Journal of Applied Physiology, Vol 81, Issue 2 573-577, Copyright © 1996 by American Physiological Society
Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia
T. Lauri
Department of Physiology, University of Oulu, Finland.
The aim of this study was to investigate the effects of beta-stimulation in
deep (25 degrees C) hypothermia. Cardiac catheterization was performed on
seven anesthetized beagle dogs. They were cooled between ice bags down to
25 degrees C and received isoproterenol administered intravenously three
times: at the normal body temperature (37 degrees C) before cooling, after
cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory
function was measured for every 1 degree C of temperature change.
Isoproterenol infusion at 37 degrees C induced cardiac acceleration,
including the increases of heart rate, cardiac output, and peak first
derivative of the left ventricular pressure curve. Systemic vascular and
mean outflow resistances and mean aortic pressure decreased. During
cooling, shivering thermogenesis continued, even down to 25 degrees C. At
25 degrees C, cardiac acceleration after isoproterenol infusion did not
exist but relaxation rate increased slightly. Systemic vascular and mean
outflow resistances decreased, but left ventricular end-diastolic and
filling pressures increased. beta-Stimulation at normal body temperature
increases shivering thermogenesis during cooling. The venous return to the
left ventricle at 25 degrees C increased after isoproterenol infusion while
systemic vascular resistance decreased, indicating systemic vasodilatation.
This increase in preload is probably due to vasoconstriction in pulmonary
vessels, which may be mediated by prejunctional beta-adrenoceptors. For
cardiac inotrophy, the isoproterenol had no physiologically significant
effects at 25 degrees C. After rewarming at 37 degrees C, the effects of
isoproterenol were physiologically similar to the effects at the same
temperature before cooling.
