CARDIAC STAIRCASE AND NMR-DETERMINED INTRACELLULAR SODIUM IN BEATING RAT HEARTS

Isolated, perfused rat hearts (30 degrees C, n = 13) were paced from 2 18 +/- 4 beats/min to 433 +/- 4 beats/min while systolic and diastolic pressure were recorded and intracellular Na+ concentration ([Na+](i)) was monitored by Na-23 nuclear magnetic resonance (NMR) spectroscopy. [Na+](i) increased progressively with increasing stimulation frequenc y. In seven hearts (group I) an initial, progressive increase in systo lic pressure was observed followed by a decrease in pressure with furt her increase in frequency. From the onset, a progressive decrease in s ystolic pressure was observed in group II (n = 6) in response to incre ased 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 o f 120 +/- 3% of control (P < 0.02). The differential pressure response between group I and group II hearts may reflect an enhanced sensitivi ty of rat hearts to the shortening of the restitution period of the sa rcoplasmic reticulum, outweighing the positive inotropic effect induce d by an increased [Na+](i). Only in rat hearts whose [Na+](i)-induced increase in pressure outweighs the restitution deficit would a complet e positive inotropic effect be anticipated.