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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Arnolda, L | en |
dc.contributor.author | McGrath, B P | en |
dc.contributor.author | Johnston, Colin I | en |
dc.date.accessioned | 2015-05-15T23:59:28Z | |
dc.date.available | 2015-05-15T23:59:28Z | |
dc.date.issued | 1991-02-01 | en |
dc.identifier.citation | The American Journal of Physiology; 260(2 Pt 2): H499-506 | en |
dc.identifier.govdoc | 1825456 | en |
dc.identifier.other | PUBMED | en |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/10521 | en |
dc.description.abstract | The 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.iso | en | en |
dc.subject.other | Acute Disease | en |
dc.subject.other | Angiotensin II.physiology | en |
dc.subject.other | Angiotensin Receptor Antagonists | en |
dc.subject.other | Angiotensin-Converting Enzyme Inhibitors.pharmacology | en |
dc.subject.other | Animals | en |
dc.subject.other | Arginine Vasopressin.antagonists & inhibitors.physiology | en |
dc.subject.other | Blood Pressure.drug effects | en |
dc.subject.other | Cardiac Output, Low.etiology.physiopathology | en |
dc.subject.other | Electroshock | en |
dc.subject.other | Female | en |
dc.subject.other | Heart Ventricles | en |
dc.subject.other | Hemodynamics.drug effects | en |
dc.subject.other | Hormones.blood | en |
dc.subject.other | Male | en |
dc.subject.other | Rabbits | en |
dc.subject.other | Receptors, Vasopressin | en |
dc.subject.other | Regional Blood Flow | en |
dc.subject.other | Vasopressins.metabolism | en |
dc.title | Systemic and regional effects of vasopressin and angiotensin in acute left ventricular failure. | en |
dc.type | Journal Article | en |
dc.identifier.journaltitle | American Journal of Physiology | en |
dc.identifier.affiliation | Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia | en |
dc.description.pages | H499-506 | en |
dc.relation.url | https://pubmed.ncbi.nlm.nih.gov/1825456 | en |
dc.type.austin | Journal Article | en |
item.fulltext | No Fulltext | - |
item.openairetype | Journal Article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.languageiso639-1 | en | - |
item.cerifentitytype | Publications | - |
Appears in Collections: | Journal articles |
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