Problems in the assessment of magnesium depletion in the rat byin vivo31P NMR

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Abstract
Prior in vitro studies, utilizing 31P nuclear magnetic resonance (31P NMR) to measure the chemical shift (σ) of β‐ATP and lengthening of the phosphocreatine spin‐spin (T2) relaxation time, suggested an assessment of their efficacy in measuring magnesium depletion in vivo. Dietary magnesium depletion (M2+↓) produced markedly lower magnesium in plasma (0.44 vs 1.13 mmol/liter) and bone (130 vs 190 μmol/g) but much smaller changes in muscle (41 vs 45 μmol/g, P 0.01), heart (42.5 vs 44.6 μmol/g), and brain (30 vs 32 μmol/g). NMR experiments in anesthetized rats in a Bruker 7‐T vertical bore magnet showed that in Mg2+↓ rats there was a significant change in brain β‐ATP shift (16.15 vs 16.03 ppm, P < 0.05). These chemical shifts gave a calculated free [Mg2+] of 0.71 mM (control) and 0.48 mM (Mg2+↓). In muscle the change in β‐ATP shift was not significant (Mg2+↓ 15.99 ppm, controls 15.96 ppm), corresponding to a calculated free MP of 0.83 and 0.95 mM, respectively. Phosphocreatine T2 (Carr‐Purcell, spin‐echo pulse sequence) was no different with M2+↓ in muscle in vivo (surface coil) (Mg2+↓ 136, control 142 ms) or in isolated perfused hearts (Helmholtz coil) (control 83, Mg2+↓ 92 ms). 31P NMR is severely limited in its ability to detect dietary magnesium depletion in vivo. Measurement of β‐ATP shift in brain may allow studies of the effects of interaction in group studies hut does not allow prediction of an individual magnesium status. © 1988 Academic Press, Inc.
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