Myocardial Sulfhydryl Pool Alterations Occur During Reperfusion After Brief and Prolonged Myocardial Ischemia In Vivo

Myocardial sulfhydryl (SH)-containing compounds, including reduced glutathione (GSH), are both defenses against and potential markers of reactive oxygen metabolite injury during ischemia and reperfusion. We examined the alterations in GSH and other myocardial SH pools during reperfusion in anestheti...

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Published in:Circulation research 1991-02, Vol.68 (2), p.605-613
Main Authors: Lesnefsky, Edward J, Dauber, Ira M, Horwitz, Lawrence D
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary Disease - metabolism
Coronary heart disease
Dogs
Female
Glutathione - analogs & derivatives
Glutathione - metabolism
Glutathione Disulfide
Heart
Male
Medical sciences
Myocardial Reperfusion
Myocardium - metabolism
Sulfhydryl Compounds - metabolism
Time Factors
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container_title Circulation research
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creator Lesnefsky, Edward J
Dauber, Ira M
Horwitz, Lawrence D
description Myocardial sulfhydryl (SH)-containing compounds, including reduced glutathione (GSH), are both defenses against and potential markers of reactive oxygen metabolite injury during ischemia and reperfusion. We examined the alterations in GSH and other myocardial SH pools during reperfusion in anesthetized dogs exposed to brief (15 minutes, n=7) or prolonged (90 minutes, n=6) regional ischemia caused by occlusion of the left anterior descending artery. Ninety minutes of ischemia followed by 5 hours of reperfusion, which resulted in myocardial necrosis of 43.9±4.0% of the area at risk, caused a 22% reduction in total myocardial SH groups (p
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We examined the alterations in GSH and other myocardial SH pools during reperfusion in anesthetized dogs exposed to brief (15 minutes, n=7) or prolonged (90 minutes, n=6) regional ischemia caused by occlusion of the left anterior descending artery. Ninety minutes of ischemia followed by 5 hours of reperfusion, which resulted in myocardial necrosis of 43.9±4.0% of the area at risk, caused a 22% reduction in total myocardial SH groups (p<0.01), a 57% decrease in nonprotein myocardial SH groups (p<0.01), a 56% decrease in GSH (p<0.01), and a 62% decrease in non-GSH, nonprotein SH groups (p<0.02). However, protein SH groups were not significantly reduced (12% decrease, p=NS). Also, myocardial release of GSH and oxidized glutathione (GSSG) into the coronary venous effluent occurred during early reperfusion. In contrast, 15 minutes of ischemia, followed by 30 minutes of reperfusion, did not alter myocardial total SH groups, protein SH groups, or GSH (9% decrease, p=NS); nor was there reperfusion release of GSH or GSSG. However, even with brief ischemia, nonprotein SH groups decreased 23% (p<0.05), due mainly to a 59% decrease in the non-GSH, nonprotein SH pool (p<0.05). These changes after brief ischemia occurred without alterations in myocardial GSSG or the GSH/GSSG ratio. Thus, the pattern of depletion of myocardial SH pools during reperfusion differs depending on the duration of the preceding ischemia. The decreases in nonprotein SH and in non-GSH, nonprotein SH pools did not occur (9% decrease and 3% decrease, respectively; both p=NS) in dogs subjected to brief occlusion (n=6) that were treated before coronary occlusion with 500 mg/kg i.v. dimethylthiourea, an intracellular scavenger of H2O2 and OH. Since only the non-GSH, nonprotein SH pool decreased significantly after brief ischemia and since this decrease could be prevented by antioxidant intervention, this pool appears to be the most sensitive SH indicator of reactive oxygen metabolite-induced myocardial ischemia/ reperfusion injury. (Circulation Research 1991:68:605–613)]]></description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.68.2.605</identifier><identifier>PMID: 1991359</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary Disease - metabolism ; Coronary heart disease ; Dogs ; Female ; Glutathione - analogs &amp; derivatives ; Glutathione - metabolism ; Glutathione Disulfide ; Heart ; Male ; Medical sciences ; Myocardial Reperfusion ; Myocardium - metabolism ; Sulfhydryl Compounds - metabolism ; Time Factors</subject><ispartof>Circulation research, 1991-02, Vol.68 (2), p.605-613</ispartof><rights>1991 American Heart Association, Inc.