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Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study
Sepsis is a life threatening condition that is characterized by the loss of vascular reactivity. The factor(s) responsible for the diminished vascular function seen in sepsis are not well understood. The purpose of this study was to characterize the vascular dysfunction from the rat cecal inoculum (...
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| Published in: | Life sciences (1973) 2015-11, Vol.141 (C), p.108-118 |
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| Main Authors: | , , , , , , , |
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| container_end_page | 118 |
| container_issue | C |
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| container_title | Life sciences (1973) |
| container_volume | 141 |
| creator | Asano, Shinichi Manne, Nandini D.P.K. Nandyala, Geeta Ma, Bing Selvaraj, Vellaisamy Arvapalli, Ravikumar Rice, Kevin M. R. Blough, Eric |
| description | Sepsis is a life threatening condition that is characterized by the loss of vascular reactivity. The factor(s) responsible for the diminished vascular function seen in sepsis are not well understood. The purpose of this study was to characterize the vascular dysfunction from the rat cecal inoculum (CI) sepsis model using cecal ligation and puncture (CLP), and lipopolysaccharide (LPS) sepsis as reference models.
Experiments were performed on isolated aorta from CI, CLP and LPS treated rats using a combination of pharmacological approaches.
Phenylephrine (PE)-induced aortic contraction was significantly decreased in each model (p |
| doi_str_mv | 10.1016/j.lfs.2015.09.020 |
| format | article |
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Experiments were performed on isolated aorta from CI, CLP and LPS treated rats using a combination of pharmacological approaches.
Phenylephrine (PE)-induced aortic contraction was significantly decreased in each model (p<0.05) and not normalized by L-NAME or indomethacin. The vascular response elicited in the CI model for acetylcholine (Ach) was more similar to that seen in the CLP than the LPS model. The removal of the endothelial layer increased sensitivity to L-NAME (p<0.05) in aortae from CI group. Inhibition of the large conductance Ca2+/voltage sensitive K+ (BKCa) channel did not normalize PE hyporesponsiveness but did abolish sepsis-induced contractile oscillation. Inhibition of the voltage dependent Kv1.5 channel was not able to reverse the vascular hyporesponsiveness, however, inhibition of the ATP dependent (KATP) channel inhibition partially restored the contractile response (p<0.05). Elevation of VCAM expression and aortic structural alternation were observed in each model.
These results suggest that the CI model may be an additional tool that could be used to investigate the mechanisms of vascular hyporesponsiveness in sepsis.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2015.09.020</identifier><identifier>PMID: 26417684</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Cecum - microbiology ; Cecum - pathology ; Enzyme Inhibitors - pharmacology ; K+ channel ; KATP Channels - drug effects ; Large-Conductance Calcium-Activated Potassium Channels - drug effects ; Ligation ; Lipopolysaccharides - pharmacology ; Male ; Muscle Contraction - drug effects ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Peritonitis - microbiology ; Peritonitis - pathology ; Phenylephrine - pharmacology ; Rats ; Rats, Sprague-Dawley ; Sepsis ; Sepsis - microbiology ; Sepsis - pathology ; Vascular Diseases - microbiology ; Vascular Diseases - pathology ; Vascular inflammation ; Vasoconstrictor Agents - pharmacology ; Vasodilator Agents - pharmacology</subject><ispartof>Life sciences (1973), 2015-11, Vol.141 (C), p.108-118</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-54af0525e9ccdcaaccf13c4cc0b0d3582a55e601df02377f8f7ac6ffdb8e8dee3</citedby><cites>FETCH-LOGICAL-c423t-54af0525e9ccdcaaccf13c4cc0b0d3582a55e601df02377f8f7ac6ffdb8e8dee3</cites><orcidid>0000-0002-5210-5336 ; 0000000252105336</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26417684$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/1359513$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Asano, Shinichi</creatorcontrib><creatorcontrib>Manne, Nandini D.P.K.</creatorcontrib><creatorcontrib>Nandyala, Geeta</creatorcontrib><creatorcontrib>Ma, Bing</creatorcontrib><creatorcontrib>Selvaraj, Vellaisamy</creatorcontrib><creatorcontrib>Arvapalli, Ravikumar</creatorcontrib><creatorcontrib>Rice, Kevin M.</creatorcontrib><creatorcontrib>R. Blough, Eric</creatorcontrib><title>Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Sepsis is a life threatening condition that is characterized by the loss of vascular reactivity. The factor(s) responsible for the diminished vascular function seen in sepsis are not well understood. The purpose of this study was to characterize the vascular dysfunction from the rat cecal inoculum (CI) sepsis model using cecal ligation and puncture (CLP), and lipopolysaccharide (LPS) sepsis as reference models.
