Abstract
Intracellular [Na^+^], [H^+^], and [ATP] and mechanical performance were measured in the isovolumic perfused rat heart during ischemia. The concentration of intracellular sodium, [Na^+^]~i~, was determined by atomic absorption spectroscopy under control conditions, and [Na^+^] was monitored by ^23^Na NMR spectroscopy at 1βmin intervals under control conditions and during global ischemia. [ATP], [H^+^], and [P~i~] were measured by ^31^PNMR in a separate group under identical conditions. The control [Na^+^]~i~ measured by atomic absorption was 30.7 Β± 3.3 m__M__(mean Β± SD, n = 6), and [Na^+^]~i~ measured by NMR was 6.2 Β± 0.5 m__M__(n = 3). Brief ischemia (10 min) was associated with a 54% increase in [Na^+^]~i~ which reversed completely with reperfusion. Developed pressure also returned to control values upon reperfusion. Prolonged ischemia (30 min) produced continuous further accumulation of sodium (0.53 m__M__/min, r^2^ = 0.99). [H^+^] also increased approximately linearly early in ischemia (0.084 ΞΌM/min, r^2^ = 0.97). The rate of increase in [Na^+^]~i~ was more than 4000 times greater than the increase in [H^+^] on a molar basis. Nevertheless, [H^+^]/[Na^+^] increased early in ischemia because the proportional change in [H^+^] was greater than that in [Na^+^] ~i~. These results indicate that (1) intracellular sodium measured by NMR in the functioning heart is about 20% of total intracellular sodium; (2) intracellular acidosis and accumulation of sodium develop simultaneously during global ischemia; (3) increased intracellular sodium content is not in itself an indicator of irreversible injury; and (4) recovery of mechanical performance is associated with return of [Na^+^] (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown. Β© 1990 Academic Press, Inc.