</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4247-f5d70baae7b66a00839eae979b37a6ba5b8e7e1ab4ed9be946fb00a53efc03dd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=4975488$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1991359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lesnefsky, Edward J</creatorcontrib><creatorcontrib>Dauber, Ira M</creatorcontrib><creatorcontrib>Horwitz, Lawrence D</creatorcontrib><title>Myocardial Sulfhydryl Pool Alterations Occur During Reperfusion After Brief and Prolonged Myocardial Ischemia In Vivo</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description><![CDATA[Myocardial sulfhydryl (SH)-containing compounds, including reduced glutathione (GSH), are both defenses against and potential markers of reactive oxygen metabolite injury during ischemia and reperfusion. We examined the alterations in GSH and other myocardial SH pools during reperfusion in anesthetized dogs exposed to brief (15 minutes, n=7) or prolonged (90 minutes, n=6) regional ischemia caused by occlusion of the left anterior descending artery. Ninety minutes of ischemia followed by 5 hours of reperfusion, which resulted in myocardial necrosis of 43.9±4.0% of the area at risk, caused a 22% reduction in total myocardial SH groups (p<0.01), a 57% decrease in nonprotein myocardial SH groups (p<0.01), a 56% decrease in GSH (p<0.01), and a 62% decrease in non-GSH, nonprotein SH groups (p<0.02). However, protein SH groups were not significantly reduced (12% decrease, p=NS). Also, myocardial release of GSH and oxidized glutathione (GSSG) into the coronary venous effluent occurred during early reperfusion. In contrast, 15 minutes of ischemia, followed by 30 minutes of reperfusion, did not alter myocardial total SH groups, protein SH groups, or GSH (9% decrease, p=NS); nor was there reperfusion release of GSH or GSSG. However, even with brief ischemia, nonprotein SH groups decreased 23% (p<0.05), due mainly to a 59% decrease in the non-GSH, nonprotein SH pool (p<0.05). These changes after brief ischemia occurred without alterations in myocardial GSSG or the GSH/GSSG ratio. Thus, the pattern of depletion of myocardial SH pools during reperfusion differs depending on the duration of the preceding ischemia. The decreases in nonprotein SH and in non-GSH, nonprotein SH pools did not occur (9% decrease and 3% decrease, respectively; both p=NS) in dogs subjected to brief occlusion (n=6) that were treated before coronary occlusion with 500 mg/kg i.v. dimethylthiourea, an intracellular scavenger of H2O2 and OH. Since only the non-GSH, nonprotein SH pool decreased significantly after brief ischemia and since this decrease could be prevented by antioxidant intervention, this pool appears to be the most sensitive SH indicator of reactive oxygen metabolite-induced myocardial ischemia/ reperfusion injury. (Circulation Research 1991:68:605–613)]]></description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Disease - metabolism</subject><subject>Coronary heart disease</subject><subject>Dogs</subject><subject>Female</subject><subject>Glutathione - analogs &amp; derivatives</subject><subject>Glutathione - metabolism</subject><subject>Glutathione Disulfide</subject><subject>Heart</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Reperfusion</subject><subject>Myocardium - metabolism</subject><subject>Sulfhydryl Compounds - metabolism</subject><subject>Time Factors</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><recordid>eNpNkUFvEzEQRi0EKmngzAnJB8Rt0_Hau14fQ2khUlGrFrhas7vjZsFZBztLlX-Po0TAwRpZ35vv8IaxNwIWQtTiAsQiUlrUzaJc1FA9YzNRlapQlRbP2QwATKGlhJfsPKUfAELJ0pyxM2GMkJWZsenLPnQY-wE9f5i8W-_7uPf8LgTPl35HEXdDGBO_7bop8o9THMZHfk9bim5KOeFLlyH-IQ7kOI49v4vBh_GRev5f8yp1a9oMyFcj_z78Dq_YC4c-0evTnLNv11dfLz8XN7efVpfLm6JTpdKFq3oNLSLptq4RoJGGkIw2rdRYt1i1DWkS2CrqTUtG1a4FwEqS60D2vZyz98febQy_Jko7uxlSR97jSGFKtgElZZmlzNnFEexiSCmSs9s4bDDurQB7EG1B2PurB1s3trRZdN54e6qe2g31__ij2Zy_O-WYOvQu4tgN6S-mjK5U02RMHbGncLCdfvrpiaJdE_rd2ub7gQRRFodWKPOvyK_U8g_n2pf_</recordid><startdate>199102</startdate><enddate>199102</enddate><creator>Lesnefsky, Edward J</creator><creator>Dauber, Ira M</creator><creator>Horwitz, Lawrence