Experiments were performed on isolated aorta from CI, CLP and LPS treated rats using a combination of pharmacological approaches.
Phenylephrine (PE)-induced aortic contraction was significantly decreased in each model (p<0.05) and not normalized by L-NAME or indomethacin. The vascular response elicited in the CI model for acetylcholine (Ach) was more similar to that seen in the CLP than the LPS model. The removal of the endothelial layer increased sensitivity to L-NAME (p<0.05) in aortae from CI group. Inhibition of the large conductance Ca2+/voltage sensitive K+ (BKCa) channel did not normalize PE hyporesponsiveness but did abolish sepsis-induced contractile oscillation. Inhibition of the voltage dependent Kv1.5 channel was not able to reverse the vascular hyporesponsiveness, however, inhibition of the ATP dependent (KATP) channel inhibition partially restored the contractile response (p<0.05). Elevation of VCAM expression and aortic structural alternation were observed in each model.
These results suggest that the CI model may be an additional tool that could be used to investigate the mechanisms of vascular hyporesponsiveness in sepsis.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Cecum - microbiology</subject><subject>Cecum - pathology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>K+ channel</subject><subject>KATP Channels - drug effects</subject><subject>Large-Conductance Calcium-Activated Potassium Channels - drug effects</subject><subject>Ligation</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Muscle Contraction - drug effects</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Peritonitis - microbiology</subject><subject>Peritonitis - pathology</subject><subject>Phenylephrine - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sepsis</subject><subject>Sepsis - microbiology</subject><subject>Sepsis - pathology</subject><subject>Vascular Diseases - microbiology</subject><subject>Vascular Diseases - pathology</subject><subject>Vascular inflammation</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp9kDuPEzEUhS0EYsPCD6BBFhVNhmt7PA-oVhEvaSUaoLWc62vhaMYOtidS_v1OlIWS6jTfOTr6GHstoBEguveHZvKlkSB0A2MDEp6wjRj6cQudEk_ZBkC2WyVB37AXpRwAQOtePWc3smtF3w3thv3aEdqJh5hwmZaZHymHmmKooXzgd5HbqVKOtoYT8Tk5mrhPmRc6llD4yZa1ZTN35-KXiDWkyEtd3Pkle-btVOjVY96yn58__dh93d5___Jtd3e_xVaqutWt9aClphHRobWIXihsEWEPTulBWq2pA-E8SNX3fvC9xc57tx9ocETqlr297qZSgykYKuFvTDESViOUHrVQK_TuCh1z-rNQqWYOBWmabKS0FCN61cp-1J1eUXFFMadSMnlzzGG2-WwEmItzczCrc3NxbmA0q_O18-ZxftnP5P41_kpegY9XgFYTp0D5cpQikgv58tOl8J_5B1zNk98</recordid><startdate>20151115</startdate><enddate>20151115</enddate><creator>Asano, Shinichi</creator><creator>Manne, Nandini D.P.K.</creator><creator>Nandyala, Geeta</creator><creator>Ma, Bing</creator><creator>Selvaraj, Vellaisamy</creator><creator>Arvapalli, Ravikumar</creator><creator>Rice, Kevin M.</creator><creator>R. Blough, Eric</creator><general>Elsevier Inc</general><general>Elsevier</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><scope>OTOTI</scope><orcidid>https://orcid.org/0000-0002-5210-5336</orcidid><orcidid>https://orcid.org/0000000252105336</orcidid></search><sort><creationdate>20151115</creationdate><title>Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study</title><author>Asano, Shinichi ; Manne, Nandini D.P.K. ; Nandyala, Geeta ; Ma, Bing ; Selvaraj, Vellaisamy ; Arvapalli, Ravikumar ; Rice, Kevin M. ; R. Blough, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-54af0525e9ccdcaaccf13c4cc0b0d3582a55e601df02377f8f7ac6ffdb8e8dee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Cecum - microbiology</topic><topic>Cecum - pathology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>K+ channel</topic><topic>KATP Channels - drug effects</topic><topic>Large-Conductance Calcium-Activated Potassium Channels - drug effects</topic><topic>Ligation</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Muscle Contraction - drug effects</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide</topic><topic>Peritonitis - microbiology</topic><topic>Peritonitis - pathology</topic><topic>Phenylephrine - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sepsis</topic><topic>Sepsis - microbiology</topic><topic>Sepsis - pathology</topic><topic>Vascular Diseases - microbiology</topic><topic>Vascular Diseases - pathology</topic><topic>Vascular inflammation</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asano, Shinichi</creatorcontrib><creatorcontrib>Manne, Nandini D.P.K.