Intracellular sodium during ischemia and calcium-free perfusion: A Na NMR study

Echteld, C.J.A. van; Kirkels, J. H.; Eijgelshoven, M. H. J.; Meer, Peter van der; Ruigrok, T. J. C.

doi:10.1016/0022-2828(91)90066-u

Cited by 98 publications

(39 citation statements)

References 48 publications

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“…[2] indicates that they cannot alone explain the 160 -280% increase in total sodium observed in our study (for MI, [Na] ϭ 0.82 ϫ {0.7 ϫ 15 ϩ 0.3 ϫ 145} ϭ 44 mmol/kg vs. 81 mmol/kg observed). This would suggest that a significant increase in [Na] in must occur in reperfused intact canine MI in vivo, which is consistent with the 23 Na MRS shift reagent studies of isolated rodent hearts (25,26).…”

Section: Extracellular Sodium and Edemasupporting

confidence: 76%

“…Thus, in reversible ischemia produced by transient coronary occlusion in isolated perfused rodent hearts, 23 Na MRS with shift reagents demonstrates an up to fivefold intracellular sodium increase following up to 30 min of ischemia, producing mechanical dysfunction which reverses upon reperfusion (25,26). Intracellular volume increases of about 13% following an hour of coronary occlusion have also been demonstrated histochemically in isolated canine hearts (27).…”

Section: Intracellular Sodiummentioning

confidence: 98%

“…Tissue volume measurements in rat and rabbit hearts using diffusible extracellular markers and microscopic analysis indicate that almost 12-19% of total tissue volume is extracellular (6,26,29). Modulation of the extracellular volume due to edema or necrosis during infarction should affect total tissue sodium content via Eq.…”

Section: Extracellular Sodium and Edemamentioning

confidence: 99%

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Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Constantinides

Kraitchman

O'Brien

et al. 2001

Magnetic Resonance in Med

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The transport of sodium and potassium between the intra-and extracellular pools and the maintenance of the transmembrane concentration gradients are important to cell function and integrity. The early disruption of the sodium pump in myocardial infarction in response to the exhaustion of energy reserves following ischemia and reperfusion results in increased intracellular (and thus total) sodium levels. In this study a method for noninvasively quantifying myocardial sodium levels directly from sodium ( 23 Na) MRI is presented. It was used to measure total myocardial sodium on a clinical 1.5T system in six normal dogs and five dogs with experimentally-induced myocardial infarction (MI). The technique was validated by comparing total sodium content measured by 23 Na MRI with that measured by atomic absorption spectrophotometry (AAS) in biopsied tissue. Total sodium measured by 23 Na MRI was significantly elevated in regions of infarction (81.3 ؎ 14.3 mmol/kg wet wt, mean ؎ SD) compared to noninfarcted myocardial tissue from both infarcted dogs (36.2 ؎ 1.1, P < 0.001) and from normal controls (34.4 ؎ 2.8, P < 0.0001). Myocardial tissue sodium content as measured by 23 Na MRI did not vary regionally in the lateral, anterior, or inferior regions in normal hearts (ANOVA, P ‫؍‬ NS). Sodium content measured by 23 Na MRI agreed with the mean AAS estimates of 31.3 ؎ 5.6 mmol/kg wet wt (P ‫؍‬ NS) in normal hearts, and did not differ significantly from AAS measurements in MI (P ‫؍‬ NS). Thus, local tissue sodium levels can be accurately quantified noninvasively using 23 Na MRI in normal and acutely reperfused MI. The detection of regional myocardial sodium elevations may help differentiate viable from nonviable, infarcted tissue.

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Section: Extracellular Sodium and Edemasupporting

confidence: 76%

Section: Intracellular Sodiummentioning

confidence: 98%

Section: Extracellular Sodium and Edemamentioning

confidence: 99%

See 1 more Smart Citation

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Constantinides

Kraitchman

O'Brien

et al. 2001

Magnetic Resonance in Med

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“…23 Na NMR spectra were quantified by integration after a Gaussian and Lorentzian multiplication and a polynomial baseline correction had been performed. NMR visibility of all Na ϩ signals was assumed to be 1.0 (26). pHi values were calculated from the chemical shift of the Pi peak by using the equation pH ϭ 6.72 Ϫ log(␦ Ϫ 5.66)/(3.27 Ϫ ␦) (13).…”

Section: Methodsmentioning

confidence: 99%

Relative contributions of Na⁺/H⁺exchange and Na⁺/HCO₃⁻cotransport to ischemic Na_i⁺overload in isolated rat hearts

