Isolated, perfused rat hearts (30 degrees C, n = 13) were paced from 218 +/- 4 beats/min to 433 +/- 4 beats/min while systolic and diastolic pressure were recorded and intracellular Na+ concentration ([Na+]i) was monitored by 23Na nuclear magnetic resonance (NMR) spectroscopy. [Na+]i increased progressively with increasing stimulation frequency. In seven hearts (group I) an initial, progressive increase in systolic pressure was observed followed by a decrease in pressure with further increase in frequency. From the onset, a progressive decrease in systolic pressure was observed in group II (n = 6) in response to increased frequency. In group I an [Na+]i increase of up to 134 +/- 7% of control (P < 0.001) was observed, whereas in group II the gain in [Na+]i with increasing pacing rate was attenuated, reaching a maximum of 120 +/- 3% of control (P < 0.02). The differential pressure response between group I and group II hearts may reflect an enhanced sensitivity of rat hearts to the shortening of the restitution period of the sarcoplasmic reticulum, outweighing the positive inotropic effect induced by an increased [Na+]i. Only in rat hearts whose [Na+]i-induced increase in pressure outweights the restitution deficit would a complete positive inotropic effect be anticipated.
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