title: Influence of global ischemia on intracellular sodium in the perfused rat heart.
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+]i was monitored by 23Na NMR spectroscopy at 1-min intervals under control conditions and during global ischemia. [ATP], [H+], and [Pi] were measured by 31P NMR 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 microM/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+]i 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+]i (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown.
authors.affiliation: Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Center, Dallas 75235-9047.
authors.forename: C R
authors.initials: CR
authors.lastname: Malloy
authors.forename: D C
authors.initials: DC
authors.lastname: Buster
authors.forename: M M
authors.initials: MM
authors.lastname: Castro
authors.forename: C F
authors.initials: CF
authors.lastname: Geraldes
authors.forename: F M
authors.initials: FM
authors.lastname: Jeffrey
authors.forename: A D
authors.initials: AD
authors.lastname: Sherry
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D006321:Heart; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000032:analysis*; D010080:Oxazoles; D010477:Perfusion; D011744:Pyrimidinones; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000032:analysis*; D013054:Spectrophotometry, Atomic; D013932:Thulium
chemical_list: D010080:Oxazoles; D011744:Pyrimidinones; C063359:2,3-dihydro-5H-oxazolo(3,2-a)thieno(3,2-d)pyrimidin-5-one; D013932:Thulium; D012964:Sodium