Action potential correlates of pressure-induced changes in cardiac conduction.

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.