[Action of potassium sulfate and potassium magnesium sulfate on the body of animals in a chronic experiment].
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Animals↗
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Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with preeclampsia.
OBJECTIVE: Does the use of nifedipine and magnesium sulfate together increase serious magnesium-related effects? STUDY DESIGN: This was a retrospective chart review of women who were admitted to BC Women's Hospital and Health Centre (1997-2001) and were given intravenous magnesium sulfate for preeclampsia. Serious magnesium-related effects were compared among 162 cases who received magnesium sulfate and contemporaneous nifedipine and 215 control subjects who received magnesium sulfate and either another antihypertensive (n=32 women) or no antihypertensive (n=183 women) medication. Chi-squared test, Fisher's exact test, or the Student t test was used for data comparison between cases and each control group. A probability value of <.05 was considered statistically significant. RESULTS: The cases had more severe preeclampsia and a longer magnesium sulfate infusion. However, cases had no excess of neuromuscular weakness (53.1%) versus control subjects who received antihypertensive medication (53.1%; P=.99) or control subjects who received no antihypertensive medication (44.8%; P=.13) or other serious magnesium-related effects. Cases versus control subjects who received antihypertensive medication had less neuromuscular blockade (odds ratio, 0.04; 95% CI, 0.002-0.80). Cases versus control subjects who received no antihypertensive medication had less maternal hypotension (41.4% vs 53.0%; P=.04). CONCLUSION: The use of nifedipine and magnesium sulfate together does not increase the risk of serious magnesium-related effects.
Adult↗
Prospective study on premature labor with magnesium sulfate.
The efficacy of magnesium sulfate was evaluated as the primary tocolytic agent in the management of patients at risk for premature delivery. Fifteen patients presenting with premature labor between 28 and 35 weeks gestation, given titrated dose intravenously magnesium sulfate till uterine contraction ceased, were prospectively studied. All patients received an additional oral beta-mimetic agent once labor was arrested till 36 weeks gestation. All cases had intact membranes and no contraindications for tocolytic therapy. Tocolysis for more than 72 hours was achieved in 14 cases (93.3%). Delayed tocolysis of more than 7 days was achieved in 13 cases (86.7%). The mean dosage to achieve tocolytic effect was 3.17 g/hr (SD 0.08). The mean serum magnesium level to achieve such effect was 5.38 mg/dl (SD 0.88). Magnesium sulfate was found to be easy to administer and clinically efficacious with minimal adverse effects. It may be used as the first line of tocolytic therapy where beta-sympathomimetic drugs are contraindicated.
Adult↗
Absorption of magnesium from orally administered magnesium sulfate in man.
The use of magnesium sulfate (Epsom salt) as a cathartic in patients with impaired renal function can lead to severe toxicity due to hypermagnesemia. Although toxicity is uncommon in healthy subjects, little is known concerning the extent of absorption of magnesium after a cathartic dose of magnesium sulfate. The bioavailability of magnesium following a large oral dose of magnesium sulfate in normal volunteers was examined in the present investigation. Baseline 24-hour urinary excretion rates of magnesium and creatinine were determined over 3 consecutive days in 6 healthy men. The oral administration of 13.9 g (56.5 mmoles) magnesium sulfate U.S.P., in 4 equal hourly increments, resulted in the urinary excretion (corrected for baseline excretion rate) of 4.0 +/- 2.9% (mean +/- SD) of the dose of magnesium during the first 24 hours and 6.9 +/- 7.0% of the dose during a 72-hour interval. Magnesium sulfate administration had no effect on the 24-hour urinary excretion rate of creatinine. The baseline excretion rate of magnesium was significantly correlated with that of creatinine (r = 0.875) and inorganic sulfate (r = 0.921). All of the subjects experienced mild or moderate diarrhea. Therefore, magnesium is absorbed to a limited and variable extent in healthy adults following a cathartic dose of magnesium sulfate.