Hove¹,

Nederhoff²,

Echteld³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Na ϩ /H ϩ exchanger (NHE) and/or the Na ϩ /HCO 3 Ϫ cotransporter (NBC) were blocked during ischemia in isolated rat hearts. Intracellular Na ϩ concentration ([Na ϩ ]i), intracellular pH (pHi), and energyrelated phosphates were measured by using simultaneous 23 Na and 31 P NMR spectroscopy. Hearts were subjected to 30 min of global ischemia and 30 min of reperfusion. Cariporide (3 M) or HCO 3 Ϫ -free HEPES buffer was used, respectively, to block NHE, NBC, or both. End-ischemic [Na ϩ ]i was 320 Ϯ 18% of baseline in HCO 3 Ϫ -perfused, untreated hearts, 184 Ϯ 6% of baseline when NHE was blocked, 253 Ϯ 19% of baseline when NBC was blocked, and 154 Ϯ 6% of baseline when both NHE and NBC were blocked. End-ischemic pHi was 6.09 Ϯ 0.06 in HCO 3 Ϫ -perfused, untreated hearts, 5.85 Ϯ 0.02 when NHE was blocked, 5.81 Ϯ 0.05 when NBC was blocked, and 5.70 Ϯ 0.01 when both NHE and NBC were blocked. NHE blockade was cardioprotective, but NBC blockade and combined blockade were not, the latter likely due to a reduction in coronary flow, because omission of HCO 3 Ϫ under conditions of NHE blockade severely impaired coronary flow. Combined blockade of NHE and NBC conserved intracellular H ϩ load during reperfusion and led to massive Na ϩ influx when blockades were lifted. Without blockade, both NHE and NBC mediate acid-equivalent efflux in exchange for Na ϩ influx during ischemia, NHE much more than NBC. Blockade of either one does not affect the other.

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“…During reperfusion, Na ϩ entry is further more potential, and as Na/K pump activity remains depressed, this leads to elevated intracellular Ca 2ϩ via the Na ϩ /Ca 2ϩ exchanger (Ca 2ϩ overload). This failure of [Na ϩ ] i to recover completely during early reperfusion contributes to cardiac I/R injury (40) and may be attributed in part to be inadequate Na/K pump activity at this time (37). Stimulating the Na/K pump back to (or beyond) basal may be expected to limit injury resulting from high levels of [Na ϩ ] i .…”

mentioning

confidence: 99%

Enhancement of Na/K pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury

Guo

Guo²,

Zhang³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Chronic intermittent hypobaric hypoxia (CIHH) has been shown to attenuate intracellular Na+ accumulation and Ca2+ overload during ischemia and reperfusion (I/R), both of which are closely related to the outcome of myocardial damage. Na/K pump plays an essential role in maintaining the equilibrium of intracellular Na+ and Ca2+ during I/R. It has been shown that enhancement of Na/K pump activity by ischemic preconditioning may be involved in the cardiac protection. Therefore, we tested whether Na/K pump was involved in the cardioprotection by CIHH. We found that Na/K pump current in cardiac myocytes of guinea pigs exposed to CIHH increased 1.45-fold. The K 1 and f 1, which reflect the portion of α1-isoform of Na/K pump, dramatically decreased or increased, respectively, in CIHH myocytes. Western blot analysis revealed that CIHH increased the protein expression of the α1-isoform by 76%, whereas the protein expression of the α2-isoform was not changed significantly. Na/K pump current was significantly suppressed in simulated I/R, and CIHH preserved the Na/K pump current. CIHH significantly improved the recovery of cell length and contraction during reperfusion. Furthermore, inhibition of Na/K pump by ouabain attenuated the protective effect afforded by CIHH. Collectively, these data suggest that the increase of Na/K pump activity following CIHH is due to the upregulating α1-isoform of Na/K pump, which may be one of the mechanisms of CIHH against I/R-induced injury.

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Intracellular sodium during ischemia and calcium-free perfusion: A Na NMR study

Cited by 98 publications

References 48 publications

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Relative contributions of Na⁺/H⁺exchange and Na⁺/HCO₃⁻cotransport to ischemic Na_i⁺overload in isolated rat hearts

Enhancement of Na/K pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury

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Intracellular sodium during ischemia and calcium-free perfusion: A Na NMR study

Cited by 98 publications

References 48 publications

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using 23Na MRI

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using 23Na MRI

Relative contributions of Na+/H+exchange and Na+/HCO3−cotransport to ischemic Nai+overload in isolated rat hearts

Enhancement of Na/K pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury

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Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using ²³Na MRI

Relative contributions of Na⁺/H⁺exchange and Na⁺/HCO₃⁻cotransport to ischemic Na_i⁺overload in isolated rat hearts