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Heat shock. A new approach for myocardial preservation in cardiac surgery

Recent studies have indicated that heat shock (HS) induces protective genes and HS protein (HSP) expression, which enhances cellular tolerance to ischemic injury. The present study sought to determine if 42 degrees C blood cardioplegia could be used to induce HSP expression and improved myocardial s...

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Published in:Circulation (New York, N.Y.) N.Y.), 1992-11, Vol.86 (5 Suppl), p.II358-II363
Main Authors: Liu, X, Engelman, R M, Moraru, I I, Rousou, J A, Flack, 3rd, J E, Deaton, D W, Maulik, N, Das, D K
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container_end_page II363
container_issue 5 Suppl
container_start_page II358
container_title Circulation (New York, N.Y.)
container_volume 86
creator Liu, X
Engelman, R M
Moraru, I I
Rousou, J A
Flack, 3rd, J E
Deaton, D W
Maulik, N
Das, D K
description Recent studies have indicated that heat shock (HS) induces protective genes and HS protein (HSP) expression, which enhances cellular tolerance to ischemic injury. The present study sought to determine if 42 degrees C blood cardioplegia could be used to induce HSP expression and improved myocardial salvage after 2 hours of cardioplegic arrest. To study this, pig hearts (n = 6) on cardiopulmonary bypass were subjected to HS by continuous infusion to the globally arrested heart of warm blood cardioplegia (K+ = 30 meq/l) at 42 degrees C for 15 minutes followed by 2 hours of intermittent hypothermic (4-6 degrees C) hyperkalemic (30 meq/l) crystalloid cardioplegic arrest and 1 hour of reperfusion (heat shock group). The control group (n = 6) was subjected to only 2 hours of hypothermic crystalloid cardioplegic arrest followed by 1 hour of reperfusion without HS. Left ventricular performance, coronary blood flow, and creatine kinase release were determined before arrest and during reperfusion. Prearrest control biopsies were taken in a separate group of pigs (n = 6) for both HSP and superoxide dismutase activity. Additional biopsies were taken for the same measurements in both control and HS groups at the completion of reperfusion. In a single additional pig in both the control and HS groups, biopsies were taken during the study to estimate changes in HSP expression. The cytosolic protein of ventricular tissue was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the HSP70 family protein was examined by Western blot analysis using monoclonal antibodies. HSP was found to be increasingly expressed from control levels after 15 minutes of HS pretreatment, increasing progressively to a level significantly above the non-HS group. Associated with this increased expression of HSP was a significant increase in superoxide dismutase activity in the HS animals and significant improvement in both global and regional functions and reduced creatine kinase release. The results show that preconditioning the heart with HS improves postischemic ventricular performance and attenuates cellular injury. HS induces a change in cellular metabolism, prompting the expression of HSP and improving antioxidant activity, leading to improved function and reduced tissue injury during ischemia and reperfusion.
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To study this, pig hearts (n = 6) on cardiopulmonary bypass were subjected to HS by continuous infusion to the globally arrested heart of warm blood cardioplegia (K+ = 30 meq/l) at 42 degrees C for 15 minutes followed by 2 hours of intermittent hypothermic (4-6 degrees C) hyperkalemic (30 meq/l) crystalloid cardioplegic arrest and 1 hour of reperfusion (heat shock group). The control group (n = 6) was subjected to only 2 hours of hypothermic crystalloid cardioplegic arrest followed by 1 hour of reperfusion without HS. Left ventricular performance, coronary blood flow, and creatine kinase release were determined before arrest and during reperfusion. Prearrest control biopsies were taken in a separate group of pigs (n = 6) for both HSP and superoxide dismutase activity. Additional biopsies were taken for the same measurements in both control and HS groups at the completion of reperfusion. In a single additional pig in both the control and HS groups, biopsies were taken during the study to estimate changes in HSP expression. The cytosolic protein of ventricular tissue was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the HSP70 family protein was examined by Western blot analysis using monoclonal antibodies. HSP was found to be increasingly expressed from control levels after 15 minutes of HS pretreatment, increasing progressively to a level significantly above the non-HS group. Associated with this increased expression of HSP was a significant increase in superoxide dismutase activity in the HS animals and significant improvement in both global and regional functions and reduced creatine kinase release. The results show that preconditioning the heart with HS improves postischemic ventricular performance and attenuates cellular injury. 