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Vol. 297, Issue 3, 1176-1183, June 2001
Anaesthesia and Intensive Care, Royal Adelaide Hospital/University
of Adelaide, North Terrace, Adelaide, Australia
The temporal relationship between the systemic and myocardial
concentrations of magnesium and some of its acute cardiovascular effects were examined after short i.v. infusion administration of
magnesium (30 mmol over 2 min) in five awake chronically instrumented sheep. Magnesium decreased mean arterial blood pressure and systemic vascular resistance (SVR) by 23 and 41% from baseline, respectively. These hemodynamic changes were consistent with magnesium producing primary reductions in SVR with partial heart rate (HR)-mediated compensation of blood pressure. Cardiac output and HR increased by 38 and 38% from baseline, respectively. Magnesium had little effect on
myocardial contractility, but substantially increased myocardial blood
flow (MBF, 77% above baseline) primarily due to direct myocardial
vasodilation. The peak arterial and coronary sinus serum magnesium
concentrations were 6.94 ± 0.26 (mean ± S.E.M.) and
6.51 ± 0.20 mM, respectively, at 2 min. Both arterial and
coronary sinus magnesium concentrations at the end of the study were
still more than 3 mM, whereas all the cardiovascular effects were back
to baseline. The myocardial kinetics of magnesium was consistent with
rapid equilibration of magnesium (half-life 0.4 min) with a small
distribution volume (71 ml) consistent with the extracellular space of
the heart. In conclusion, magnesium was shown to have a rapid
equilibration between the plasma/serum concentrations of magnesium and
its extracellular concentration in the myocardium. However, the primary
cardiovascular effect of magnesium (reductions in SVR) preceded its
extracellular concentrations, and was a direct function of its arterial
concentration. A "threshold" model for changes in SVR was preferred
when linked to the arterial magnesium concentration.