Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction
Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the devel...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1997-02, Vol.29 (2), p.753-763 |
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| creator | Yamaguchi, Fuminari Sanbe, Atsushi Takeo, Satoshi |
| description | Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25–0.5 min with 10−5mCa2+(53–70%) and when preloaded with 10−6mCa2+and then exposed to 0.1–1mmcaffeine (39–87%). The results suggest that the rate of Ca2+uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+released from SR decreased due to decreased Ca2+uptake rate of SR and down-regulation of the SR Ca2+-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction. |
| doi_str_mv | 10.1006/jmcc.1996.0319 |
| format | Article |
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The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25–0.5 min with 10−5mCa2+(53–70%) and when preloaded with 10−6mCa2+and then exposed to 0.1–1mmcaffeine (39–87%). The results suggest that the rate of Ca2+uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+released from SR decreased due to decreased Ca2+uptake rate of SR and down-regulation of the SR Ca2+-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.1996.0319</identifier><identifier>PMID: 9140832</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Caffeine - pharmacology ; Calcium - metabolism ; Calcium - pharmacokinetics ; Calcium release ; Calcium sensitivity ; Calcium uptake ; Cell Membrane - metabolism ; Central Nervous System Stimulants - pharmacology ; Heart Failure - physiopathology ; Hemodynamics ; Histocytological Preparation Techniques ; Male ; Muscle Fibers, Skeletal - chemistry ; Muscle Fibers, Skeletal - metabolism ; Myocardial Contraction - drug effects ; Myocardial Infarction - physiopathology ; Myocardium - metabolism ; Papillary Muscles - chemistry ; Papillary Muscles - metabolism ; Proteins - metabolism ; Rats ; Rats, Wistar ; Ryanodine - metabolism ; Ryanodine receptor ; Sarcoplasmic Reticulum - metabolism ; Skinned fiber</subject><ispartof>Journal of molecular and cellular cardiology, 1997-02, Vol.29 (2), p.753-763</ispartof><rights>1997 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c339t-4315cc92d130066edabf60ad96eca79fcf44fa16ce6a11c8810704d5f0a336633</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/jmcc.1996.0319$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9140832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamaguchi, Fuminari</creatorcontrib><creatorcontrib>Sanbe, Atsushi</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><title>Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25–0.5 min with 10−5mCa2+(53–70%) and when preloaded with 10−6mCa2+and then exposed to 0.1–1mmcaffeine (39–87%). The results suggest that the rate of Ca2+uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+released from SR decreased due to decreased Ca2+uptake rate of SR and down-regulation of the SR Ca2+-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.</description><subject>Animals</subject><subject>Caffeine - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium - pharmacokinetics</subject><subject>Calcium release</subject><subject>Calcium sensitivity</subject><subject>Calcium uptake</subject><subject>Cell Membrane - metabolism</subject><subject>Central Nervous System Stimulants - pharmacology</subject><subject>Heart Failure - physiopathology</subject><subject>Hemodynamics</subject><subject>Histocytological Preparation Techniques</subject><subject>Male</subject><subject>Muscle Fibers, Skeletal - chemistry</subject><subject>Muscle Fibers, Skeletal - metabolism</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Papillary Muscles - chemistry</subject><subject>Papillary Muscles - metabolism</subject><subject>Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ryanodine - metabolism</subject><subject>Ryanodine receptor</subject><subject>Sarcoplasmic Reticulum - metabolism</subject><subject>Skinned fiber</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFP3DAQha0KRLfQa2-VfOKWxY4Tr31EKxaQQEi0nK1hMileOfFiJ0X8-ybsqjdOc3hvPul9jP2QYimF0BfbDnEprdVLoaT9whZS2LowtamO2EKIsixKU5qv7FvOWyGErZQ6YSdWVsKocsG2a0iNB-S_IGHcBcidR_5Ig8cxQOKbscfBx577nj_CkPmbH174-iXFfurdEKSBb8CHMRHfxBDim-__8Pv3iB_cwG_7diLPiDN23ELI9P1wT9nT5ur3-qa4e7i-XV_eFaiUHYpKyRrRlo1U0z5NDTy3WkBjNSGsbIttVbUgNZIGKdEYKVaiaupWgFJaK3XKzvfcXYqvI-XBdT4jhQA9xTG7lbHW1Lacist9EVPMOVHrdsl3kN6dFG6W62a5bpbrZrnTw88DeXzuqPlfP9iccrPPaZr311NyGT31SI1PhINrov8M_Q-gWonx</recordid><startdate>19970201</startdate><enddate>19970201</enddate><creator>Yamaguchi, Fuminari</creator><creator>Sanbe, Atsushi</creator><creator>Takeo, Satoshi</creator><general>Elsevier Ltd</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>7X8</scope></search><sort><creationdate>19970201</creationdate><title>Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction</title><author>Yamaguchi, Fuminari ; Sanbe, Atsushi ; Takeo, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-4315cc92d130066edabf60ad96eca79fcf44fa16ce6a11c8810704d5f0a336633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Caffeine - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium - pharmacokinetics</topic><topic>Calcium release</topic><topic>Calcium sensitivity</topic><topic>Calcium uptake</topic><topic>Cell Membrane - metabolism</topic><topic>Central Nervous System Stimulants - pharmacology</topic><topic>Heart Failure - physiopathology</topic><topic>Hemodynamics</topic><topic>Histocytological Preparation Techniques</topic><topic>Male</topic><topic>Muscle Fibers, Skeletal - chemistry</topic><topic>Muscle Fibers, Skeletal - metabolism</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Papillary Muscles - chemistry</topic><topic>Papillary Muscles - metabolism</topic><topic>Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ryanodine - metabolism</topic><topic>Ryanodine receptor</topic><topic>Sarcoplasmic Reticulum - metabolism</topic><topic>Skinned fiber</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamaguchi, Fuminari</creatorcontrib><creatorcontrib>Sanbe, Atsushi</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><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>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamaguchi, Fuminari</au><au>Sanbe, Atsushi</au><au>Takeo, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1997-02-01</date><risdate>1997</risdate><volume>29</volume><issue>2</issue><spage>753</spage><epage>763</epage><pages>753-763</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25–0.5 min with 10−5mCa2+(53–70%) and when preloaded with 10−6mCa2+and then exposed to 0.1–1mmcaffeine (39–87%). The results suggest that the rate of Ca2+uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+released from SR decreased due to decreased Ca2+uptake rate of SR and down-regulation of the SR Ca2+-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>9140832</pmid><doi>10.1006/jmcc.1996.0319</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Caffeine - pharmacology Calcium - metabolism Calcium - pharmacokinetics Calcium release Calcium sensitivity Calcium uptake Cell Membrane - metabolism Central Nervous System Stimulants - pharmacology Heart Failure - physiopathology Hemodynamics Histocytological Preparation Techniques Male Muscle Fibers, Skeletal - chemistry Muscle Fibers, Skeletal - metabolism Myocardial Contraction - drug effects Myocardial Infarction - physiopathology Myocardium - metabolism Papillary Muscles - chemistry Papillary Muscles - metabolism Proteins - metabolism Rats Rats, Wistar Ryanodine - metabolism Ryanodine receptor Sarcoplasmic Reticulum - metabolism Skinned fiber |
| title | Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction |
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