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Effect of inotropic stimulation on cytosolic mg 2+ in isolated rat heart: a 31 p magnetic resonance study
Author(s) -
Headrick John P,
Willis Roger J.
Publication year - 1989
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1910120305
Subject(s) - ouabain , ibmx , inotrope , medicine , endocrinology , stimulation , chemistry , cytosol , creatine , sodium , biochemistry , enzyme , forskolin , organic chemistry
Alterations in cytosolic metabolites and [Mg 2+ ], were monitored using 31 P magnetic resonance spectroscopy during inotropic stimulation of isolated rat heart [10 n M isoproterenol, 0.6 μ M isobutyl‐1‐methylxanthine (IBMX), 5 μ M ouabain]. All drugs significantly elevated contractile function (rate‐pressure product) and MVO 2 by approximately 100‐150% ( P 0.001), decreased cytosolic [creatine phosphate] ([CrP]) and [ATP] (approximately 65 and 80% of control values, respectively) ( P 0.001), increased [ P i ] to more than 180% of pretreatment values, and decreased [ H + ] by less than 15% ( P 0.05). A significant relative shift in the α‐P and β‐P resonances of ATP ( P 0.01) occurred with inotropic stimulation. [Mg 2+ ], calculated on the basis of these shifts was found to be 0.78 ± 0.1 m M in control hearts, and increased to maxima of 1.9 ± 0.2,2.0 ±0.2, and 2.9 ± 0.2 m M during infusion of isoproterenol, IBMX, and ouabain, respectively. Changes in [Mg 2+ ], correlate with cytosolic [ATP] + [CrP] in all hearts ( r = 0.89, 0.91, and 0.88 in isoproterenol‐, IBMX‐, and ouabain‐treated hearts, respectively). The significantly higher [Mg 2+ ], with ouabain infusion ( P 0.01) at similar workloads and [ATP] + [CrP] supports the proposal that a ouabain‐inhibited Mg 2+ pump exists in the plasma membrane. The data support acute changes in [ Mg 2+ ] i during alterations in inotropic state that may be important in modulating metabolic and contractile function. © 1989 Academic Press, Inc.