Bronchodilating Effect of Intravenous Magnesium Sulfate in Acute Severe Bronchial Asthma: DISCUSSION
Few contolled data are available on the bronchodilating effect of intravenous MgS04 in bronchial asthma. In 1987, Okayama et al showed that MgS04 relieved bronchoconstriction in mild asthma in a dose-dependant manner. Maximal responses were similar to the effects of additional albuterol inhalation. Bronchodilation occurred soon after the beginning of MgS04 infusion and reached its maximum at the end of the 20 min of infusion. Ten minutes after ending the infusion, respiratory parameters had returned to pre-treatment values. Spivey et al compared intravenous MgS04 with saline placebo for the treatment of moderate to severe asthmatic subjects who failed to respond to conventional beta-agonists (two metapro- terenol or albuterol nebulized treatments 45 min apart, and solumedrol). If PEFR 15 min after the second nebulized treatment had not doubled from the initial values, either saline solution or MgS04 (1.2 g over 20 min equiv 0.246 mmol/min) was injected. Infusion of MgS04 resulted in significantly better bronchodilation than did saline infusion, indicating that MgS04 may be a useful adjunct to conventional beta-agonist therapy in the emergency treatment of moderate to severe bronchospasm.
In our study we evaluated the bronchodilating effect of intravenous MgS04 in patients with severe acute asthma. Infusion of MgS04 caused a significant improvement in FEV, (0.94 ±0.39 L to 1.3 ±0.44 L), and an improvement in clinical signs and symptoms in ten out of 12 administrations. tadalis sx
Thirty minutes after the infusion period, FEV1 had not returned to the preinfusion values in our patients, in contrast with the findings of Okayama et al,suggesting some persistence of the bronchodilating effect. This is in accordance with data of Spivey et alwhich also show that the MgS04 -induced bronchodilation persists for more than 20 min.
Again in contrast with the findings of Okayama et al, the bronchodilating effect of MgS04 was significantly less than that of subsequent albuterol inhalation (FEV! improvement from 1.13±0.41 L to 1.72±0.49 L); however, the fact that FEVt had not returned to preinfusion values 30 min after stopping the MgS04 infusion could account for the greater improvement of FEV1 after albuterol inhalation, since MgS04 and beta2-agonists may have additive bronchodilating effects.
Another reason for the lesser potency of MgS04 in our study could reside in the difference between the populations studied: “our” patients had significantly more severe asthma when entering the study (mean 30.25 percent predicted FEV\ vs mean 61.8 percent predicted FEV1 in the Japanese study). Although patients of Spivey et al (who also had “severe asthma”) showed a marked bronchodilation after MgS04 infusion, the data presented do not allow comparison of PEFR changes in their patients between beta-agonist therapy and MgS04 infusion.
The mechanism of the observed Mg-induced bronchodilation is not clear. Hypomagnesemia has been reported in patients with asthma; we do not think, however, that repletion of Mg deficiency can be considered in our patients since pretreatment serum and intracellular Mg concentrations were within normal limits, and since no patient was at risk for hypomagnesemia. Intravenous beta-agonists (ie, albuterol), in a therapeutic dose, can cause a significant fall in serum magnesium concentrations, probably due to a beta-adrenergic-induced intracellular shift of Mg. Although all our patients regularly used betag- agonists, no albuterol or other betas-agonist were given at least 4 h before the Mg infusion. canadian pharmacy viagra
Calcium channel blockers have been shown to blunt or abolish the bronchoconstrictor response to exercise, histamine and metacholine; the effect of Mg is similar to that observed with calcium-channel blockers. This, and experimental data, suggest that Mg may exert its effect on the final common path of bronchoconstriction by interfering with calcium handling of the bronchial smooth muscle cells.
Magnesium sulfate also is used in the treatment of seizures associated with acute nephritis and with eclampsia of pregnancy: typically, 4 g of MgS04 is injected over 5 min, followed by 10 to 20 g in drip infusion at the rate of approximately 1 g of MgS04 per hour. Magnesium concentrations of 6 to 8 mEq/L (equiv 3 to 4 mmol/L) are within the therapeutic range. Respiratory failure can occur at concentrations of approximately 12 to 15 mEq/L (6 to 7.5 mmol/L).
We decided to inject 3 g of MgS04 (in Belgium, MgS04 is available in ampules of 3 g MgS04 in a 30 percent solution) over a 20-min period, in analogy to Okayama et al, resulting in an infusion rate of 0.615 mmol/min. Maximal Mg concentrations observed were far within safety limits.
We conclude that intravenous MgS04 infusion causes significant bronchodilation and subjective improvement in patients with severe bronchial asthma; we therefore consider it a safe and efficient adjunct to classic beta2-agonist therapy in cases of severe acute asthma.