AJP - Cell Physiology, Vol 234, Issue 3 115-C121, Copyright © 1978 by American Physiological Society
Magnesium net fluxes and distribution in rabbit myocardium in irreversible contracture
N. F. Paradise, G. W. Beeler Jr and M. B. Visscher
Distribution of magnesium (Mg) in heart muscle was studied by measuring
fluxes of Mg and transmembrane potentials as a function of perfusate [Mg2+]
after a massive increase in permeability of the sarcolemma was induced in
the Langendorff prepared heart from the Nembutal-anesthetized rabbit. After
onset of 0 mM [Ca2+] perfusion which produced excitation-contraction (E-C)
uncoupling and mechanical arrest, action potentials recorded from
subepicardial cells showed an increase in duration and decrease in
amplitude, which progressed until no transmembrane potentials could be
observed. Restoration of physiological salt solution perfusion after 15 min
of [Ca2+]-free perfusion caused an irreversible contracture that was
associated with 1) efflux of potassium (K) and myoglobin, 2) perfusate
[Mg2+]-dependent flux of Mg, and 3) transmembrane potentials of 0 mV. The
magnitude of net efflux of K and myoglobin during contracture was
unaffected by perfusate [Mg2+]. During the first 2 min of contracture, net
efflux of Mg (mumoles per gram wet muscle +/- SE) was 1.37 +/- 0.09 and
0.48 +/- 0.19 during 0 mM and 2.5 mM [Mg2+] perfusion, respectively; but a
net influx of 0.56 +/- 0.23 occurred during 5 mM [Mg2+] perfusion. Total
sarcoplasmic [Mg] may correspond to perfusate [Mg2+] of 3.6 mM, which was
found by interpolation to prevent any net flux of Mg during contracture.
3.6 mM may, therefore, represent the upper limit of the intracellular
free-ionized Mg concentration in rabbit heart.
