Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10521
Title: Systemic and regional effects of vasopressin and angiotensin in acute left ventricular failure.
Authors: Arnolda, L;McGrath, B P;Johnston, Colin I
Affiliation: Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
Issue Date: 1-Feb-1991
Citation: The American Journal of Physiology; 260(2 Pt 2): H499-506
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.
Internal ID Number: 1825456
URI: http://ahro.austin.org.au/austinjspui/handle/1/10521
URL: http://www.ncbi.nlm.nih.gov/pubmed/1825456
Type: Journal Article
Subjects: Acute Disease
Angiotensin II.physiology
Angiotensin Receptor Antagonists
Angiotensin-Converting Enzyme Inhibitors.pharmacology
Animals
Arginine Vasopressin.antagonists & inhibitors.physiology
Blood Pressure.drug effects
Cardiac Output, Low.etiology.physiopathology
Electroshock
Female
Heart Ventricles
Hemodynamics.drug effects
Hormones.blood
Male
Rabbits
Receptors, Vasopressin
Regional Blood Flow
Vasopressins.metabolism
Appears in Collections:Journal articles

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