TY - JOUR
T1 - Use of a specific mesenteric vasodilator peptide, urotensin I, to reduce afterload in the dog
AU - MacCanneli, K.
AU - Giraud, G.
AU - Lederis, K.
AU - Groves, G.
PY - 1980
Y1 - 1980
N2 - The authors have previously demonstrated that urotensin I, a peptide derived from the urophysis of bony fish, reduced arterial blood pressure of anesthetized dogs by selective dilation of the mesenteric vascular bed. In the present experiments, intavenous infusions of urotensin I produced a sustained increase in cardiac output and decrease in peripheral resistance. The magnitude of the hypotensive response and of reflex effects on the heart appeared to be limited quantitatively by the unique mechanism of action. Coronary artery flow was maintained in spite of a decrease in coronary filling pressure, presumably as a consequence of coronary autoregulation and the increased cardiac output. No direct cardiac effects were observed on close-arterial injection into a coronary artery. An agent with these characteristics which will decrease left ventricle after load is of interest in the management of myocardial failure and possibly of cardiogenic shock. In dogs in which minimal myocardial injury was produced by injection of thrombin into a coronary artery, intravenous infusions of urotensin I restored minimal but statistically significant elevations in right and left ventricular end-diastolic pressures to preinsult levels.
AB - The authors have previously demonstrated that urotensin I, a peptide derived from the urophysis of bony fish, reduced arterial blood pressure of anesthetized dogs by selective dilation of the mesenteric vascular bed. In the present experiments, intavenous infusions of urotensin I produced a sustained increase in cardiac output and decrease in peripheral resistance. The magnitude of the hypotensive response and of reflex effects on the heart appeared to be limited quantitatively by the unique mechanism of action. Coronary artery flow was maintained in spite of a decrease in coronary filling pressure, presumably as a consequence of coronary autoregulation and the increased cardiac output. No direct cardiac effects were observed on close-arterial injection into a coronary artery. An agent with these characteristics which will decrease left ventricle after load is of interest in the management of myocardial failure and possibly of cardiogenic shock. In dogs in which minimal myocardial injury was produced by injection of thrombin into a coronary artery, intravenous infusions of urotensin I restored minimal but statistically significant elevations in right and left ventricular end-diastolic pressures to preinsult levels.
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U2 - 10.1139/y80-214
DO - 10.1139/y80-214
M3 - Article
C2 - 7237239
AN - SCOPUS:0019295932
SN - 0008-4212
VL - 58
SP - 1412
EP - 1417
JO - Canadian Journal of Physiology and Pharmacology
JF - Canadian Journal of Physiology and Pharmacology
IS - 12
ER -