Hydrostatic pressure and mammalian cardiac-pacemaker function

The effects of hydrostatic pressure on pacemaker function were examined using sinus node preparations isolated from mouse, rat, guinea pig, rabbit, and dog hearts. In all species studied, an increase in hydrostatic pressure produced a reduction in beating frequency the magnitude of which varied directly with the magnitude of the intrinsic beating frequency of each species at 1 atm. Such slowing was evident over a wide temperature range (22.5-37°C) and persisted in the presence of atropine and propranalol. Adaptational changes were seen after long exposures to elevated pressure. For example, decompression after 2-3 hours at 150 atm resulted in beating frequencies faster than initial 1-atm control values. Additional evidence for the negative chronotropic action of pressure was provided by the finding that elevated pressure increased the suppression of spontaneous rate normally following periods of raplid stimulation, i.e., enhanced overdrive suppression. Microelectrode analysis of spontaneously beating Purkinje fibers revealed that the major cellular action of elevated pressure to cause slowing was a decrease in the rate of diastolic depolarization. It was concluded that hydrostatic pressure acting directly at the level of the pacemaker cell membrane represents an important factor modulating heart rate in diving man. However, other changes occurring simultaneously with pressure-induced bradycardia indicate that conduction disturbances may also develop under these conditions.