[abstract] HYDROSTATIC PRESSURE AND CARDIAC PACEMAKER FUNCTION

Abstract

We have reported previously that elevated hydrostatic pressure slows the beating frequency of mammalian sinus nodes. The present study examined: 1) the affect of pressure on the voltage determinants of automaticity in single pacemaker cells, and 2) the adaptational changes in pacemaker function associated with prolonged exposure to pressure. Spontaneously beating canine Purkinje fibers were subjected to 100 atm of hydrostatic pressure. Intracellular micro-electrode recordings correlated pressure-induced slowing (from 74.5 +/- 4.5 to 60.5 +/- 3.8 beats/min) with a significant reduction in the rate of dyastolic depolarization (from 34.0 +/- 3.1 to 22.5 +/- 3.2 mv/sec). This result suggests that pressure may modify the kinetics of K+ conductance during diastole. Elevated pressure also increased the degree of overdrive suppression of the spontaneous rate, providing further evidence for the negative chronotropic action of pressure. Long-term adaptational responses were demonstrated using the mouse sinus node preparation. After 3 hours of exposure to 150 atm, decompression to 1atm resulted in a beating frequency faster than the initial 1atm control value. The large overshoot indicates that heart rate adapts to high pressure environments. This finding may explain the gradual disappearance of hyperbaric bradycardia noted in human subjects during long periods at elevated pressure.