Administration, Oral↗
Urinary magnesium, calcium, and phosphate excretion during magnesium sulfate infusion.
Urinary excretion of magnesium, calcium, and phosphate was measured in 20 preeclamptic pregnant women treated with intravenous magnesium sulfate. Blood levels of these substances, as well as of parathyroid hormone and calcitonin, were also measured. Urinary magnesium excretion increased 20-fold during magnesium sulfate infusion. Seventy-five percent of the infused magnesium was excreted during the infusion, and 90% within 24 hours after treatment. Urinary calcium concentration increased 4.5-fold during magnesium sulfate infusion, and the urinary calcium excretion rate was 3 times that observed in controls. Urinary phosphate concentration and excretion rate were the same in treated and control subjects. During treatment, maternal serum total calcium fell 25%, ionized calcium fell 12%, and parathyroid hormone rose 26%. Magnesium sulfate therapy depresses maternal calcium levels by increasing urinary calcium loss, and increased parathyroid hormone output prevents more marked hypocalcemia.
Calcitonin↗
Effect of intravenous magnesium sulfate on cardiac arrhythmias in critically ill patients with low serum ionized magnesium.
Magnesium affects cardiac function, although until the recent development of a new ion-selective electrode no method existed for measuring the physiologically active form of magnesium, free ions (iMg2+), in the blood. We investigated the antiarrhythmic effect of magnesium sulfate administered to critically ill patients with cardiac arrhythmias and reduced iMg2+ as determined using the ion-selective electrode. Eight patients with a low iMg2+ level (less than 0.40 mmol/L) were given intravenous magnesium sulfate (group L). Magnesium sulfate was also administered to patients with a normal iMg2+ level (more than 0.40 mmol/L) but who did not respond to conventional antiarrhythmic drugs (group N). Intravenous magnesium sulfate significantly increased the iMg2+ level in patients in group L from 0.35 +/- 0.06 mmol/L (mean +/- SD) to 0.54 +/- 0.09 mmol/L (p < 0.01), and had an antiarrhythmic effect in 7 of the 8 patients (88%). However, in group N patients, intravenous magnesium sulfate had an antiarrhythmic effect in only 1 of the 6 patients (17%) (p < 0.05 vs group L). These results suggest that intravenous magnesium sulfate may be effective in the acute management of cardiac arrhythmias in patients with a low serum iMg2+ level.
Aged↗
Ventricular fibrillation in acute experimental myocardial ischemia: protection by magnesium sulfate.
1. The efficacy of magnesium sulfate for prevention of ventricular fibrillation was compared with that of the calcium blocker verapamil and other antiarrhythmic drugs in 54 open-chested anesthetized dogs during a 3-h ligation of the circumflex coronary artery. Latency time to fibrillation, incidence of fibrillation and hemodynamic parameters were assessed. 2. Ventricular fibrillation occurred in 11 of 14 (79%) control dogs, in 2 of 8 (25%) dogs treated with magnesium sulfate (100 mg/kg) and in none of 8 animals treated with verapamil (0.2 mg/kg) (P = 0.014 and P = 0.0004, respectively, in comparison with controls); lidocaine (60 mg followed by 4 mg/min), amiodarone (5 mg/kg) and propafenone (4 mg/kg) had no effect on the incidence of fibrillation. 3. The latency time to fibrillation was 11.6 +/- 9.1 min in controls and it was shortened to 4.0 +/- 3.8 min (P = 0.039) in dogs treated with propafenone, but was unaffected by other drugs. 4. There was no correlation between pre-occlusion heart rate or blood pressure and fibrillation incidence. 5. In this experimental model, magnesium sulfate infusion had a protective effect against ventricular fibrillation that was similar to verapamil, suggesting that magnesium sulfate may be useful as an antifibrillatory agent during acute ischemia.
Analysis of Variance↗
Magnesium sulfate tocolysis: time to quit.
