The α-MSH analogue AP214 attenuates rise in pulmonary pressure and fall in ejection fraction in lipopolysaccharide-induced systemic inflammatory response syndrome in pigs
Summary Background: The effect of an α‐melanocyte stimulating hormone (α‐MSH) analogue (AP214) on experimentally endotoxin‐induced systemic inflammatory response syndrome (SIRS) was studied, because α‐MSH in rodent models has shown promise in attenuating inflammatory response markers and associated...
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| creator | Kristensen, Jens Jonassen, Thomas E. N. Rehling, Michael Tønnesen, Else Sloth, Erik Nielsen, Søren Frøkiær, Jørgen |
| description | Summary
Background: The effect of an α‐melanocyte stimulating hormone (α‐MSH) analogue (AP214) on experimentally endotoxin‐induced systemic inflammatory response syndrome (SIRS) was studied, because α‐MSH in rodent models has shown promise in attenuating inflammatory response markers and associated organ damage in SIRS. SIRS is associated with considerable morbidity and mortality. Consequently, new treatment modalities are still warranted to address the different aspects of the pathophysiological process.
Methods: SIRS was induced by lipopolysaccharide (LPS) (Escherichia coli endotoxin) infusion in anaesthetized Danish Landrace pigs (20–25 kg). The pigs received an α‐MSH analogue (AP214) or saline as a bolus at the initiation of the LPS infusion. The hemodynamic response was registered as well as echocardiographic indices of left ventricular function.
Results: The cardiovascular response was recorded together with echocardiographic indices of left ventricular function in control and in intervention animals. AP214 reduced the early peak in pulmonary pressure and pulmonary vascular resistance by approximately 33%. Furthermore, AP214 prevented the decline in left ventricular fractional shortening as observed in the control group. Mean change and standard deviation in fractional shortening (ΔFS) in control group: ‐ 7·3 (4·7), AP214 (low dose): 0·9 (8·2) and AP214 (high dose) 4·1 (6·0), P |
| doi_str_mv | 10.1111/j.1475-097X.2010.00979.x |
| format | Article |
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Background: The effect of an α‐melanocyte stimulating hormone (α‐MSH) analogue (AP214) on experimentally endotoxin‐induced systemic inflammatory response syndrome (SIRS) was studied, because α‐MSH in rodent models has shown promise in attenuating inflammatory response markers and associated organ damage in SIRS. SIRS is associated with considerable morbidity and mortality. Consequently, new treatment modalities are still warranted to address the different aspects of the pathophysiological process.
Methods: SIRS was induced by lipopolysaccharide (LPS) (Escherichia coli endotoxin) infusion in anaesthetized Danish Landrace pigs (20–25 kg). The pigs received an α‐MSH analogue (AP214) or saline as a bolus at the initiation of the LPS infusion. The hemodynamic response was registered as well as echocardiographic indices of left ventricular function.
Results: The cardiovascular response was recorded together with echocardiographic indices of left ventricular function in control and in intervention animals. AP214 reduced the early peak in pulmonary pressure and pulmonary vascular resistance by approximately 33%. Furthermore, AP214 prevented the decline in left ventricular fractional shortening as observed in the control group. Mean change and standard deviation in fractional shortening (ΔFS) in control group: ‐ 7·3 (4·7), AP214 (low dose): 0·9 (8·2) and AP214 (high dose) 4·1 (6·0), P < 0·05 for both intervention groups versus control.
