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Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload
Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University School of Medicine, Atlanta, Georgia Submitted 31 December 2003 ; accepted in final form 21 November 2004 We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., p...
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| Published in: | American journal of physiology. Heart and circulatory physiology 2005-04, Vol.288 (4), p.H1900-H1908 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 288 |
| creator | Sun, He-Ying Wang, Ning-Ping Kerendi, Faraz Halkos, Michael Kin, Hajime Guyton, Robert A Vinten-Johansen, Jakob Zhao, Zhi-Qing |
| description | Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University School of Medicine, Atlanta, Georgia
Submitted 31 December 2003
; accepted in final form 21 November 2004
We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca 2+ overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca 2+ concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca 2+ concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca 2+ overload.
reactive oxygen species; hypoxia; reoxygenation; superoxide; ischemia; reperfusion
Address for reprint requests and other correspondence: Z.-Q. Zhao, Cardiothorac |
| doi_str_mv | 10.1152/ajpheart.01244.2003 |
| format | article |
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Submitted 31 December 2003
; accepted in final form 21 November 2004
We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca 2+ overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca 2+ concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca 2+ concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca 2+ overload.
reactive oxygen species; hypoxia; reoxygenation; superoxide; ischemia; reperfusion
Address for reprint requests and other correspondence: Z.-Q. Zhao, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center/Crawford Long Hospital, Emory Univ. School of Medicine, 550 Peachtree St. NE, Atlanta, GA 30308-2225 (E-mail: zzhao{at}emory.edu )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01244.2003</identifier><identifier>PMID: 15563525</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Calcium - metabolism ; Cell Communication - physiology ; Cell Survival - physiology ; Cells, Cultured ; Cytochromes c - metabolism ; Hydrogen Peroxide - metabolism ; Hypoxia - metabolism ; Hypoxia - pathology ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; L-Lactate Dehydrogenase - metabolism ; Luminescent Measurements ; Malondialdehyde - metabolism ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - metabolism ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Superoxide Dismutase - metabolism ; Superoxides - metabolism</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2005-04, Vol.288 (4), p.H1900-H1908</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15563525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, He-Ying</creatorcontrib><creatorcontrib>Wang, Ning-Ping</creatorcontrib><creatorcontrib>Kerendi, Faraz</creatorcontrib><creatorcontrib>Halkos, Michael</creatorcontrib><creatorcontrib>Kin, Hajime</creatorcontrib><creatorcontrib>Guyton, Robert A</creatorcontrib><creatorcontrib>Vinten-Johansen, Jakob</creatorcontrib><creatorcontrib>Zhao, Zhi-Qing</creatorcontrib><title>Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University School of Medicine, Atlanta, Georgia
Submitted 31 December 2003
; accepted in final form 21 November 2004
We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca 2+ overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca 2+ concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca 2+ concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca 2+ overload.
reactive oxygen species; hypoxia; reoxygenation; superoxide; ischemia; reperfusion
Address for reprint requests and other correspondence: Z.-Q. Zhao, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center/Crawford Long Hospital, Emory Univ. School of Medicine, 550 Peachtree St. NE, Atlanta, GA 30308-2225 (E-mail: zzhao{at}emory.edu )</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Cell Communication - physiology</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>Cytochromes c - metabolism</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - pathology</subject><subject>In Vitro Techniques</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Luminescent Measurements</subject><subject>Malondialdehyde - metabolism</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxides - metabolism</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNp1kU1r3DAQhkVpaTZpf0Eh6NRL8UYfK9mip7I02UAg0KZnMWuN1wpay5HsJP738ZIPculpDu_zzAwzhHzjbMm5Emdw27cIaVgyLlarpWBMfiCLOREFV9J8JAsmtSw0l-qIHOd8yxhTpZafyRFXSksl1IL0m6mPj76mfcxDHTvnBx873-1oQjfWmGkNyfm4n2I9DUhDzJluJ-q71m9ndgb_XP-lO-wwwUGl0Lk5HRLUGMIYINE1iB803mMKEdwX8qmBkPHrSz0h_85_36w3xdX1xeX611XRClMORaV4iYDaiRIlY4YrtoIGy9JVyLTgbitlYxAMmNJwoVyjndRNIwCkMILJE_L9uW-f4t2IebB7nw8rQYdxzFaX8wSuqxk8fQHH7R6d7ZPfQ5rs641m4OwZaP2uffAJbd9O2ccQd5N9fYIVVWVXdsMNO8z--X_jfAzhBh-HN_WdaXvXyCd5p5NA</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Sun, He-Ying</creator><creator>Wang, Ning-Ping</creator><creator>Kerendi, Faraz</creator><creator>Halkos, Michael</creator><creator>Kin, Hajime</creator><creator>Guyton, Robert