Open AccessThe Role of Beta Receptors in the Peripheral Vasculature of Calves with a Total Artificial Heart
Author(s) -
Lauri K. Kalanges,
Kevin Murray,
Philip F. Binkley,
E. Paul Howanitz,
Timothy A. Galbraith,
Kim M. Watson,
Patty A. Lowe,
Paul D. Myerowitz
Publication year - 1989
Publication title -
asaio transactions
Language(s) - English
Resource type - Journals
eISSN - 2375-0952
pISSN - 0889-7190
DOI - 10.1097/00002480-198907000-00033
Subject(s) - preload , propranolol , blockade , medicine , cardiac output , heart rate , beta (programming language) , agonist , antagonist , isoprenaline , cardiology , venous return curve , endocrinology , receptor , anesthesia , hemodynamics , blood pressure , stimulation , computer science , programming language
Drugs given to a total artificial heart (TAH) calf isolate their vascular effects independent of the myocardium. During experiments, the TAH maintains full ejection, constant heart rate, and percent systole, and uses no vacuum. Cardiac output (CO) varies solely and directly with preload. Six calves received an infusion of isoproterenol, a beta agonist, and three calves received propranolol, a beta antagonist. The isoproterenol was resumed after beta blockade. Isoproterenol alone caused a significant increase in CO, an effect that was attenuated but not eliminated with beta blockade. Both isoproterenol and propranolol decreased AoP, but only isoproterenol increased preload. Beta receptors play a significant role in decreasing venous capacitance with increased preload and CO, independent of the myocardium.