Positive inotropic effect on the rat atrial myocardium compressed to 5, 10 and 30 bar

The contractile activity of spontaneously beating auricular preparations from the rat was studied during and after pressure exposure to 5, 10 and 30 bar in three series of experiments (compression and decompression rate: I bar min^‐1). The preparations were mounted in an organ bath within a pressure chamber and perfused with oxygenated preheated Krebs‐Henseleit solution (37 °C, pH = 7.45) containing α, β‐ and muscarinic‐receptor blockers and blockers of the neuronal and extraneuronal uptake mechanisms. No change in chronotropy of the cardiac preparations were observed during or after exposures to the pressures tested. Significant increase in cardiac contractility (20–40%, P < 0.01) described by the peak tension (T_max), the maximal velocity of tension rise (T'_max) and fall (T'_max) were apparent at 5 and 10 bar. Further significant elevations (6–80%, P < 0.05) in T'_max, T' and T'_min were detected during exposure to 30 bar. The cardiac contractility increased rapidly with pressure, was approximately unchanged during stable elevated pressures at 5, 10 and 30 bar, but was maintained above control values 15 min after completed decompression. Since no change in chronotropy and loading of the preparations occurred, it is concluded that the increased contractility is due to a positive inotropy generated by the hydrostatic pressure. Furthermore, it is indicated that this positive inotropy is not related to adrenoceptor activation since the effect was achieved in the presence of α, and β‐adrenoceptor blockade.