Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart
Background and purpose: Carbon monoxide (CO) generated by the enzyme haeme oxygenase‐1 (HO‐1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide‐releasing molecules (CO‐RMs) exerts inotro...
Gespeichert in:
| Veröffentlicht in: | British journal of pharmacology 2006-12, Vol.149 (8), p.1104-1112 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1112 |
|---|---|
| container_issue | 8 |
| container_start_page | 1104 |
| container_title | British journal of pharmacology |
| container_volume | 149 |
| creator | Musameh, M D Fuller, B J Mann, B E Green, C J Motterlini, R |
| description | Background and purpose:
Carbon monoxide (CO) generated by the enzyme haeme oxygenase‐1 (HO‐1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide‐releasing molecules (CO‐RMs) exerts inotropic effects on the myocardium.
Experimental approach:
Rat isolated hearts perfused either at constant flow or constant pressure were used to test the effect of CO‐RMs.
Key results:
CORM‐3, a fast CO releaser, produced a direct positive inotropic effect when cumulative doses (3, 10 and 30 μg min−1) or a single dose (5 μM) were infused at either constant coronary pressure (CCP) or constant coronary flow (CCF). The inotropic effect mediated by CORM‐3 was abolished by blockade of soluble guanylate cyclase or Na+/H+ exchanger, but not by inhibitors of L‐type Ca2+ channels and protein kinase C. CORM‐3 also caused a slight reduction in heart rate but did not alter coronary flow. In contrast, the slow CO releaser CORM‐A1 produced significant coronary vasodilatation when given at the highest concentration (30 μg min−1) but exerted no effect on myocardial contractility or heart rate.
Conclusion and implications:
A rapid CO release from CORM‐3 exerts a direct positive inotropic effect on rat isolated perfused hearts, whereas CO slowly released by CORM‐A1 had no effect on myocardial contractility but caused significant coronary vasodilatation. Both cGMP and Na+/H+ exchange appear to be involved in this effect but further work is needed to determine the relative contribution of each pathway in CO‐mediated inotropic effect.
British Journal of Pharmacology (2006) 149, 1104–1112. doi:10.1038/sj.bjp.0706939 |
| doi_str_mv | 10.1038/sj.bjp.0706939 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2014642</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1179170871</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4881-27e222160ba063029ff1b039775736898b83b544ab4db7e5150d8a7b42156ba83</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhS0EotPCliWKkKhgkcF_iZ1NJRgBRSpqhWBt2c5Nx5EnTu2k0B2PwDPyJLiaiAIbVr7y-Xx87IPQE4LXBDP5KvVr049rLHDdsOYeWhEu6rJiktxHK4yxKAmR8gAdptRjnEVRPUQHROAqT9UKXV2E5CZ3DYUbwhTD6GwBXQd2SkXoCqujCUOxC0P45lr4-f1HBA86ueEyb3qws4dUvNicZ-XTx_QyuxTTNpul4PUEbTFC7OaUh6inYgs6To_Qg077BI-X9Qh9eff28-a0PDt__2Hz-qy0XEpSUgGUUlJjo3HNMG26jhjMmhxbsFo20khmKs614a0RUJEKt1ILwympaqMlO0Ine99xNjtoLQxT1F6N0e10vFFBO_W3MritugzXiuZvqjnNBseLQQxXM6RJ7Vyy4L0eIMxJ1ZIyKhjP4LN_wD7McciPU5QI0lSEkQyt95CNIaUI3e8kBKvbKlXqVa5SLVXmA0__zH-HL91l4PkC6GS176IerEt3nGSck-bWiO65r87DzX-uVW8uTmkO_AtwoLpK</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>217195131</pqid></control><display><type>article</type><title>Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Musameh, M D ; Fuller, B J ; Mann, B E ; Green, C J ; Motterlini, R</creator><creatorcontrib>Musameh, M D ; Fuller, B J ; Mann, B E ; Green, C J ; Motterlini, R</creatorcontrib><description>Background and purpose:
Carbon monoxide (CO) generated by the enzyme haeme oxygenase‐1 (HO‐1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide‐releasing molecules (CO‐RMs) exerts inotropic effects on the myocardium.
