Magnesium as a relaxing factor of airway smooth muscles

in the search for effective treatment of a life-threatening asthma attack, intravenous magnesium infusion has been studied in asthmatic patients becau se of its potential effect to reverse bronchospasm and improve pulmonary fu nction. To determine whether magnesium sulfate inhibits airway smooth muscl e contraction and the possible mechanism of its action, in vitro experiment s were performed on rabbit tracheas. Tracheal muscle strips were obtained f rom 12 rabbits. Initially, the muscle strip was pretreated with a solution containing MgSO4 (concentrations 10(-4) to 2 M) and 85 mM KCl. The response curve of the muscle was recorded. Application of the above solution led to a 40% relaxation at a magnesium concentration of 10(-1) M. The time to pea k and to wash-out remained unchanged, and fixed to 66.6 and 123.3 sec, resp ectively, not influenced by magnesium concentration. On a second phase, the muscle strip was pretreated with KCI alone, and only after a full contract ile response was obtained did we add 10(-1) M MgSO4, which led to full rela xation. We follow the same protocol using 10(-4) M acetylcholine (ACH). In this case, simultaneous application of 10(-1) M MgSO4 caused a 55.1% decrea se in muscle contraction and a 60% decrease in time to peak. On a second ph ase, we added magnesium as we did with KCI, but without the same result. Ma gnesium caused a full relaxation when the constrictor agent was KCI, but a residual contraction was observed when the constrictor was ACH. Based on th e knowledge that ACH and KCI cause Ca2+ influx into the cells and subsequen t contraction by acting on different Ca2+ channels, we concluded that magne sium inhibits Ca2+ influx by blocking the voltage-dependent calcium channel s.