Conclusions: In the porcine model, the peak increase in pulmonary pressure was attenuated, and the LPS‐induced decline in left ventricular function was prevented.</description><identifier>ISSN: 1475-0961</identifier><identifier>EISSN: 1475-097X</identifier><identifier>DOI: 10.1111/j.1475-097X.2010.00979.x</identifier><identifier>PMID: 21029328</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>alpha-MSH - analogs & derivatives ; alpha-MSH - pharmacology ; Analogue ; Animals ; Attenuation ; Biological and medical sciences ; Echocardiography ; Ejection ; Endotoxins - pharmacology ; experimental ; Female ; Fundamental and applied biological sciences. Psychology ; Glomerular Filtration Rate - drug effects ; Heart Ventricles - diagnostic imaging ; Heart Ventricles - drug effects ; Heart Ventricles - physiopathology ; Hemodynamics - drug effects ; Imaging ; Inflammatory response ; Lipopolysaccharides ; Lung - blood supply ; Lung - drug effects ; Lung - physiopathology ; Physiology ; Pigs ; sepsis ; Swine ; Systemic Inflammatory Response Syndrome - chemically induced ; Systemic Inflammatory Response Syndrome - diagnostic imaging ; Systemic Inflammatory Response Syndrome - drug therapy ; Systemic Inflammatory Response Syndrome - physiopathology ; Vascular Resistance - drug effects ; Ventricular Function, Left - drug effects ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Clinical physiology and functional imaging, 2011-01, Vol.31 (1), p.54-60</ispartof><rights>2010 The Authors. Clinical Physiology and Functional Imaging © 2010 Scandinavian Society of Clinical Physiology and Nuclear Medicine</rights><rights>2015 INIST-CNRS</rights><rights>2010 The Authors. Clinical Physiology and Functional Imaging © 2010 Scandinavian Society of Clinical Physiology and Nuclear Medicine.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4189-50118cd5f2b482583362654982c2ef2a465190c87bbc1329c13c1eb78cbea1533</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1475-097X.2010.00979.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1475-097X.2010.00979.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,4024,27923,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23624081$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21029328$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kristensen, Jens</creatorcontrib><creatorcontrib>Jonassen, Thomas E. N.</creatorcontrib><creatorcontrib>Rehling, Michael</creatorcontrib><creatorcontrib>Tønnesen, Else</creatorcontrib><creatorcontrib>Sloth, Erik</creatorcontrib><creatorcontrib>Nielsen, Søren</creatorcontrib><creatorcontrib>Frøkiær, Jørgen</creatorcontrib><title>The α-MSH analogue AP214 attenuates rise in pulmonary pressure and fall in ejection fraction in lipopolysaccharide-induced systemic inflammatory response syndrome in pigs</title><title>Clinical physiology and functional imaging</title><addtitle>Clin Physiol Funct Imaging</addtitle><description>Summary
Background: The effect of an α‐melanocyte stimulating hormone (α‐MSH) analogue (AP214) on experimentally endotoxin‐induced systemic inflammatory response syndrome (SIRS) was studied, because α‐MSH in rodent models has shown promise in attenuating inflammatory response markers and associated organ damage in SIRS. SIRS is associated with considerable morbidity and mortality. Consequently, new treatment modalities are still warranted to address the different aspects of the pathophysiological process.
Methods: SIRS was induced by lipopolysaccharide (LPS) (Escherichia coli endotoxin) infusion in anaesthetized Danish Landrace pigs (20–25 kg). The pigs received an α‐MSH analogue (AP214) or saline as a bolus at the initiation of the LPS infusion. The hemodynamic response was registered as well as echocardiographic indices of left ventricular function.
Results: The cardiovascular response was recorded together with echocardiographic indices of left ventricular function in control and in intervention animals. AP214 reduced the early peak in pulmonary pressure and pulmonary vascular resistance by approximately 33%. Furthermore, AP214 prevented the decline in left ventricular fractional shortening as observed in the control group. Mean change and standard deviation in fractional shortening (ΔFS) in control group: ‐ 7·3 (4·7), AP214 (low dose): 0·9 (8·2) and AP214 (high dose) 4·1 (6·0), P < 0·05 for both intervention groups versus control.
