Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes
Departments of 1 Physiology II and 2 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara; and 3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan Submitted 8 October 2004 ; accepted in final form 22 December 2004 We have recently...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2005-04, Vol.288 (4), p.H1699-H1707 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
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| creator | Hagihara, Hiroji Yoshikawa, Yoshiro Ohga, Yoshimi Takenaka, Chikako Murata, Ken-ya Taniguchi, Shigeki Takaki, Miyako |
| description | Departments of 1 Physiology II and 2 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara; and 3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan
Submitted 8 October 2004
; accepted in final form 22 December 2004
We have recently reported that exposure of rat hearts to high Ca 2+ produces a Ca 2+ overload-induced contractile failure in rat hearts, which was associated with proteolysis of -fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca 2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVA mLVV ) was significantly decreased from 5.89 ± 1.55 to 3.83 ± 1.16 mmHg·ml·beat 1 ·g 1 ( n = 6). Mean myocardial oxygen consumption per beat (V O 2 ) intercept of (V O 2 -PVA linear relation was significantly decreased from 0.21 ± 0.05 to 0.15 ± 0.03 µl O 2 ·beat 1 ·g 1 without change in its slope. Initial 30-min reperfusion with a Na + /Ca 2+ exchanger (NCX) inhibitor KB-R7943 (KBR; 10 µmol/l) significantly reduced the decrease in mean PVA mLVV and V O 2 intercept ( n = 6). Although V O 2 for the Ca 2+ handling was finally decreased, it transiently but significantly increased from the control for 1015 min after I/R. This increase in V O 2 for the Ca 2+ handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. -Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca 2+ infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.
calcium overload; mechanoenergetics; KB-R7943; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp ) |
| doi_str_mv | 10.1152/ajpheart.01033.2004 |
| format | Article |
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Submitted 8 October 2004
; accepted in final form 22 December 2004
We have recently reported that exposure of rat hearts to high Ca 2+ produces a Ca 2+ overload-induced contractile failure in rat hearts, which was associated with proteolysis of -fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca 2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVA mLVV ) was significantly decreased from 5.89 ± 1.55 to 3.83 ± 1.16 mmHg·ml·beat 1 ·g 1 ( n = 6). Mean myocardial oxygen consumption per beat (V O 2 ) intercept of (V O 2 -PVA linear relation was significantly decreased from 0.21 ± 0.05 to 0.15 ± 0.03 µl O 2 ·beat 1 ·g 1 without change in its slope. Initial 30-min reperfusion with a Na + /Ca 2+ exchanger (NCX) inhibitor KB-R7943 (KBR; 10 µmol/l) significantly reduced the decrease in mean PVA mLVV and V O 2 intercept ( n = 6). Although V O 2 for the Ca 2+ handling was finally decreased, it transiently but significantly increased from the control for 1015 min after I/R. This increase in V O 2 for the Ca 2+ handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. -Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca 2+ infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.
