File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Endothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide-treated rats: Interaction with nitric oxide

TitleEndothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide-treated rats: Interaction with nitric oxide
Authors
KeywordsCoronary perfusion pressure
Endothelin
Lipopolysaccharide
Myocardial depression
Nitric oxide
Issue Date2004
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical And Experimental Pharmacology And Physiology, 2004, v. 31 n. 9, p. 571-574 How to Cite?
Abstract1. The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO). 2. Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded. 3. In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/- dP/dt max). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly. 4. Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats.
Persistent Identifierhttp://hdl.handle.net/10722/81174
ISSN
2012 Impact Factor: 2.16
2015 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTu, Jen_HK
dc.contributor.authorShan, Qen_HK
dc.contributor.authorJin, Hen_HK
dc.contributor.authorBourreau, JPen_HK
dc.contributor.authorXia, Qen_HK
dc.date.accessioned2010-09-06T08:14:40Z-
dc.date.available2010-09-06T08:14:40Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical And Experimental Pharmacology And Physiology, 2004, v. 31 n. 9, p. 571-574en_HK
dc.identifier.issn0305-1870en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81174-
dc.description.abstract1. The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO). 2. Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded. 3. In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/- dP/dt max). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly. 4. Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEPen_HK
dc.relation.ispartofClinical and Experimental Pharmacology and Physiologyen_HK
dc.subjectCoronary perfusion pressureen_HK
dc.subjectEndothelinen_HK
dc.subjectLipopolysaccharideen_HK
dc.subjectMyocardial depressionen_HK
dc.subjectNitric oxideen_HK
dc.titleEndothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide-treated rats: Interaction with nitric oxideen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1870&volume=31&spage=571&epage=574&date=2004&atitle=Endothelin-1-Mediated+Coronary+vasoconstriction+deteriorates+myocardial+depression+in+hearts+isolated+from+lipopolysaccharide-treated+rats:+interaction+with+nitric+oxideen_HK
dc.identifier.emailBourreau, JP: bourreau@hkucc.hku.hken_HK
dc.identifier.authorityBourreau, JP=rp00389en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1681.2004.04049.xen_HK
dc.identifier.pmid15479162-
dc.identifier.scopuseid_2-s2.0-4944232609en_HK
dc.identifier.hkuros95657en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4944232609&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue9en_HK
dc.identifier.spage571en_HK
dc.identifier.epage574en_HK
dc.identifier.isiWOS:000224248600002-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridTu, J=36836674300en_HK
dc.identifier.scopusauthoridShan, Q=7007145043en_HK
dc.identifier.scopusauthoridJin, H=7403073384en_HK
dc.identifier.scopusauthoridBourreau, JP=7003927886en_HK
dc.identifier.scopusauthoridXia, Q=7202871577en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats