Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10521
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dc.contributor.authorArnolda, Len
dc.contributor.authorMcGrath, B Pen
dc.contributor.authorJohnston, Colin Ien
dc.date.accessioned2015-05-15T23:59:28Z
dc.date.available2015-05-15T23:59:28Z
dc.date.issued1991-02-01en
dc.identifier.citationThe American Journal of Physiology; 260(2 Pt 2): H499-506en
dc.identifier.govdoc1825456en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10521en
dc.description.abstractThe systemic and regional hemodynamic effects of arginine vasopressin receptor antagonism (AVPA) and angiotensin-converting enzyme inhibition (ACEi) were examined in rabbits with acute left ventricular failure induced by repetitive direct current (DC) shock. Hemodynamic measurements in 24 rabbits 24 h after DC shock compared with 6 sham-operated controls demonstrated a lowered cardiac output (602 +/- 26 vs. 920 +/- 35 ml/min, P less than 0.01), increased left ventricular end-diastolic pressure (LVEDP, 13.6 +/- 1.3 vs. 1.9 +/- 0.5 mmHg, P less than 0.01) and a raised peripheral resistance (9,734 +/- 495 vs. 6,479 +/- 305 dyn.s.cm-5, P less than 0.01). Cerebral blood flow was not altered in rabbits with acute left ventricular failure but intestinal (29 +/- 2 vs. 53 +/- 9 ml/min, P less than 0.01) and renal (82 +/- 6 vs. 130 +/- 8 ml/min, P less than 0.01) blood flows were significantly reduced. No hemodynamic changes were observed after AVPA alone in the acute heart failure group and ACEi alone reduced LVEDP and increased renal vascular conductance. Treatment with both drugs (i.e., AVPA + ACEi) resulted in a significant increase in cardiac output (21%) and a decrease in blood pressure (19%) and peripheral resistance (34%) and restored renal and intestinal blood flows to near normal levels. Thus both vasopressin and angiotensin contribute to the overall increase in peripheral resistance in this model and to the decrease in intestinal and renal blood flow observed. Presumably blockade of one system produced little hemodynamic change because of compensatory increases in the other system.en
dc.language.isoenen
dc.subject.otherAcute Diseaseen
dc.subject.otherAngiotensin II.physiologyen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherArginine Vasopressin.antagonists & inhibitors.physiologyen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherCardiac Output, Low.etiology.physiopathologyen
dc.subject.otherElectroshocken
dc.subject.otherFemaleen
dc.subject.otherHeart Ventriclesen
dc.subject.otherHemodynamics.drug effectsen
dc.subject.otherHormones.blooden
dc.subject.otherMaleen
dc.subject.otherRabbitsen
dc.subject.otherReceptors, Vasopressinen
dc.subject.otherRegional Blood Flowen
dc.subject.otherVasopressins.metabolismen
dc.titleSystemic and regional effects of vasopressin and angiotensin in acute left ventricular failure.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican Journal of Physiologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pagesH499-506en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1825456en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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