Journal of Applied Physiology, Vol 47, Issue 6 1169-1175, Copyright © 1979 by American Physiological Society
Action potential correlates of pressure-induced changes in cardiac conduction
T. J. Doubt and P. M. Hogan
Microelectrode studies were undertaken to determine the cellular bases for
hydrostatic pressure effects on impulse propagation and refractoriness in
cardiac muscle. Canine Purkinje fibers, at 37 degrees C, were exposed to
increases in hydrostatic pressure to 150 ATA. At 150 ATA membrane
excitability was depressed and the maximum upstroke velocity (Vmax) of the
action potential was reduced by 10%. Furthermore, the curve relating Vmax
to takeoff potential (membrane responsiveness relation) shifted downward
and to the right with the half inactivation voltage shifting in the
hyperpolarizing direction by about 4 mV. Decreases in excitability and
responsiveness occurred concomitantly with pressure-induced decreases in
impulse conduction. Action potential duration (APD) increased significantly
at 150 ATA. APD measured at -20 mV, -60 mV, and at maximum repolarization
averaged 20.7, 15.5, and 13.5% longer than their respective 1-ATA values.
The combined effects of increased APD and depressed responsiveness account
for increased tissue refractoriness. The implications of the findings with
regard to the arrhythmogenic nature of high hydrostatic pressure are
discussed.