calcium overload; mechanoenergetics; KB-R7943; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01033.2004</identifier><identifier>PMID: 15626686</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Blotting, Western ; Calcium - metabolism ; Cardiotonic Agents - pharmacology ; Carrier Proteins - metabolism ; Electrophoresis, Polyacrylamide Gel ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Heart Ventricles - metabolism ; Immunohistochemistry ; Male ; Microfilament Proteins - metabolism ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Myocardium - metabolism ; Oxygen Consumption - physiology ; Rats ; Rats, Wistar ; Sodium-Calcium Exchanger - antagonists & inhibitors ; Sodium-Calcium Exchanger - metabolism ; Thiourea - analogs & derivatives ; Thiourea - pharmacology ; Ventricular Function, Left - drug effects ; Ventricular Function, Left - physiology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2005-04, Vol.288 (4), p.H1699-H1707</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15626686$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hagihara, Hiroji</creatorcontrib><creatorcontrib>Yoshikawa, Yoshiro</creatorcontrib><creatorcontrib>Ohga, Yoshimi</creatorcontrib><creatorcontrib>Takenaka, Chikako</creatorcontrib><creatorcontrib>Murata, Ken-ya</creatorcontrib><creatorcontrib>Taniguchi, Shigeki</creatorcontrib><creatorcontrib>Takaki, Miyako</creatorcontrib><title>Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Departments of 1 Physiology II and 2 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara; and 3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan
Submitted 8 October 2004
; accepted in final form 22 December 2004
We have recently reported that exposure of rat hearts to high Ca 2+ produces a Ca 2+ overload-induced contractile failure in rat hearts, which was associated with proteolysis of -fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca 2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVA mLVV ) was significantly decreased from 5.89 ± 1.55 to 3.83 ± 1.16 mmHg·ml·beat 1 ·g 1 ( n = 6). Mean myocardial oxygen consumption per beat (V O 2 ) intercept of (V O 2 -PVA linear relation was significantly decreased from 0.21 ± 0.05 to 0.15 ± 0.03 µl O 2 ·beat 1 ·g 1 without change in its slope. Initial 30-min reperfusion with a Na + /Ca 2+ exchanger (NCX) inhibitor KB-R7943 (KBR; 10 µmol/l) significantly reduced the decrease in mean PVA mLVV and V O 2 intercept ( n = 6). Although V O 2 for the Ca 2+ handling was finally decreased, it transiently but significantly increased from the control for 1015 min after I/R. This increase in V O 2 for the Ca 2+ handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. -Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca 2+ infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.
calcium overload; mechanoenergetics; KB-R7943; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp )</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Blotting, Western</subject><subject>Calcium - metabolism</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Carrier Proteins - metabolism</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Heart Ventricles - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Microfilament Proteins - metabolism</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Oxygen Consumption - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sodium-Calcium Exchanger - antagonists & inhibitors</subject><subject>Sodium-Calcium Exchanger - metabolism</subject><subject>Thiourea - analogs & derivatives</subject><subject>Thiourea - pharmacology</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Function, Left - physiology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtr3DAQx0VoSbZJPkGg6NRL8K4etmzTU1mapLC0l_QsJHtsaeNXJZldf_sqyS70UhgYhvn_5onQHSVrSjO2UfvJgHJhTSjhfM0ISS_QKmZYQjNefkArwgVPBOXZFfrk_Z4QkuWCX6IrmgkmRCFWaPmp7jdbxe4xHCujhhawHYzVNthxwJMbA1TB42AAOxXwW0PcuLHH1lcGeqsSBxO4ZvavgB32s1uwjtaN1YsdWgwDuHZJDsqH1zCWrMB78DfoY6M6D7cnf41-P3x_3j4lu1-PP7bfdolhZR4SYEVWg05TKkhJCiiJIDquJ3hTQykamqWsKFJBmC5qpXIgutaF1hp4ralO-TX68l43dv4zgw-yj6ND16kBxtlLkWeMiiKPws8n4ax7qOXkbK_cIs_HioKv7wJjW3OwDuRklrh2N7aLfJi77hmOQZ7fEqeSqXyioizlVDeR3vyfPkPyH4r_BZt8lqM</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Hagihara, Hiroji</creator><creator>Yoshikawa, Yoshiro</creator><creator>Ohga, Yoshimi</creator><creator>Takenaka, Chikako</creator><creator>Murata, Ken-ya</creator><creator>Taniguchi, Shigeki</creator><creator>Takaki, Miyako</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>Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes</title><author>Hagihara, Hiroji ; Yoshikawa, Yoshiro ; Ohga, Yoshimi ; Takenaka, Chikako ; Murata, Ken-ya ; Taniguchi, Shigeki ; Takaki, Miyako</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h297t-e285deb44160908e9060b53963fde96f1542884602b8daa7e0bdb8bbbe3db1b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Blotting, Western</topic><topic>Calcium - metabolism</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Carrier Proteins - metabolism</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Energy Metabolism - drug effects</topic><topic>Energy Metabolism - physiology</topic><topic>Heart Ventricles - metabolism</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Microfilament Proteins - metabolism</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Oxygen Consumption - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sodium-Calcium Exchanger - antagonists & inhibitors</topic><topic>Sodium-Calcium Exchanger - metabolism</topic><topic>Thiourea - analogs & derivatives</topic><topic>Thiourea - pharmacology</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Function, Left - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hagihara, Hiroji</creatorcontrib><creatorcontrib>Yoshikawa, Yoshiro</creatorcontrib><creatorcontrib>Ohga, Yoshimi</creatorcontrib><creatorcontrib>Takenaka, Chikako</creatorcontrib><creatorcontrib>Murata, Ken-ya</creatorcontrib><creatorcontrib>Taniguchi, Shigeki</creatorcontrib><creatorcontrib>Takaki, Miyako</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. 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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>H1699</spage><epage>H1707</epage><pages>H1699-H1707</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Departments of 1 Physiology II and 2 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara; and 3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan
Submitted 8 October 2004
; accepted in final form 22 December 2004
We have recently reported that exposure of rat hearts to high Ca 2+ produces a Ca 2+ overload-induced contractile failure in rat hearts, which was associated with proteolysis of -fodrin. We hypothesized that contractile failure after ischemia-reperfusion (I/R) is similar to that after high Ca 2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts, which were subjected to 15 min global ischemia and 60 min reperfusion. Sixty minutes after I/R, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume (mLVV) (PVA mLVV ) was significantly decreased from 5.89 ± 1.55 to 3.83 ± 1.16 mmHg·ml·beat 1 ·g 1 ( n = 6). Mean myocardial oxygen consumption per beat (V O 2 ) intercept of (V O 2 -PVA linear relation was significantly decreased from 0.21 ± 0.05 to 0.15 ± 0.03 µl O 2 ·beat 1 ·g 1 without change in its slope. Initial 30-min reperfusion with a Na + /Ca 2+ exchanger (NCX) inhibitor KB-R7943 (KBR; 10 µmol/l) significantly reduced the decrease in mean PVA mLVV and V O 2 intercept ( n = 6). Although V O 2 for the Ca 2+ handling was finally decreased, it transiently but significantly increased from the control for 1015 min after I/R. This increase in V O 2 for the Ca 2+ handling was completely blocked by KBR, suggesting an inhibition of reverse-mode NCX by KBR. -Fodrin proteolysis, which was significantly increased after I/R, was also significantly reduced by KBR. Our study shows that the contractile failure after I/R is similar to that after high Ca 2+ infusion, although the contribution of reverse-mode NCX to the contractile failure is different. An inhibition of reverse-mode NCX during initial reperfusion protects the heart against reperfusion injury.
calcium overload; mechanoenergetics; KB-R7943; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp )</abstract><cop>United States</cop><pmid>15626686</pmid><doi>10.1152/ajpheart.01033.2004</doi></addata></record> |
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| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Anti-Arrhythmia Agents - pharmacology Blotting, Western Calcium - metabolism Cardiotonic Agents - pharmacology Carrier Proteins - metabolism Electrophoresis, Polyacrylamide Gel Energy Metabolism - drug effects Energy Metabolism - physiology Heart Ventricles - metabolism Immunohistochemistry Male Microfilament Proteins - metabolism Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Myocardium - metabolism Oxygen Consumption - physiology Rats Rats, Wistar Sodium-Calcium Exchanger - antagonists & inhibitors Sodium-Calcium Exchanger - metabolism Thiourea - analogs & derivatives Thiourea - pharmacology Ventricular Function, Left - drug effects Ventricular Function, Left - physiology |
| title | Na+/Ca2+ exchange inhibition protects the rat heart from ischemia-reperfusion injury by blocking energy-wasting processes |
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