D</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199102</creationdate><title>Myocardial Sulfhydryl Pool Alterations Occur During Reperfusion After Brief and Prolonged Myocardial Ischemia In Vivo</title><author>Lesnefsky, Edward J ; Dauber, Ira M ; Horwitz, Lawrence D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4247-f5d70baae7b66a00839eae979b37a6ba5b8e7e1ab4ed9be946fb00a53efc03dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Disease - metabolism</topic><topic>Coronary heart disease</topic><topic>Dogs</topic><topic>Female</topic><topic>Glutathione - analogs &amp; derivatives</topic><topic>Glutathione - metabolism</topic><topic>Glutathione Disulfide</topic><topic>Heart</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Reperfusion</topic><topic>Myocardium - metabolism</topic><topic>Sulfhydryl Compounds - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lesnefsky, Edward J</creatorcontrib><creatorcontrib>Dauber, Ira M</creatorcontrib><creatorcontrib>Horwitz, Lawrence D</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lesnefsky, Edward J</au><au>Dauber, Ira M</au><au>Horwitz, Lawrence D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial Sulfhydryl Pool Alterations Occur During Reperfusion After Brief and Prolonged Myocardial Ischemia In Vivo</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1991-02</date><risdate>1991</risdate><volume>68</volume><issue>2</issue><spage>605</spage><epage>613</epage><pages>605-613</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract><![CDATA[Myocardial sulfhydryl (SH)-containing compounds, including reduced glutathione (GSH), are both defenses against and potential markers of reactive oxygen metabolite injury during ischemia and reperfusion. We examined the alterations in GSH and other myocardial SH pools during reperfusion in anesthetized dogs exposed to brief (15 minutes, n=7) or prolonged (90 minutes, n=6) regional ischemia caused by occlusion of the left anterior descending artery. Ninety minutes of ischemia followed by 5 hours of reperfusion, which resulted in myocardial necrosis of 43.9±4.0% of the area at risk, caused a 22% reduction in total myocardial SH groups (p<0.01), a 57% decrease in nonprotein myocardial SH groups (p<0.01), a 56% decrease in GSH (p<0.01), and a 62% decrease in non-GSH, nonprotein SH groups (p<0.02). However, protein SH groups were not significantly reduced (12% decrease, p=NS). Also, myocardial release of GSH and oxidized glutathione (GSSG) into the coronary venous effluent occurred during early reperfusion. In contrast, 15 minutes of ischemia, followed by 30 minutes of reperfusion, did not alter myocardial total SH groups, protein SH groups, or GSH (9% decrease, p=NS); nor was there reperfusion release of GSH or GSSG. However, even with brief ischemia, nonprotein SH groups decreased 23% (p<0.05), due mainly to a 59% decrease in the non-GSH, nonprotein SH pool (p<0.05). These changes after brief ischemia occurred without alterations in myocardial GSSG or the GSH/GSSG ratio. Thus, the pattern of depletion of myocardial SH pools during reperfusion differs depending on the duration of the preceding ischemia. The decreases in nonprotein SH and in non-GSH, nonprotein SH pools did not occur (9% decrease and 3% decrease, respectively; both p=NS) in dogs subjected to brief occlusion (n=6) that were treated before coronary occlusion with 500 mg/kg i.v. dimethylthiourea, an intracellular scavenger of H2O2 and OH. Since only the non-GSH, nonprotein SH pool decreased significantly after brief ischemia and since this decrease could be prevented by antioxidant intervention, this pool appears to be the most sensitive SH indicator of reactive oxygen metabolite-induced myocardial ischemia/ reperfusion injury. (Circulation Research 1991:68:605–613)]]></abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>1991359</pmid><doi>10.1161/01.res.68.2.605</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary Disease - metabolism
Coronary heart disease
Dogs
Female
Glutathione - analogs & derivatives
Glutathione - metabolism
Glutathione Disulfide
Heart
Male
Medical sciences
Myocardial Reperfusion
Myocardium - metabolism
Sulfhydryl Compounds - metabolism
Time Factors
title Myocardial Sulfhydryl Pool Alterations Occur During Reperfusion After Brief and Prolonged Myocardial Ischemia In Vivo
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