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 23Na NMR spectroscopy at 1‐min intervals under control conditions and during global ischemia. [ATP], [H+], and [Pi] were measured by 31PNMR in a separate group under identical conditions. The control [Na+]i measured by atomic absorption was 30.7 ± 3.3 mM(mean ± SD, n = 6), and [Na+]i measured by NMR was 6.2 ± 0.5 mM(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 mM/min, r2 = 0.99). [H+] also increased approximately linearly early in ischemia (0.084 μM/min, r2 = 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. © 1990 Academic Press, Inc.
ASJC Scopus subject areas
- Radiology Nuclear Medicine and imaging