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Am J Physiol Heart Circ Physiol 275: H917-H929, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 3, H917-H929, September 1998

Functional and metabolic effects of extracellular magnesium in normoxic and ischemic myocardium

John P. Headrick, James C. McKirdy, and Roger J. Willis

Rotary Centre for Cardiovascular Research, School of Health Science, Griffith University Gold Coast Campus, Southport, Queensland 4217, Australia

Metabolic and functional responses to extracellular Mg2+ concentration ([Mg2+]o) were studied in perfused rat heart. Elevations of [Mg2+]o from 1.2 to 2.4, 5.0, and 8.0 mM dose dependently reduced contractile function and myocardial oxygen consumption (MVO2) up to 80%. Intracellular Mg2+ concentration ([Mg2+]i) remained stable (0.45-0.50 mM) during perfusion with 1.2-5.0 mM [Mg2+]o but increased to 0.81 ± 0.14 mM with 8.0 mM [Mg2+]o. Myocardial ATP was unaffected by [Mg2+]o, phosphocreatine (PCr) increased up to 25%, and Pi declined by up to 50%. Free energy of ATP hydrolysis (Delta GATP) increased from -60 to -64 kJ/mol. Adenosine efflux declined in parallel with changes in MVO2 and [AMP]. At comparable workload and MVO2, the effects of [Mg2+]o on cytosolic free energy were mimicked by reduced extracellular Ca2+ concentration ([Ca2+]o) or Ca2+ antagonism with verapamil. Moreover, functional and energetic effects of [Mg2+]o were reversed by elevated [Ca2+]o. Despite similar reductions in preischemic function and MVO2, metabolic and functional recovery from 30 min of global ischemia was enhanced in hearts treated with 8.0 mM [Mg2+]o vs. 2.0 µM verapamil. It is concluded that 1) 1.2-8.0 mM [Mg2+]o improves myocardial cytosolic free energy indirectly by reducing metabolic rate and Ca2+ entry; 2) [Mg2+]i does not respond rapidly to elevations in [Mg2+]o from 1.2 to 5.0 mM and is uninvolved in acute functional and metabolic responses to [Mg2+]o; 3) adenosine formation in rat heart is indirectly reduced during elevated [Mg2+]o; and 4) 8.0 mM [Mg2+]o provides superior protection during ischemia-reperfusion compared with functionally equipotent Ca2+ channel blockade.

adenosine; calcium; cardioplegia; free energy of adenosine 5'-triphosphate hydrolysis; phosphorus-31 nuclear magnetic resonance spectroscopy; rat hearts


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