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A new approach for myocardial preservation in cardiac surgery</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Recent studies have indicated that heat shock (HS) induces protective genes and HS protein (HSP) expression, which enhances cellular tolerance to ischemic injury. The present study sought to determine if 42 degrees C blood cardioplegia could be used to induce HSP expression and improved myocardial salvage after 2 hours of cardioplegic arrest. To study this, pig hearts (n = 6) on cardiopulmonary bypass were subjected to HS by continuous infusion to the globally arrested heart of warm blood cardioplegia (K+ = 30 meq/l) at 42 degrees C for 15 minutes followed by 2 hours of intermittent hypothermic (4-6 degrees C) hyperkalemic (30 meq/l) crystalloid cardioplegic arrest and 1 hour of reperfusion (heat shock group). 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A new approach for myocardial preservation in cardiac surgery</title><author>Liu, X ; Engelman, R M ; Moraru, I I ; Rousou, J A ; Flack, 3rd, J E ; Deaton, D W ; Maulik, N ; Das, D K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p206t-913dbfeaf62a2a3e4166487e9dc6f1bad54cc7d85b4c1179d443a0a5aa253ea23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Blood</topic><topic>Blotting, Western</topic><topic>Coronary Circulation - physiology</topic><topic>Creatine Kinase - blood</topic><topic>Female</topic><topic>Gene Expression - physiology</topic><topic>Heart Arrest, Induced - methods</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Hot Temperature</topic><topic>Male</topic><topic>Myocardial Reperfusion - methods</topic><topic>Myocardial Reperfusion Injury - prevention &amp; control</topic><topic>Myocardium - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Time Factors</topic><topic>Ventricular Function, Left - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Engelman, R M</creatorcontrib><creatorcontrib>Moraru, I I</creatorcontrib><creatorcontrib>Rousou, J A</creatorcontrib><creatorcontrib>Flack, 3rd, J E</creatorcontrib><creatorcontrib>Deaton, D W</creatorcontrib><creatorcontrib>Maulik, N</creatorcontrib><creatorcontrib>Das, D K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, X</au><au>Engelman, R M</au><au>Moraru, I I</au><au>Rousou, J A</au><au>Flack, 3rd, J E</au><au>Deaton, D W</au><au>Maulik, N</au><au>Das, D K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heat shock. A new approach for myocardial preservation in cardiac surgery</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1992-11-01</date><risdate>1992</risdate><volume>86</volume><issue>5 Suppl</issue><spage>II358</spage><epage>II363</epage><pages>II358-II363</pages><issn>0009-7322</issn><abstract>Recent studies have indicated that heat shock (HS) induces protective genes and HS protein (HSP) expression, which enhances cellular tolerance to ischemic injury. The present study sought to determine if 42 degrees C blood cardioplegia could be used to induce HSP expression and improved myocardial salvage after 2 hours of cardioplegic arrest. To study this, pig hearts (n = 6) on cardiopulmonary bypass were subjected to HS by continuous infusion to the globally arrested heart of warm blood cardioplegia (K+ = 30 meq/l) at 42 degrees C for 15 minutes followed by 2 hours of intermittent hypothermic (4-6 degrees C) hyperkalemic (30 meq/l) crystalloid cardioplegic arrest and 1 hour of reperfusion (heat shock group). The control group (n = 6) was subjected to only 2 hours of hypothermic crystalloid cardioplegic arrest followed by 1 hour of reperfusion without HS. Left ventricular performance, coronary blood flow, and creatine kinase release were determined before arrest and during reperfusion. Prearrest control biopsies were taken in a separate group of pigs (n = 6) for both HSP and superoxide dismutase activity. Additional biopsies were taken for the same measurements in both control and HS groups at the completion of reperfusion. In a single additional pig in both the control and HS groups, biopsies were taken during the study to estimate changes in HSP expression. The cytosolic protein of ventricular tissue was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the HSP70 family protein was examined by Western blot analysis using monoclonal antibodies. HSP was found to be increasingly expressed from control levels after 15 minutes of HS pretreatment, increasing progressively to a level significantly above the non-HS group. Associated with this increased expression of HSP was a significant increase in superoxide dismutase activity in the HS animals and significant improvement in both global and regional functions and reduced creatine kinase release. The results show that preconditioning the heart with HS improves postischemic ventricular performance and attenuates cellular injury. HS induces a change in cellular metabolism, prompting the expression of HSP and improving antioxidant activity, leading to improved function and reduced tissue injury during ischemia and reperfusion.</abstract><cop>United States</cop><pmid>1424025</pmid></addata></record>
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subjects Animals
Blood
Blotting, Western
Coronary Circulation - physiology
Creatine Kinase - blood
Female
Gene Expression - physiology
Heart Arrest, Induced - methods
Heat-Shock Proteins - metabolism
Hot Temperature
Male
Myocardial Reperfusion - methods
Myocardial Reperfusion Injury - prevention & control
Myocardium - metabolism
Superoxide Dismutase - metabolism
Time Factors
Ventricular Function, Left - physiology
title Heat shock. A new approach for myocardial preservation in cardiac surgery
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