Additional limitations in the available evidence relate to differences in the dose, route, and precise method of administration of magnesium and it remains possible that alternative dose regimens may have different effects. This is problematic because, outside of clinical trials, it is often those patients presenting with life-threatening features who are considered for magnesium therapy when standard treatment regimens fail to control the disease. Furthermore, many studies exclude patients with life-threatening asthma, making it difficult to generalise the findings to this patient population. Given the heterogeneous nature of asthma, this is an important caveat. Some studies have suggested that magnesium treatment, particularly via the intravenous route, has a particular benefit in patients who present with severe features but, again, interpretation of the data here is difficult due to inconsistencies in the definition and categorisation of severity. The use of systemic corticosteroids, nebulised beta 2 agonists, and additional nebulised ipratropium is widely considered by clinicians to provide optimum treatment and we have evaluated the evidence for magnesium as an additional treatment rather than an alternative bronchodilator. Particularly important are the differences in treatments given to control populations, which reflect variation in standard treatment guidelines between different healthcare settings. Interpretation of the studies of inhaled and intravenous magnesium sulfate in acute asthma in adults is hindered by wide variations in study methods. Its safety and efficacy have not previously been confirmed, and its use has been considered controversial. Magnesium sulfate is an airway smooth muscle relaxant that has been used as a bronchodilator in patients with acute asthma. This updated overview focuses on magnesium sulfate (iv) alone and magnesium sulfate (nebulised) plus short-acting beta 2 agonists. The previous version of this overview on treatments for acute asthma in adults included a range of comparisons, such as controlled oxygen supplementation, corticosteroids, corticosteroids (inhaled), education about acute asthma, formoterol (inhaled), helium-oxygen mixture (heliox), ipratropium bromide (inhaled) plus short-acting beta 2 agonists (inhaled), magnesium sulfate (nebulised), mechanical ventilation for people with severe acute asthma, oral corticosteroids alone, short-acting beta 2 agonists, short-acting beta 2 agonists delivered by metered-dose inhalers plus spacer devices/holding chambers, and specialist care. We conclude that MgSO4 mediates enhanced production of PGI2 by vascular endothelium, thereby potentially enhancing its thromboresistant properties.Inhaled short-acting beta 2 agonists given in conjunction with systemic corticosteroids are considered the mainstay of treatment for acute asthma exacerbations. Finally, PGI2 production was 2- to 5-fold greater by HUVEC incubated with plasma obtained from preeclamptic patients undergoing MgSO4 therapy than by HUVEC incubated with pretherapy plasma. In separate experiments, MgSO4 overcame the enhanced adherence of platelets to HUVEC exhausted by repeated exposure to thrombin. By radioimmunoassay for 6-keto-PGF1 alpha, the stable metabolite of PGI2, it was shown that MgSO4 amplifies release of PGI2 by HUVEC in a dose-dependent manner, with a peak occurring between 2 and 3 mM. By platelet aggregometry, the known antiaggregatory effect of intact HUVEC was enhanced by MgSO4. We studied the effect of MgSO4 on PGI2 release by cultured human umbilical vein endothelial cells (HUVEC) by several methods. Traditional therapy utilizes infusions of large amounts of MgSO4, but the physiologic basis for this is not clear. There is evidence from a number of studies that production of prostacyclin (prostaglandin I2, PGI2), a potent vasodilator and inhibitor of platelet aggregation, is deficient in preeclamptic compared to normal pregnancy. Preeclampsia is a disorder of pregnancy characterized clinically by hypertension, proteinuria, and edema and characterized pathologically in its late stages by widespread microvascular thrombi.
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