Intravenous magnesium sulfate tocolysis remains a North American anomaly. This therapy rose to prominence based on poor science and the recommendations of authorities. However, a Cochrane systematic review concluded that magnesium sulfate is ineffective as a tocolytic. The review found no benefit in preventing preterm or very preterm birth. Moreover, the risk of total pediatric mortality was significantly higher for infants exposed to magnesium sulfate (relative risk 2.8; 95% confidence interval 1.2-6.6). Given its lack of benefit, possible harms, and expense, magnesium sulfate should not be used for tocolysis. Any further use of magnesium sulfate for tocolysis should be restricted to formal clinical trials with approval by an institutional review board and signed informed consent for participants. Should tocolysis be desired, calcium channel blockers, such as nifedipine, seem preferable.
Biomedical Research↗
The adsorption of metronidazole and tinidazole to activated charcoal and the effect of magnesium sulfate.
The effect of magnesium sulfate on the in vitro adsorption of metronidazole and tinidazole to activated charcoal was studied. Solutions of metronidazole and tinidazole were prepared at low concentrations of 6.25, 12.5, 25.0 and 50 micrograms/ml and at simulated toxic concentrations of 0.5, 1.0, 2.0, 5.0 and 10 mg/ml in distilled water. Drug charcoal slurries were vortex-mixed, centrifuged and analyzed for free drug. Metronidazole gave adsorption capacities of 62.2-82.7% with 50 and 200 mg activated charcoal. Fifty and 200 mg activated charcoal adsorbed 80-90% of tinidazole. Metronidazole at 0.5 mg/ml had 16.7, 30.0, 56.7, 75.0 and 83.3% adsorption with 12.5, 50, 125, 250 and 500 mg charcoal respectively. There was a corresponding increase in the adsorption of metronidazole and tinidazole at the increasing concentrations of activated charcoal. The adsorption of metronidazole and tinidazole also seemed to be dose dependent. Magnesium sulfate (7.5 mg/ml) enhanced the adsorption of metronidazole to activated charcoal, but had no effect on tinidazole-charcoal adsorption.
Charcoal↗
The adsorption of quinine and quinidine to activated charcoal with and without magnesium sulfate.
The effect of magnesium sulfate on the in vitro adsorption of quinine and quinidine to activated charcoal (AC) was studied. Solutions of quinine and quinidine were prepared at concentrations of 5 and 10 micrograms/ml and at simulated toxic concentrations of 62.5, 125 and 250 micrograms/ml in distilled water. Drug-charcoal slurries were vortex mixed, centrifuged and analysed for free drug in the supernatant. Quinine had adsorption capacities of 78.2 to 100% with 12.5 or 50 mg AC; 12.5 or 50 mg AC adsorbed 29.5-87.2% of the quinidine. Quinine (250 micrograms/ml) had adsorption capacities of 0.0, 21.1, 52.4, 78.3 or 93.8% to 12.5, 50, 125, 250 or 500 mg AC, respectively. There was a corresponding increase quinine and quinidine adsorption at increasing concentrations of AC. The adsorption of quinine and quinidine seemed dose dependent. Magnesium sulfate (7.5 mg/ml) enhanced the adsorption of quinine to AC, but increased the amount of AC required for quinidine-charcoal adsorption.
Adsorption↗
The effects of systemic magnesium sulfate infusion on brain magnesium concentrations and energy state during hypoxia-ischemia in newborn miniswine.