Experimental approach:
Rat isolated hearts perfused either at constant flow or constant pressure were used to test the effect of CO‐RMs.
Key results:
CORM‐3, a fast CO releaser, produced a direct positive inotropic effect when cumulative doses (3, 10 and 30 μg min−1) or a single dose (5 μM) were infused at either constant coronary pressure (CCP) or constant coronary flow (CCF). The inotropic effect mediated by CORM‐3 was abolished by blockade of soluble guanylate cyclase or Na+/H+ exchanger, but not by inhibitors of L‐type Ca2+ channels and protein kinase C. CORM‐3 also caused a slight reduction in heart rate but did not alter coronary flow. In contrast, the slow CO releaser CORM‐A1 produced significant coronary vasodilatation when given at the highest concentration (30 μg min−1) but exerted no effect on myocardial contractility or heart rate.
Conclusion and implications:
A rapid CO release from CORM‐3 exerts a direct positive inotropic effect on rat isolated perfused hearts, whereas CO slowly released by CORM‐A1 had no effect on myocardial contractility but caused significant coronary vasodilatation. Both cGMP and Na+/H+ exchange appear to be involved in this effect but further work is needed to determine the relative contribution of each pathway in CO‐mediated inotropic effect.
British Journal of Pharmacology (2006) 149, 1104–1112. doi:10.1038/sj.bjp.0706939</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706939</identifier><identifier>PMID: 17057755</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Alkaloids - pharmacology ; Amiloride - analogs & derivatives ; Amiloride - pharmacology ; Animals ; Benzophenanthridines - pharmacology ; Biological and medical sciences ; Boranes - metabolism ; Boranes - pharmacology ; Calcium Channel Blockers - pharmacology ; Carbon Monoxide - metabolism ; carbon monoxide‐releasing molecules (CO‐RMs) ; Carbonates - metabolism ; Carbonates - pharmacology ; Cardiotonic Agents - pharmacology ; Enzyme Inhibitors - pharmacology ; guanylate cyclase ; Heart - drug effects ; inotropic effect ; Kinetics ; Male ; Medical sciences ; Myocardium - metabolism ; Na+/H+ exchanger ; Nifedipine - pharmacology ; Organometallic Compounds - pharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Lew ; Research Papers ; Signal Transduction - drug effects</subject><ispartof>British journal of pharmacology, 2006-12, Vol.149 (8), p.1104-1112</ispartof><rights>2006 British Pharmacological Society</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2006</rights><rights>Copyright 2006, Nature Publishing Group 2006 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4881-27e222160ba063029ff1b039775736898b83b544ab4db7e5150d8a7b42156ba83</citedby><cites>FETCH-LOGICAL-c4881-27e222160ba063029ff1b039775736898b83b544ab4db7e5150d8a7b42156ba83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014642/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014642/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18344199$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17057755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Musameh, M D</creatorcontrib><creatorcontrib>Fuller, B J</creatorcontrib><creatorcontrib>Mann, B E</creatorcontrib><creatorcontrib>Green, C J</creatorcontrib><creatorcontrib>Motterlini, R</creatorcontrib><title>Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose:
Carbon monoxide (CO) generated by the enzyme haeme oxygenase‐1 (HO‐1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide‐releasing molecules (CO‐RMs) exerts inotropic effects on the myocardium.
Experimental approach:
Rat isolated hearts perfused either at constant flow or constant pressure were used to test the effect of CO‐RMs.
Key results:
CORM‐3, a fast CO releaser, produced a direct positive inotropic effect when cumulative doses (3, 10 and 30 μg min−1) or a single dose (5 μM) were infused at either constant coronary pressure (CCP) or constant coronary flow (CCF). The inotropic effect mediated by CORM‐3 was abolished by blockade of soluble guanylate cyclase or Na+/H+ exchanger, but not by inhibitors of L‐type Ca2+ channels and protein kinase C. CORM‐3 also caused a slight reduction in heart rate but did not alter coronary flow. In contrast, the slow CO releaser CORM‐A1 produced significant coronary vasodilatation when given at the highest concentration (30 μg min−1) but exerted no effect on myocardial contractility or heart rate.
