Cardioprotective effects of a novel calpain inhibitor SNJ-1945 for reperfusion injury after cardioplegic cardiac arrest
Departments of 1 Physiology II and 2 Thoracic-Cardiovascular Surgery, Nara Medical University School of Medicine, Kashihara, Nara, Japan Submitted September 8, 2009 ; accepted in final form November 25, 2009 We have previously indicated that calpain inhibitor-1 prevents the heart from ischemia- repe...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2010-02, Vol.298 (2), p.H643-H651 |
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| creator | Yoshikawa, Yoshiro Zhang, Guo-Xing Obata, Koji Ohga, Yoshimi Matsuyoshi, Hiroko Taniguchi, Shigeki Takaki, Miyako |
| description | Departments of 1 Physiology II and
2 Thoracic-Cardiovascular Surgery, Nara Medical University School of Medicine, Kashihara, Nara, Japan
Submitted September 8, 2009
; accepted in final form November 25, 2009
We have previously indicated that calpain inhibitor-1 prevents the heart from ischemia- reperfusion injury associated with the impairment of total Ca 2+ handling by inhibiting the proteolysis of -fodrin. However, this inhibitor is insoluble with water and inappropriate for clinical application. The aim of the present study was to investigate the protective effect of a newly developed calpain inhibitor, SNJ-1945 (SNJ), with good aqueous solubility on left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts. SNJ (150 µM) was added to KCl (30 meq) cardioplegia (CP). Mean end-systolic pressure at midrange LV volume (ESP mLVV ) and systolic pressure-volume area (PVA) at mLVV (PVA mLVV ; a total mechanical energy per beat) were hardly changed after CP plus SNJ arrest-reperfusion (post-CP + SNJ), whereas ESP mLVV and PVA mLVV in post-CP group were significantly ( P < 0.01) decreased. Mean myocardial oxygen consumption for the total Ca 2+ handling in excitation-contraction coupling did not significantly decrease in post-CP + SNJ group, whereas it was significantly ( P < 0.01) decreased in post-CP group. The mean amounts of 145- and 150-kDa fragments of -fodrin in the post-CP group were significantly larger than those in normal and post-CP + SNJ groups. In contrast, the mean amounts of L-type Ca 2+ channel and sarcoplasmic reticulum Ca 2+ -ATPase were not significantly different among normal, post-CP, and post-CP + SNJ groups. Our results indicate that soluble SNJ attenuates cardiac dysfunction due to CP arrest-reperfusion injury associated with the impairment of the total Ca 2+ handling in excitation-contraction coupling by inhibiting the proteolysis of -fodrin.
cardiac function; systolic pressure-volume area; oxygen consumption; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ. School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (e-mail: mtakaki{at}naramed-u.ac.jp ). |
| doi_str_mv | 10.1152/ajpheart.00849.2009 |
| format | Article |
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2 Thoracic-Cardiovascular Surgery, Nara Medical University School of Medicine, Kashihara, Nara, Japan
Submitted September 8, 2009
; accepted in final form November 25, 2009
We have previously indicated that calpain inhibitor-1 prevents the heart from ischemia- reperfusion injury associated with the impairment of total Ca 2+ handling by inhibiting the proteolysis of -fodrin. However, this inhibitor is insoluble with water and inappropriate for clinical application. The aim of the present study was to investigate the protective effect of a newly developed calpain inhibitor, SNJ-1945 (SNJ), with good aqueous solubility on left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts. SNJ (150 µM) was added to KCl (30 meq) cardioplegia (CP). Mean end-systolic pressure at midrange LV volume (ESP mLVV ) and systolic pressure-volume area (PVA) at mLVV (PVA mLVV ; a total mechanical energy per beat) were hardly changed after CP plus SNJ arrest-reperfusion (post-CP + SNJ), whereas ESP mLVV and PVA mLVV in post-CP group were significantly ( P < 0.01) decreased. Mean myocardial oxygen consumption for the total Ca 2+ handling in excitation-contraction coupling did not significantly decrease in post-CP + SNJ group, whereas it was significantly ( P < 0.01) decreased in post-CP group. The mean amounts of 145- and 150-kDa fragments of -fodrin in the post-CP group were significantly larger than those in normal and post-CP + SNJ groups. In contrast, the mean amounts of L-type Ca 2+ channel and sarcoplasmic reticulum Ca 2+ -ATPase were not significantly different among normal, post-CP, and post-CP + SNJ groups. Our results indicate that soluble SNJ attenuates cardiac dysfunction due to CP arrest-reperfusion injury associated with the impairment of the total Ca 2+ handling in excitation-contraction coupling by inhibiting the proteolysis of -fodrin.