The mechanism of neuroprotection associated with systemically administered magnesium remains unclear. This investigation examined the acute effects of systemically administered MgSO4 on brain extracellular ([Mg]ecf) and intracellular ([Mg]i) fluid Mg concentrations, specific brain phosphorylated metabolites, and brain intracellular pH. Miniswine were studied with P-31 magnetic resonance spectra, to derive [Mg]i, and brain microdialysis probes, to measure [Mg]ecf. Animals were infused with MgSO4 (n = 5, 275 mg/kg over 30 min followed by 100 mg/kg over 30 min, designated MgHI) or Na2SO4 (n = 5, designated NaHI), and both groups underwent hypoxia-ischemia (HI) over the last 15 min of the infusions. Groups differed in plasma [Mg] at the completion of HI (9.1 +/- 1.5 versus 1.1 +/- 0.6 mM for MgHI and NaHI, respectively, p < 0.05). MgHI had elevations of [Mg]ecf (0.23 +/- 0.11 and 0.40 +/- 0.14 mM at control and completion of HI, respectively), and [Mg]ecf was unchanged for NaHI (p < 0.05 versus MgHI). At the completion of HI, MgHI had greater decreases in nucleoside triphosphate (NTP) (48 +/- 6% of control), and more brain acidosis after HI (6.01 +/- 0.07) compared with NaHI (NTP, 70 +/- 3% of control; brain pH, 6.51 +/- 0.14, both p < 0.05 versus MgHI). [Mg]i increased to elevated values during HI in both MgHI and NaHI (p < 0.05 versus control of each group) and remained higher in MgHI over the next 25 min (p < 0.05 versus NaHI). There were inverse correlations during HI between [Mg]i and brain NTP (r2 = 0.73 and 0.59 for MgHI and NaHI, respectively), and brain acidosis (r2 = 0.85 and 0.85 for MgHI and NaHI, respectively) in each group. These findings indicate complex effects of Mg on the brain. Elevation of [Mg]ecf may be beneficial with regards to excitatory neurotransmitters. However, greater disturbance of brain NTP concentration, more acidosis, and the increase in [Mg]i may offset any benefit. The results warrant further investigation using indicators of neuronal injury to determine whether Mg supplementation provides neuroprotection.
Animals↗
Is magnesium sulfate for prevention or only therapeutic in preeclampsia?
Intravenously administered magnesium sulfate is effective in reducing the incidence of eclampsia in women with severe preeclampsia. However, the routine use of magnesium sulfate in all cases of preeclampsia is not justified as the incidence of eclampsia is likely to be lower in milder cases than in those with severe disease, and also in view of the adverse effects of magnesium sulfate. Magnesium sulfate should be considered for women with preeclampsia for whom there is concern about the risk of eclampsia, such as hyperreflexia, frontal headache, blurred vision, and epigastric tenderness. As it is an inexpensive drug, it is especially suitable for use in low income countries. Intravenous administration is preferable, where there are appropriate resources, as side effects and injection site problems seem lower. Duration of treatment should not normally exceed 24 hours, and if the intravenous route is used for maintenance therapy the dose should not exceed 1 g/hour Serum monitoring is not necessary. Clinical monitoring of respiration, tendon reflexes and urine out put are enough for monitoring of magnesium toxicity. Administration and clinical monitoring of magnesium sulfate can be done by medical, a midwife or nursing staff provided they are appropriately trained. However, the use of magnesium sulfate should not be misconstrued as a license for reduced surveillance of preeclamptic women. Progression from mild to severe disease and development of serious maternal complications during antepartum, intrapartum and postpartum cannot be predicted without close maternal surveillance. Therefore, continued close antepartum, intrapartum, and postpartum surveillance is crucial for optimal maternal and perinatal outcomes.
Female↗
Successful magnesium sulfate tocolysis: is "weaning" the drug necessary?