Conclusion and implications:
A rapid CO release from CORM‐3 exerts a direct positive inotropic effect on rat isolated perfused hearts, whereas CO slowly released by CORM‐A1 had no effect on myocardial contractility but caused significant coronary vasodilatation. Both cGMP and Na+/H+ exchange appear to be involved in this effect but further work is needed to determine the relative contribution of each pathway in CO‐mediated inotropic effect.
British Journal of Pharmacology (2006) 149, 1104–1112. doi:10.1038/sj.bjp.0706939</description><subject>Alkaloids - pharmacology</subject><subject>Amiloride - analogs & derivatives</subject><subject>Amiloride - pharmacology</subject><subject>Animals</subject><subject>Benzophenanthridines - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Boranes - metabolism</subject><subject>Boranes - pharmacology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Carbon Monoxide - metabolism</subject><subject>carbon monoxide‐releasing molecules (CO‐RMs)</subject><subject>Carbonates - metabolism</subject><subject>Carbonates - pharmacology</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>guanylate cyclase</subject><subject>Heart - drug effects</subject><subject>inotropic effect</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - metabolism</subject><subject>Na+/H+ exchanger</subject><subject>Nifedipine - pharmacology</subject><subject>Organometallic Compounds - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Research Papers</subject><subject>Signal Transduction - drug effects</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc1u1DAUhS0EotPCliWKkKhgkcF_iZ1NJRgBRSpqhWBt2c5Nx5EnTu2k0B2PwDPyJLiaiAIbVr7y-Xx87IPQE4LXBDP5KvVr049rLHDdsOYeWhEu6rJiktxHK4yxKAmR8gAdptRjnEVRPUQHROAqT9UKXV2E5CZ3DYUbwhTD6GwBXQd2SkXoCqujCUOxC0P45lr4-f1HBA86ueEyb3qws4dUvNicZ-XTx_QyuxTTNpul4PUEbTFC7OaUh6inYgs6To_Qg077BI-X9Qh9eff28-a0PDt__2Hz-qy0XEpSUgGUUlJjo3HNMG26jhjMmhxbsFo20khmKs614a0RUJEKt1ILwympaqMlO0Ine99xNjtoLQxT1F6N0e10vFFBO_W3MritugzXiuZvqjnNBseLQQxXM6RJ7Vyy4L0eIMxJ1ZIyKhjP4LN_wD7McciPU5QI0lSEkQyt95CNIaUI3e8kBKvbKlXqVa5SLVXmA0__zH-HL91l4PkC6GS176IerEt3nGSck-bWiO65r87DzX-uVW8uTmkO_AtwoLpK</recordid><startdate>200612</startdate><enddate>200612</enddate><creator>Musameh, M D</creator><creator>Fuller, B J</creator><creator>Mann, B E</creator><creator>Green, C J</creator><creator>Motterlini, R</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200612</creationdate><title>Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart</title><author>Musameh, M D ; Fuller, B J ; Mann, B E ; Green, C J ; Motterlini, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4881-27e222160ba063029ff1b039775736898b83b544ab4db7e5150d8a7b42156ba83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Alkaloids - pharmacology</topic><topic>Amiloride - analogs & derivatives</topic><topic>Amiloride - pharmacology</topic><topic>Animals</topic><topic>Benzophenanthridines - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Boranes - metabolism</topic><topic>Boranes - pharmacology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Carbon Monoxide - metabolism</topic><topic>carbon monoxide‐releasing molecules (CO‐RMs)</topic><topic>Carbonates - metabolism</topic><topic>Carbonates - pharmacology</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>guanylate cyclase</topic><topic>Heart - drug effects</topic><topic>inotropic effect</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - metabolism</topic><topic>Na+/H+ exchanger</topic><topic>Nifedipine - pharmacology</topic><topic>Organometallic Compounds - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Research Papers</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Musameh, M D</creatorcontrib><creatorcontrib>Fuller, B J</creatorcontrib><creatorcontrib>Mann, B E</creatorcontrib><creatorcontrib>Green, C J</creatorcontrib><creatorcontrib>Motterlini, R</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Musameh, M D</au><au>Fuller, B J</au><au>Mann, B E</au><au>Green, C J</au><au>Motterlini, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2006-12</date><risdate>2006</risdate><volume>149</volume><issue>8</issue><spage>1104</spage><epage>1112</epage><pages>1104-1112</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose:
Carbon monoxide (CO) generated by the enzyme haeme oxygenase‐1 (HO‐1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide‐releasing molecules (CO‐RMs) exerts inotropic effects on the myocardium.