cardiac function; systolic pressure-volume area; oxygen consumption; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ. School of Medicine, 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.00849.2009</identifier><identifier>PMID: 19966051</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adenosine triphosphatase ; Animals ; Blood pressure ; Calcium - metabolism ; Calcium Channels, L-Type - metabolism ; Calpain - antagonists & inhibitors ; Carbamates - therapeutic use ; Cardiotonic Agents - therapeutic use ; Carrier Proteins - metabolism ; Disease Models, Animal ; Heart ; Heart Arrest, Induced - adverse effects ; Male ; Microfilament Proteins - metabolism ; Myocardial Reperfusion Injury - etiology ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention & control ; Oxygen Consumption - physiology ; Rats ; Rats, Wistar ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism ; Studies ; Veins & arteries ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2010-02, Vol.298 (2), p.H643-H651</ispartof><rights>Copyright American Physiological Society Feb 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-766f82587753db98286df18344797bacdcb607bc56e66d5ca786fc06dac953c73</citedby><cites>FETCH-LOGICAL-c436t-766f82587753db98286df18344797bacdcb607bc56e66d5ca786fc06dac953c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19966051$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshikawa, Yoshiro</creatorcontrib><creatorcontrib>Zhang, Guo-Xing</creatorcontrib><creatorcontrib>Obata, Koji</creatorcontrib><creatorcontrib>Ohga, Yoshimi</creatorcontrib><creatorcontrib>Matsuyoshi, Hiroko</creatorcontrib><creatorcontrib>Taniguchi, Shigeki</creatorcontrib><creatorcontrib>Takaki, Miyako</creatorcontrib><title>Cardioprotective effects of a novel calpain inhibitor SNJ-1945 for reperfusion injury after cardioplegic cardiac arrest</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 School of Medicine, Kashihara, Nara, Japan
Submitted September 8, 2009
; accepted in final form November 25, 2009
We have previously indicated that calpain inhibitor-1 prevents the heart from ischemia- reperfusion injury associated with the impairment of total Ca 2+ handling by inhibiting the proteolysis of -fodrin. However, this inhibitor is insoluble with water and inappropriate for clinical application. The aim of the present study was to investigate the protective effect of a newly developed calpain inhibitor, SNJ-1945 (SNJ), with good aqueous solubility on left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts. SNJ (150 µM) was added to KCl (30 meq) cardioplegia (CP). Mean end-systolic pressure at midrange LV volume (ESP mLVV ) and systolic pressure-volume area (PVA) at mLVV (PVA mLVV ; a total mechanical energy per beat) were hardly changed after CP plus SNJ arrest-reperfusion (post-CP + SNJ), whereas ESP mLVV and PVA mLVV in post-CP group were significantly ( P < 0.01) decreased. Mean myocardial oxygen consumption for the total Ca 2+ handling in excitation-contraction coupling did not significantly decrease in post-CP + SNJ group, whereas it was significantly ( P < 0.01) decreased in post-CP group. The mean amounts of 145- and 150-kDa fragments of -fodrin in the post-CP group were significantly larger than those in normal and post-CP + SNJ groups. In contrast, the mean amounts of L-type Ca 2+ channel and sarcoplasmic reticulum Ca 2+ -ATPase were not significantly different among normal, post-CP, and post-CP + SNJ groups. Our results indicate that soluble SNJ attenuates cardiac dysfunction due to CP arrest-reperfusion injury associated with the impairment of the total Ca 2+ handling in excitation-contraction coupling by inhibiting the proteolysis of -fodrin.
cardiac function; systolic pressure-volume area; oxygen consumption; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ. School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (e-mail: mtakaki{at}naramed-u.ac.jp ).</description><subject>Adenosine triphosphatase</subject><subject>Animals</subject><subject>Blood pressure</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels, L-Type - metabolism</subject><subject>Calpain - antagonists & inhibitors</subject><subject>Carbamates - therapeutic use</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Carrier Proteins - metabolism</subject><subject>Disease Models, Animal</subject><subject>Heart</subject><subject>Heart Arrest, Induced - adverse effects</subject><subject>Male</subject><subject>Microfilament Proteins - metabolism</subject><subject>Myocardial Reperfusion Injury - etiology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Oxygen Consumption - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</subject><subject>Studies</subject><subject>Veins & arteries</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU9v1DAQxS0EokvhEyAhiwunLP4Tj-MjWhUKqtpD4Ww5jr3xKhsHO2m13x5vd1GlnuyRf--NZx5CHylZUyrYV7ObemfSvCakqdWaEaJeoVV5YRUVXL1GK8KBV0C5uEDvct4RQoQE_hZdUKUAiKAr9LgxqQtxSnF2dg4PDjvvyy3j6LHBY3xwA7ZmmEwYcRj70IY5Jnx_-6uiqhbYlyK5ySW_5BCPyG5JB2z87FLRPXkPbhvsqTAWm5Rcnt-jN94M2X04n5foz_er35vr6ubux8_Nt5vK1hzmSgL4holGSsG7VjWsgc7Thte1VLI1trMtENlaAQ6gE9bIBrwl0BmrBLeSX6IvJ98y4d-lNNb7kK0bBjO6uGQtOQfKOK0L-fkFuYtLGsvnNGMKOCndC8RPkE0x5-S8nlLYm3TQlOhjKvp_KvopFX1Mpag-na2Xdu-6Z805hgKsT0Aftv1jSE5P_aHsc4jbw7MjU41m-hpqzv8BKdmb1w</recordid><startdate>20100201</startdate><enddate>20100201</enddate><creator>Yoshikawa, Yoshiro</creator><creator>Zhang, Guo-Xing</creator><creator>Obata, Koji</creator><creator>Ohga, Yoshimi</creator><creator>Matsuyoshi, Hiroko</creator><creator>Taniguchi, Shigeki</creator><creator>Takaki, Miyako</creator><general>American