Conclusions: In the porcine model, the peak increase in pulmonary pressure was attenuated, and the LPS‐induced decline in left ventricular function was prevented.</description><subject>alpha-MSH - analogs & derivatives</subject><subject>alpha-MSH - pharmacology</subject><subject>Analogue</subject><subject>Animals</subject><subject>Attenuation</subject><subject>Biological and medical sciences</subject><subject>Echocardiography</subject><subject>Ejection</subject><subject>Endotoxins - pharmacology</subject><subject>experimental</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Heart Ventricles - diagnostic imaging</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hemodynamics - drug effects</subject><subject>Imaging</subject><subject>Inflammatory response</subject><subject>Lipopolysaccharides</subject><subject>Lung - blood supply</subject><subject>Lung - drug effects</subject><subject>Lung - physiopathology</subject><subject>Physiology</subject><subject>Pigs</subject><subject>sepsis</subject><subject>Swine</subject><subject>Systemic Inflammatory Response Syndrome - chemically induced</subject><subject>Systemic Inflammatory Response Syndrome - diagnostic imaging</subject><subject>Systemic Inflammatory Response Syndrome - drug therapy</subject><subject>Systemic Inflammatory Response Syndrome - physiopathology</subject><subject>Vascular Resistance - drug effects</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>1475-0961</issn><issn>1475-097X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAQxyMEoqXwCsgXxCmL7Xw5Epdq1d0iSimiCG6W40xaL44T7ERsnokTL8IzMSHLcsQHezTz-8_IMxNFhNEVw_Nqt2JpkcW0LL6sOEUvRbNc7R9Ep8fAw6Ods5PoSQg7SlmRpMXj6IQzysuEi9Pox-09kF8_43cfL4lyynZ3I5DzG85SooYB3KgGCMSbAMQ40o-27ZzyE-k9hDB6QFFNGmXtHIYd6MF0jjReLQY6rem7vrNTUFrfK29qiI2rRw01CVMYoDUascaqtlVDh6kxc985LBgmV_uuXSqbu_A0eoSVAjw7vGfRp83F7foyvnq_fbM-v4p1ykQZZ5Qxoeus4VUqeCaSJOd5lpaCaw4NV2mesZJqUVSVZgkv8dIMqkLoChTLkuQsernk7X33bYQwyNYEDdYqB90YpMhnClP-n8Q-ClakGZLPD-RYtVDL3psW-yj_TgKBFwdABa0sdtBpE_5x-ImUCobc64X7bixMxzijct4MuZPz0OW8AHLeDPlnM-Rerm82aKA8XuQGW78_ypX_KvMiQeXn661km-stL99y-SH5DRazvcQ</recordid><startdate>201101</startdate><enddate>201101</enddate><creator>Kristensen, Jens</creator><creator>Jonassen, Thomas E. N.</creator><creator>Rehling, Michael</creator><creator>Tønnesen, Else</creator><creator>Sloth, Erik</creator><creator>Nielsen, Søren</creator><creator>Frøkiær, Jørgen</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>201101</creationdate><title>The α-MSH analogue AP214 attenuates rise in pulmonary pressure and fall in ejection fraction in lipopolysaccharide-induced systemic inflammatory response syndrome in pigs</title><author>Kristensen, Jens ; Jonassen, Thomas E. N. ; Rehling, Michael ; Tønnesen, Else ; Sloth, Erik ; Nielsen, Søren ; Frøkiær, Jørgen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4189-50118cd5f2b482583362654982c2ef2a465190c87bbc1329c13c1eb78cbea1533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>alpha-MSH - analogs & derivatives</topic><topic>alpha-MSH - pharmacology</topic><topic>Analogue</topic><topic>Animals</topic><topic>Attenuation</topic><topic>Biological and medical sciences</topic><topic>Echocardiography</topic><topic>Ejection</topic><topic>Endotoxins - pharmacology</topic><topic>experimental</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Heart Ventricles - diagnostic imaging</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hemodynamics - drug effects</topic><topic>Imaging</topic><topic>Inflammatory response</topic><topic>Lipopolysaccharides</topic><topic>Lung - blood supply</topic><topic>Lung - drug effects</topic><topic>Lung - physiopathology</topic><topic>Physiology</topic><topic>Pigs</topic><topic>sepsis</topic><topic>Swine</topic><topic>Systemic Inflammatory Response Syndrome - chemically induced</topic><topic>Systemic Inflammatory Response Syndrome - diagnostic imaging</topic><topic>Systemic Inflammatory Response Syndrome - drug therapy</topic><topic>Systemic Inflammatory Response Syndrome - physiopathology</topic><topic>Vascular Resistance - drug effects</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kristensen, Jens</creatorcontrib><creatorcontrib>Jonassen, Thomas E. N.