Role of intracellular Na+ in Ca2+ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Possible involvement of H+-Na+ and Na+-Ca2+ exchange.

Tani, Masato; Neely, James R.

doi:10.1161/01.res.65.4.1045

Cited by 715 publications

(303 citation statements)

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“…23 The metabolome experiences imbalances that cause the failure of aerobic production of ATP, disruption of membrane-mediated transport (i.e., rapid gains in calcium, the loss of intracellular potassium and gain of sodium) and intracellular acidosis with pH approaching 4. [23][24][25][26] While select mammalian species have evolved mechanism supportive of whole-body hypothermia (i.e., hibernators) 27,28 or seasonally adaptive heterothermy, 29,30 few human cells in vivo tolerate low temperature exposure beyond a few hours. Hypothermia without manipulative intervention yields progressive cell injury during each of its three phases (cooling, maintenance in the cold and rewarming).…”

Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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“…Characteristic features of myocardial ischemia include intracellular acidosis resulting from anaerobic glycolysis during ischemia (Tani and Neely, 1989). Intracellular acidosis is known to stimulate several pH regulating systems including Na + / H + exchanger (NHE) (Grinstein et al, 1992;Noel and Pouyssegur, 1995).…”

Section: Introductionmentioning

confidence: 99%

KR-32570, a novel Na+/H+ exchanger-1 inhibitor, attenuates hypoxia-induced cell death through inhibition of intracellular Ca2+ overload and mitochondrial death pathway in H9c2 cells

Kim

Moon

Kim

et al. 2005

European Journal of Pharmacology

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“…Obviously, these mechanisms are interrelated, because pH can alter ATP hydrolysis, and, conversely, ATP is required for pH regulation. Furthermore, recent work by Tani and Neely (22) in mature rat hearts suggests that N~+ -H + and ~a + -~a~+ exchange may be involved in ischemic myocardial dysfunction. It has been proposcd that intracellular H+ exchanges with Naf during ischemia.…”

Section: Discussionmentioning

confidence: 99%

Mechanical and Metabolic Characterization of Ischemic Contracture in the Neonatal Pig Heart

et al. 1995

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Isolated, paced, isovolumetrically beating piglet hearts ( n = 37) underwent retrograde aortic perfusion with a crystalloid solution during three periods: 1) baseline (coronary perfusion pressure 60 mm Hg), 2) ischemia (coronary flow 10% of baseline for -80 min), and 3) reperfusion (perfusion pressure returned to baseline). In one group of hearts, glycolysis (using "H,o formation from [3H]glucose) was assessed. During baseline, peak systolic pressure (PSP) was 101.1 i 5.0 mm Hg, end diastolic pressure (EDP) 4.4 z 0.5 mm Hg, glycolysis 970.5 -C 65.3 nmol/min/g,,,, and myocardial glycogen 234.8 2 12.0 pmoll g,,,. During ischemia, PSI' decreased to 23.3 t 2.7 mm Hg, BDP increased to 12.3 2 0.7 mm Hg, myocardial glycogen decreased to 181.5 2 30.3 pmol/g,,,, and lactate (-154 pmoll g,,,) and glycerol (-930 nmol/g,,,) were released. Myocardial contracture correlated with a decrease in lactate release. Glycolysis decreased to -400 nmol/min/g,,, and remained stable, accounting for =SO% of the lactate producetl. During reperfusion, PSP recovered to 79.8 2 3.5 mm llg, EDP 6.6 2 1.7 mm Hg, and glycolysis 1103.9 + 81 nmol/rnin/g,,,. In a second group of hearts, with similar mechanical responses, giucose oxidation (using "CO, formation from ['4C]glucose) was evaluated. During baseline, glucose oxidation was 165.4 -t 15.9 nmol/min/g,,, and correlated closely (r = 0.957) with rnechanical activity. With ischemia, glucose oxidation decreased to =17Myocardial contracture represents a state of decreased diastolic compliance of the ventricle secondary to a depletion of high energy stores in the region of the contractile apparatus (1).With ischemia, contracture occurs as a consequence of myocardial underperfusion, which results in inadequate substrate delivery and impaired ATP production. Insufficient ATP leads to a progressive increase in the number of myocin-actin complexes that are unable to dissociate and to derangements in resting cytosolic calcium levels (2). (3,4). Little is known about myocardial contracture in the setting of low-flow ischemia, where hearts are beating, and there is washout of metabolites. Additionally, the modalities of energy production and utilization associated with contracture are poorly understood, yet these processes ultimately determine myocardial viability. An understanding of these processes in neonatal hearts has significant clinical ramifications, because contracture is thought to represent a precursor to an irreversible myocardial injury (5).The objectives of the present investigation were to study myocardial contracture in isolated, isovolumetrically beating, neonatal pig hearts subjected to normothermic, low-flow isch-

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Role of intracellular Na+ in Ca2+ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Possible involvement of H+-Na+ and Na+-Ca2+ exchange.

Cited by 715 publications

References 29 publications

Cryopreservation

Cryopreservation

KR-32570, a novel Na+/H+ exchanger-1 inhibitor, attenuates hypoxia-induced cell death through inhibition of intracellular Ca2+ overload and mitochondrial death pathway in H9c2 cells

Mechanical and Metabolic Characterization of Ischemic Contracture in the Neonatal Pig Heart

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