Physiological Society</general><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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20100201</creationdate><title>Cardioprotective effects of a novel calpain inhibitor SNJ-1945 for reperfusion injury after cardioplegic cardiac arrest</title><author>Yoshikawa, Yoshiro ; Zhang, Guo-Xing ; Obata, Koji ; Ohga, Yoshimi ; Matsuyoshi, Hiroko ; Taniguchi, Shigeki ; Takaki, Miyako</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-766f82587753db98286df18344797bacdcb607bc56e66d5ca786fc06dac953c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adenosine triphosphatase</topic><topic>Animals</topic><topic>Blood pressure</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels, L-Type - metabolism</topic><topic>Calpain - antagonists & inhibitors</topic><topic>Carbamates - therapeutic use</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Carrier Proteins - metabolism</topic><topic>Disease Models, Animal</topic><topic>Heart</topic><topic>Heart Arrest, Induced - adverse effects</topic><topic>Male</topic><topic>Microfilament Proteins - metabolism</topic><topic>Myocardial Reperfusion Injury - etiology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Oxygen Consumption - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</topic><topic>Studies</topic><topic>Veins & arteries</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshikawa, Yoshiro</creatorcontrib><creatorcontrib>Zhang, Guo-Xing</creatorcontrib><creatorcontrib>Obata, Koji</creatorcontrib><creatorcontrib>Ohga, Yoshimi</creatorcontrib><creatorcontrib>Matsuyoshi, Hiroko</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>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Yoshikawa, Yoshiro</au><au>Zhang, Guo-Xing</au><au>Obata, Koji</au><au>Ohga, Yoshimi</au><au>Matsuyoshi, Hiroko</au><au>Taniguchi, Shigeki</au><au>Takaki, Miyako</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardioprotective effects of a novel calpain inhibitor SNJ-1945 for reperfusion injury after cardioplegic cardiac arrest</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2010-02-01</date><risdate>2010</risdate><volume>298</volume><issue>2</issue><spage>H643</spage><epage>H651</epage><pages>H643-H651</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>Departments of 1 Physiology II and
2 Thoracic-Cardiovascular Surgery, Nara Medical University School of Medicine, Kashihara, Nara, Japan
Submitted September 8, 2009
; accepted in final form November 25, 2009
We have previously indicated that calpain inhibitor-1 prevents the heart from ischemia- reperfusion injury associated with the impairment of total Ca 2+ handling by inhibiting the proteolysis of -fodrin. However, this inhibitor is insoluble with water and inappropriate for clinical application. The aim of the present study was to investigate the protective effect of a newly developed calpain inhibitor, SNJ-1945 (SNJ), with good aqueous solubility on left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts. SNJ (150 µM) was added to KCl (30 meq) cardioplegia (CP). Mean end-systolic pressure at midrange LV volume (ESP mLVV ) and systolic pressure-volume area (PVA) at mLVV (PVA mLVV ; a total mechanical energy per beat) were hardly changed after CP plus SNJ arrest-reperfusion (post-CP + SNJ), whereas ESP mLVV and PVA mLVV in post-CP group were significantly ( P < 0.01) decreased. Mean myocardial oxygen consumption for the total Ca 2+ handling in excitation-contraction coupling did not significantly decrease in post-CP + SNJ group, whereas it was significantly ( P < 0.01) decreased in post-CP group. The mean amounts of 145- and 150-kDa fragments of -fodrin in the post-CP group were significantly larger than those in normal and post-CP + SNJ groups. In contrast, the mean amounts of L-type Ca 2+ channel and sarcoplasmic reticulum Ca 2+ -ATPase were not significantly different among normal, post-CP, and post-CP + SNJ groups. Our results indicate that soluble SNJ attenuates cardiac dysfunction due to CP arrest-reperfusion injury associated with the impairment of the total Ca 2+ handling in excitation-contraction coupling by inhibiting the proteolysis of -fodrin.
cardiac function; systolic pressure-volume area; oxygen consumption; -fodrin
Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ. School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (e-mail: mtakaki{at}naramed-u.ac.jp ).</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>19966051</pmid><doi>10.1152/ajpheart.00849.2009</doi></addata></record> |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adenosine triphosphatase Animals Blood pressure Calcium - metabolism Calcium Channels, L-Type - metabolism Calpain - antagonists & inhibitors Carbamates - therapeutic use Cardiotonic Agents - therapeutic use Carrier Proteins - metabolism Disease Models, Animal Heart Heart Arrest, Induced - adverse effects Male Microfilament Proteins - metabolism Myocardial Reperfusion Injury - etiology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Oxygen Consumption - physiology Rats Rats, Wistar Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Studies Veins & arteries Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology |
| title | Cardioprotective effects of a novel calpain inhibitor SNJ-1945 for reperfusion injury after cardioplegic cardiac arrest |
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