small intestine

Background & Aims: Induction of heat-shock protein 72 is associated with enhanced tolerance to subsequent nonthermal stresses. This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. Methods: Groups of nonheated and heated rats und...

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Veröffentlicht in:Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 1995-08, Vol.109 (2), p.505-515
Hauptverfasser: Stojadinovic, Alexander, Kiang, Juliann, Smallridge, Robert, Galloway, Richard, Shea-Donohue, Terez
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container_end_page 515
container_issue 2
container_start_page 505
container_title Gastroenterology (New York, N.Y. 1943)
container_volume 109
creator Stojadinovic, Alexander
Kiang, Juliann
Smallridge, Robert
Galloway, Richard
Shea-Donohue, Terez
description Background & Aims: Induction of heat-shock protein 72 is associated with enhanced tolerance to subsequent nonthermal stresses. This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. Methods: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5–42°C for 15–20 minutes was followed by passive cooling 2–3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E 2 and leukotriene B 4 and for histological assessment of mucosal injury and number of neutrophils. Results: Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B 4 production. Levels of leukotriene B 4 and numbers of neutrophils were well correlated in nonheated ( r = 0.72) but not in heated groups ( r = −0.16). The elevation of prostaglandin E 2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. Conclusions: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B 4 production and subsequent prevention of neutrophil activation and chemotaxis.
doi_str_mv 10.1016/0016-5085(95)90339-9
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This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. Methods: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5–42°C for 15–20 minutes was followed by passive cooling 2–3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E 2 and leukotriene B 4 and for histological assessment of mucosal injury and number of neutrophils. Results: Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B 4 production. Levels of leukotriene B 4 and numbers of neutrophils were well correlated in nonheated ( r = 0.72) but not in heated groups ( r = −0.16). The elevation of prostaglandin E 2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. Conclusions: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B 4 production and subsequent prevention of neutrophil activation and chemotaxis.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1016/0016-5085(95)90339-9</identifier><identifier>PMID: 7615200</identifier><identifier>CODEN: GASTAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - physiology ; Fever ; Gastroenterology. Liver. Pancreas. Abdomen ; Heart Rate - physiology ; Heat-Shock Proteins - biosynthesis ; HSP72 Heat-Shock Proteins ; Intestinal Mucosa - blood supply ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine, Small - blood supply ; Intestine, Small - metabolism ; Intestine, Small - pathology ; Leukotriene B4 - biosynthesis ; Male ; Medical sciences ; Neutrophils - physiology ; Other diseases. Semiology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention &amp; control ; Stomach. Duodenum. Small intestine. Colon. Rectum. 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This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. Methods: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5–42°C for 15–20 minutes was followed by passive cooling 2–3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E 2 and leukotriene B 4 and for histological assessment of mucosal injury and number of neutrophils. Results: Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B 4 production. Levels of leukotriene B 4 and numbers of neutrophils were well correlated in nonheated ( r = 0.72) but not in heated groups ( r = −0.16). The elevation of prostaglandin E 2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. Conclusions: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B 4 production and subsequent prevention of neutrophil activation and chemotaxis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - physiology</subject><subject>Fever</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Heart Rate - physiology</subject><subject>Heat-Shock Proteins - biosynthesis</subject><subject>HSP72 Heat-Shock Proteins</subject><subject>Intestinal Mucosa - blood supply</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine, Small - blood supply</subject><subject>Intestine, Small - metabolism</subject><subject>Intestine, Small - pathology</subject><subject>Leukotriene B4 - biosynthesis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neutrophils - physiology</subject><subject>Other diseases. Semiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention &amp; control</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Heart Rate - physiology</topic><topic>Heat-Shock Proteins - biosynthesis</topic><topic>HSP72 Heat-Shock Proteins</topic><topic>Intestinal Mucosa - blood supply</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine, Small - blood supply</topic><topic>Intestine, Small - metabolism</topic><topic>Intestine, Small - pathology</topic><topic>Leukotriene B4 - biosynthesis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neutrophils - physiology</topic><topic>Other diseases. Semiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - prevention &amp; control</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stojadinovic, Alexander</creatorcontrib><creatorcontrib>Kiang, Juliann</creatorcontrib><creatorcontrib>Smallridge, Robert</creatorcontrib><creatorcontrib>Galloway, Richard</creatorcontrib><creatorcontrib>Shea-Donohue, Terez</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stojadinovic, Alexander</au><au>Kiang, Juliann</au><au>Smallridge, Robert</au><au>Galloway, Richard</au><au>Shea-Donohue, Terez</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of heat-shock protein 72 protects against ischemia/reperfusion in rat small intestine</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>1995-08-01</date><risdate>1995</risdate><volume>109</volume><issue>2</issue><spage>505</spage><epage>515</epage><pages>505-515</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><coden>GASTAB</coden><abstract>Background &amp; Aims: Induction of heat-shock protein 72 is associated with enhanced tolerance to subsequent nonthermal stresses. This study evaluated whether induction of heat-shock protein 72 protects against intestinal ischemia/reperfusion injury. Methods: Groups of nonheated and heated rats underwent sham operation, 30 minutes of ischemia by occlusion of the superior mesenteric artery, or ischemia followed by 60 minutes of reperfusion. Whole-body hyperthermia to a core temperature of 41.5–42°C for 15–20 minutes was followed by passive cooling 2–3 hours before the experiment. Samples of small intestine were obtained for determination of heat-shock protein 72 production and ex vivo generation of prostaglandin E 2 and leukotriene B 4 and for histological assessment of mucosal injury and number of neutrophils. Results: Hyperthermia significantly increased heat-shock protein 72 production and significantly reduced ischemia/reperfusion-induced mucosal injury, neutrophilic infiltration, and leukotriene B 4 production. Levels of leukotriene B 4 and numbers of neutrophils were well correlated in nonheated ( r = 0.72) but not in heated groups ( r = −0.16). The elevation of prostaglandin E 2 levels in response to ischemia and reperfusion was unaltered by hyperthermia. Conclusions: The mechanism of heat stress-induced protection against intestinal ischemia/reperfusion injury involves inhibition of leukotriene B 4 production and subsequent prevention of neutrophil activation and chemotaxis.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>7615200</pmid><doi>10.1016/0016-5085(95)90339-9</doi><tpages>11</tpages></addata></record>
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subjects Animals
Biological and medical sciences
Blood Pressure - physiology
Fever
Gastroenterology. Liver. Pancreas. Abdomen
Heart Rate - physiology
Heat-Shock Proteins - biosynthesis
HSP72 Heat-Shock Proteins
Intestinal Mucosa - blood supply
Intestinal Mucosa - metabolism
Intestinal Mucosa - pathology
Intestine, Small - blood supply
Intestine, Small - metabolism
Intestine, Small - pathology
Leukotriene B4 - biosynthesis
Male
Medical sciences
Neutrophils - physiology
Other diseases. Semiology
Rats
Rats, Sprague-Dawley
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Reperfusion Injury - prevention & control
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
title Induction of heat-shock protein 72 protects against ischemia/reperfusion in rat small intestine
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