AJP - Heart and Circulatory Physiology, Vol 251, Issue 4 734-H741, Copyright © 1986 by American Physiological Society
Direct cardiac effects of vasopressin and their reversal by a vascular antagonist
W. A. Boyle 3rd and L. D. Segel
We studied the direct cardiac effects of arginine vasopressin (AVP) by use
of an isolated working rat heart model perfused with Krebs-Henseleit
medium. At a concentration of 878 +/- 15 pg/ml, AVP produced significant (P
less than 0.05) decreases in coronary flow (-31 +/- 2%); myocardial O2
consumption (-12 +/- 2%); left ventricular peak systolic pressure (-5 +/-
1%); dP/dtmax (-7 +/- 1%); -dP/dtmax (-6 +/- 3%); peak aortic flow rate (-5
+/- 1%); stroke work (-3 +/- 1%); peak power (-8 +/- 1%); and total output
(-3 +/- 1%). Aortic output increased significantly (+7 +/- 1%) as did
arteriovenous O2 difference (+108 +/- 14 mmHg); left ventricular
end-diastolic pressure (+0.4 +/- 0.1 mmHg); efficiency (+1.5 +/- 0.4%); and
rate of lactate release (+1.27 +/- 0.21 nmol/ml perfusate/min).
Dose-response relationships were studied at 9 +/- 1, 25 +/- 1, 75 +/- 3,
303 +/- 15, and 817 +/- 42 pg AVP/ml. Significant dose-dependent depression
of coronary flow occurred at the three highest AVP concentrations; cardiac
function was significantly depressed at the highest dose. The AVP analogue
d(CH2)5[Tyr(Me)]AVP (20 ng/ml) completely reversed the cardiac effects
attributed to AVP. The data indicate that AVP is a potent direct coronary
constrictor that produces myocardial ischemia and decreased contractile
function at AVP concentrations that are observed in some pathophysiologic
states.(ABSTRACT TRUNCATED AT 250 WORDS)