Experimental approach:
Rat isolated hearts perfused either at constant flow or constant pressure were used to test the effect of CO‐RMs.
Key results:
CORM‐3, a fast CO releaser, produced a direct positive inotropic effect when cumulative doses (3, 10 and 30 μg min−1) or a single dose (5 μM) were infused at either constant coronary pressure (CCP) or constant coronary flow (CCF). The inotropic effect mediated by CORM‐3 was abolished by blockade of soluble guanylate cyclase or Na+/H+ exchanger, but not by inhibitors of L‐type Ca2+ channels and protein kinase C. CORM‐3 also caused a slight reduction in heart rate but did not alter coronary flow. In contrast, the slow CO releaser CORM‐A1 produced significant coronary vasodilatation when given at the highest concentration (30 μg min−1) but exerted no effect on myocardial contractility or heart rate.
Conclusion and implications:
A rapid CO release from CORM‐3 exerts a direct positive inotropic effect on rat isolated perfused hearts, whereas CO slowly released by CORM‐A1 had no effect on myocardial contractility but caused significant coronary vasodilatation. Both cGMP and Na+/H+ exchange appear to be involved in this effect but further work is needed to determine the relative contribution of each pathway in CO‐mediated inotropic effect.
British Journal of Pharmacology (2006) 149, 1104–1112. doi:10.1038/sj.bjp.0706939</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17057755</pmid><doi>10.1038/sj.bjp.0706939</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-1188 |
| ispartof | British journal of pharmacology, 2006-12, Vol.149 (8), p.1104-1112 |
| issn | 0007-1188 1476-5381 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2014642 |
| source | MEDLINE; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | Alkaloids - pharmacology Amiloride - analogs & derivatives Amiloride - pharmacology Animals Benzophenanthridines - pharmacology Biological and medical sciences Boranes - metabolism Boranes - pharmacology Calcium Channel Blockers - pharmacology Carbon Monoxide - metabolism carbon monoxide‐releasing molecules (CO‐RMs) Carbonates - metabolism Carbonates - pharmacology Cardiotonic Agents - pharmacology Enzyme Inhibitors - pharmacology guanylate cyclase Heart - drug effects inotropic effect Kinetics Male Medical sciences Myocardium - metabolism Na+/H+ exchanger Nifedipine - pharmacology Organometallic Compounds - pharmacology Pharmacology. Drug treatments Rats Rats, Inbred Lew Research Papers Signal Transduction - drug effects |
| title | Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T12%3A44%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Positive%20inotropic%20effects%20of%20carbon%20monoxide%E2%80%90releasing%20molecules%20(CO%E2%80%90RMs)%20in%20the%20isolated%20perfused%20rat%20heart&rft.jtitle=British%20journal%20of%20pharmacology&rft.au=Musameh,%20M%20D&rft.date=2006-12&rft.volume=149&rft.issue=8&rft.spage=1104&rft.epage=1112&rft.pages=1104-1112&rft.issn=0007-1188&rft.eissn=1476-5381&rft.coden=BJPCBM&rft_id=info:doi/10.1038/sj.bjp.0706939&rft_dat=%3Cproquest_pubme%3E1179170871%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=217195131&rft_id=info:pmid/17057755&rfr_iscdi=true |