</creatorcontrib><creatorcontrib>Rehling, Michael</creatorcontrib><creatorcontrib>Tønnesen, Else</creatorcontrib><creatorcontrib>Sloth, Erik</creatorcontrib><creatorcontrib>Nielsen, Søren</creatorcontrib><creatorcontrib>Frøkiær, Jørgen</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Clinical physiology and functional imaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kristensen, Jens</au><au>Jonassen, Thomas E. N.</au><au>Rehling, Michael</au><au>Tønnesen, Else</au><au>Sloth, Erik</au><au>Nielsen, Søren</au><au>Frøkiær, Jørgen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The α-MSH analogue AP214 attenuates rise in pulmonary pressure and fall in ejection fraction in lipopolysaccharide-induced systemic inflammatory response syndrome in pigs</atitle><jtitle>Clinical physiology and functional imaging</jtitle><addtitle>Clin Physiol Funct Imaging</addtitle><date>2011-01</date><risdate>2011</risdate><volume>31</volume><issue>1</issue><spage>54</spage><epage>60</epage><pages>54-60</pages><issn>1475-0961</issn><eissn>1475-097X</eissn><abstract>Summary
Background: The effect of an α‐melanocyte stimulating hormone (α‐MSH) analogue (AP214) on experimentally endotoxin‐induced systemic inflammatory response syndrome (SIRS) was studied, because α‐MSH in rodent models has shown promise in attenuating inflammatory response markers and associated organ damage in SIRS. SIRS is associated with considerable morbidity and mortality. Consequently, new treatment modalities are still warranted to address the different aspects of the pathophysiological process.
Methods: SIRS was induced by lipopolysaccharide (LPS) (Escherichia coli endotoxin) infusion in anaesthetized Danish Landrace pigs (20–25 kg). The pigs received an α‐MSH analogue (AP214) or saline as a bolus at the initiation of the LPS infusion. The hemodynamic response was registered as well as echocardiographic indices of left ventricular function.
Results: The cardiovascular response was recorded together with echocardiographic indices of left ventricular function in control and in intervention animals. AP214 reduced the early peak in pulmonary pressure and pulmonary vascular resistance by approximately 33%. Furthermore, AP214 prevented the decline in left ventricular fractional shortening as observed in the control group. Mean change and standard deviation in fractional shortening (ΔFS) in control group: ‐ 7·3 (4·7), AP214 (low dose): 0·9 (8·2) and AP214 (high dose) 4·1 (6·0), P < 0·05 for both intervention groups versus control.
Conclusions: In the porcine model, the peak increase in pulmonary pressure was attenuated, and the LPS‐induced decline in left ventricular function was prevented.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21029328</pmid><doi>10.1111/j.1475-097X.2010.00979.x</doi><tpages>7</tpages></addata></record> |
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| subjects | alpha-MSH - analogs & derivatives alpha-MSH - pharmacology Analogue Animals Attenuation Biological and medical sciences Echocardiography Ejection Endotoxins - pharmacology experimental Female Fundamental and applied biological sciences. Psychology Glomerular Filtration Rate - drug effects Heart Ventricles - diagnostic imaging Heart Ventricles - drug effects Heart Ventricles - physiopathology Hemodynamics - drug effects Imaging Inflammatory response Lipopolysaccharides Lung - blood supply Lung - drug effects Lung - physiopathology Physiology Pigs sepsis Swine Systemic Inflammatory Response Syndrome - chemically induced Systemic Inflammatory Response Syndrome - diagnostic imaging Systemic Inflammatory Response Syndrome - drug therapy Systemic Inflammatory Response Syndrome - physiopathology Vascular Resistance - drug effects Ventricular Function, Left - drug effects Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | The α-MSH analogue AP214 attenuates rise in pulmonary pressure and fall in ejection fraction in lipopolysaccharide-induced systemic inflammatory response syndrome in pigs |
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