A</creator><creator>Vinten-Johansen, Jakob</creator><creator>Zhao, Zhi-Qing</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20050401</creationdate><title>Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload</title><author>Sun, He-Ying ; Wang, Ning-Ping ; Kerendi, Faraz ; Halkos, Michael ; Kin, Hajime ; Guyton, Robert A ; Vinten-Johansen, Jakob ; Zhao, Zhi-Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h297t-8517eae6d27e30091504afe77d8e0621db33f9ea9a979125df6d36ff2aa329203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Cell Communication - physiology</topic><topic>Cell Survival - physiology</topic><topic>Cells, Cultured</topic><topic>Cytochromes c - metabolism</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - pathology</topic><topic>In Vitro Techniques</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Luminescent Measurements</topic><topic>Malondialdehyde - metabolism</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, He-Ying</creatorcontrib><creatorcontrib>Wang, Ning-Ping</creatorcontrib><creatorcontrib>Kerendi, Faraz</creatorcontrib><creatorcontrib>Halkos, Michael</creatorcontrib><creatorcontrib>Kin, Hajime</creatorcontrib><creatorcontrib>Guyton, Robert A</creatorcontrib><creatorcontrib>Vinten-Johansen, Jakob</creatorcontrib><creatorcontrib>Zhao, Zhi-Qing</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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, He-Ying</au><au>Wang, Ning-Ping</au><au>Kerendi, Faraz</au><au>Halkos, Michael</au><au>Kin, Hajime</au><au>Guyton, Robert A</au><au>Vinten-Johansen, Jakob</au><au>Zhao, Zhi-Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>288</volume><issue>4</issue><spage>H1900</spage><epage>H1908</epage><pages>H1900-H1908</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University School of Medicine, Atlanta, Georgia
Submitted 31 December 2003
; accepted in final form 21 November 2004
We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by hypoxic postconditioning (Postcon) is associated with a reduction in the generation of reactive oxygen species (ROS) and intracellular Ca 2+ overload. Primary cultured neonatal rat cardiomyocytes were exposed to 3 h of hypoxia followed by 6 h of reoxygenation. Cardiomyocytes were postconditioned after the 3-h index hypoxia by three cycles of 5 min of reoxygenation and 5 min of rehypoxia applied before 6 h of reoxygenation. Relative to sham control and hypoxia alone, the generation of ROS (increased lucigenin-enhanced chemiluminescence, SOD-inhibitable cytochrome c reduction, and generation of hydrogen peroxide) was significantly augmented after immediate reoxygenation as was the production of malondialdehyde, a product of lipid peroxidation. Concomitant with these changes, intracellular and mitochondrial Ca 2+ concentrations, which were detected by fluorescent fluo-4 AM and X-rhod-1 AM staining, respectively, were elevated. Cell viability assessed by propidium iodide staining was decreased consistent with increased levels of lactate dehydrogenase after reoxygenation. Postcon treatment at the onset of reoxygenation reduced ROS generation and malondialdehyde concentration in media and attenuated cardiomyocyte death assessed by propidium iodide and lactate dehydrogenase. Postcon treatment was associated with a decrease in intracellular and mitochondrial Ca 2+ concentrations. These data suggest that Postcon treatment reduces reoxygenation-induced injury in cardiomyocytes and is potentially mediated by attenuation of ROS generation, lipid peroxidation, and intracellular and mitochondrial Ca 2+ overload.
reactive oxygen species; hypoxia; reoxygenation; superoxide; ischemia; reperfusion
Address for reprint requests and other correspondence: Z.-Q. Zhao, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center/Crawford Long Hospital, Emory Univ. School of Medicine, 550 Peachtree St. NE, Atlanta, GA 30308-2225 (E-mail: zzhao{at}emory.edu )</abstract><cop>United States</cop><pmid>15563525</pmid><doi>10.1152/ajpheart.01244.2003</doi></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2005-04, Vol.288 (4), p.H1900-H1908 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_pubmed_primary_15563525 |
| source | American Physiological Society Free |
| subjects | Animals Calcium - metabolism Cell Communication - physiology Cell Survival - physiology Cells, Cultured Cytochromes c - metabolism Hydrogen Peroxide - metabolism Hypoxia - metabolism Hypoxia - pathology In Vitro Techniques Ischemic Preconditioning, Myocardial L-Lactate Dehydrogenase - metabolism Luminescent Measurements Malondialdehyde - metabolism Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes, Cardiac - cytology Myocytes, Cardiac - metabolism Rats Rats, Wistar Reactive Oxygen Species - metabolism Superoxide Dismutase - metabolism Superoxides - metabolism |
| title | Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload |
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