</creatorcontrib><creatorcontrib>Nandyala, Geeta</creatorcontrib><creatorcontrib>Ma, Bing</creatorcontrib><creatorcontrib>Selvaraj, Vellaisamy</creatorcontrib><creatorcontrib>Arvapalli, Ravikumar</creatorcontrib><creatorcontrib>Rice, Kevin M.</creatorcontrib><creatorcontrib>R. Blough, Eric</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><collection>OSTI.GOV</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asano, Shinichi</au><au>Manne, Nandini D.P.K.</au><au>Nandyala, Geeta</au><au>Ma, Bing</au><au>Selvaraj, Vellaisamy</au><au>Arvapalli, Ravikumar</au><au>Rice, Kevin M.</au><au>R. Blough, Eric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2015-11-15</date><risdate>2015</risdate><volume>141</volume><issue>C</issue><spage>108</spage><epage>118</epage><pages>108-118</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Sepsis is a life threatening condition that is characterized by the loss of vascular reactivity. The factor(s) responsible for the diminished vascular function seen in sepsis are not well understood. The purpose of this study was to characterize the vascular dysfunction from the rat cecal inoculum (CI) sepsis model using cecal ligation and puncture (CLP), and lipopolysaccharide (LPS) sepsis as reference models.
Experiments were performed on isolated aorta from CI, CLP and LPS treated rats using a combination of pharmacological approaches.
Phenylephrine (PE)-induced aortic contraction was significantly decreased in each model (p<0.05) and not normalized by L-NAME or indomethacin. The vascular response elicited in the CI model for acetylcholine (Ach) was more similar to that seen in the CLP than the LPS model. The removal of the endothelial layer increased sensitivity to L-NAME (p<0.05) in aortae from CI group. Inhibition of the large conductance Ca2+/voltage sensitive K+ (BKCa) channel did not normalize PE hyporesponsiveness but did abolish sepsis-induced contractile oscillation. Inhibition of the voltage dependent Kv1.5 channel was not able to reverse the vascular hyporesponsiveness, however, inhibition of the ATP dependent (KATP) channel inhibition partially restored the contractile response (p<0.05). Elevation of VCAM expression and aortic structural alternation were observed in each model.
These results suggest that the CI model may be an additional tool that could be used to investigate the mechanisms of vascular hyporesponsiveness in sepsis.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>26417684</pmid><doi>10.1016/j.lfs.2015.09.020</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5210-5336</orcidid><orcidid>https://orcid.org/0000000252105336</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Life sciences (1973), 2015-11, Vol.141 (C), p.108-118 |
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| language | eng |
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| source | Elsevier |
| subjects | Acetylcholine - pharmacology Animals Cecum - microbiology Cecum - pathology Enzyme Inhibitors - pharmacology K+ channel KATP Channels - drug effects Large-Conductance Calcium-Activated Potassium Channels - drug effects Ligation Lipopolysaccharides - pharmacology Male Muscle Contraction - drug effects NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Peritonitis - microbiology Peritonitis - pathology Phenylephrine - pharmacology Rats Rats, Sprague-Dawley Sepsis Sepsis - microbiology Sepsis - pathology Vascular Diseases - microbiology Vascular Diseases - pathology Vascular inflammation Vasoconstrictor Agents - pharmacology Vasodilator Agents - pharmacology |
| title | Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study |
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