OBJECTIVE: Magnesium sulfate is the most commonly used tocolytic agent for preterm labor. A common clinical practice is to slowly discontinue the drug (wean) after successful tocolysis. Our objective was to determine the necessity of this practice. STUDY DESIGN: A prospective, randomized clinical trial was performed from June 1993 to July 1996. After successful magnesium sulfate tocolysis, patients with preterm labor were randomized to two groups: stopping the drug abruptly (no weaning) or gradually weaning the drug (approximately 1 gm every 4 hours). Preterm labor was defined as documented cervical change with regular uterine contractions or regular uterine contractions with a cervix of 2 cm and 75% effacement. The primary outcome variable was the necessity to reinstitute magnesium sulfate therapy within 24 hours of discontinuation of successful tocolysis. RESULTS: One hundred forty-one patients completed the study. No patient in the no-wean group required retocolysis within 24 hours of magnesium discontinuation. However, eight patients in the wean group required retocolysis within 24 hours of magnesium discontinuation (p = 0.01). Significantly more patients in the wean group had retocolysis during pregnancy (3 vs 12, p = 0.03). Patients in the wean group were also in the labor and delivery unit longer and, as would be anticipated, received magnesium sulfate significantly longer. No differences in the neonatal outcomes were noted between the two groups. Seventy-seven percent of the patients in the study were delivered prematurely. CONCLUSION: This study demonstrated an increased need for retocolysis in the group weaned from magnesium sulfate. We also found that patients in the wean group had an increased labor and delivery time and a longer administration time of magnesium sulfate. Thus weaning magnesium sulfate increases health care cost. The practice of weaning magnesium sulfate does not appear beneficial.
Adult↗
Magnesium sulfate as a tocolytic agent.
Although magnesium sulfate is widely used as a tocolytic agent in the hope of preventing spontaneous preterm birth, there is a paucity of data from large well-designed randomized clinical studies demonstrating the efficacy of magnesium sulfate therapy. Given the potential for untoward side effects and the inherent risks of magnesium sulfate therapy, a thorough understanding of the potential risks and benefits of this agent is needed. To accomplish this understanding we have provided a detailed review the history, pharmacology, physiology, maternal/fetal side effects, and tocolytic efficacy of magnesium sulfate.
Adrenergic beta-Agonists↗
A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia.
BACKGROUND: Magnesium sulfate is used widely to prevent eclamptic seizures in pregnant women with hypertension, but few studies have compared the efficacy of magnesium sulfate with that of other drugs. Anticonvulsant prophylaxis with phenytoin for eclampsia has been recommended, but there are virtually no data to support its efficacy. Our objective was to compare magnesium sulfate with phenytoin in preventing seizures in hypertensive women during labor. METHODS: We randomly assigned women with hypertension who were admitted for delivery to receive either magnesium sulfate or phenytoin. The magnesium sulfate regimen consisted of a 10-g intramuscular loading dose followed by a maintenance dose of 5 g given intramuscularly every four hours. For women with severe preeclampsia, an additional 4-g loading dose was given intravenously. The phenytoin regimen included a 1000-mg loading dose infused over a period of 1 hour, followed by a 500-mg oral dose 10 hours later. With either regimen, anticonvulsant therapy was continued for 24 hours post partum. RESULTS: Ten of 1089 women randomly assigned to the phenytoin regimen had eclamptic convulsions, as compared with none of 1049 women randomly assigned to magnesium sulfate (P = 0.004). There were no significant differences in any risk factors for eclampsia between the two study groups. Maternal and infant outcomes were also similar in the two study groups. CONCLUSIONS: Magnesium sulfate is superior to phenytoin for the prevention of eclampsia in hypertensive pregnant women. These results validate the long-practiced use of magnesium sulfate in the prevention of eclampsia.
Adolescent↗
Obstetrical accidents involving intravenous magnesium sulfate: recommendations to promote patient safety.
Magnesium sulfate is commonly used in obstetrical practice both as seizure prophylaxis in women with preeclampsia, as well as to inhibit preterm labor contractions. However, despite (and perhaps because of) years of use and provider familiarity, the administration of magnesium sulfate occasionally results in accidental overdose and patient harm. Fortunately, in most instances when potentially fatal amounts of magnesium sulfate are given, the error is recognized before permanent adverse outcomes occur. Nevertheless, a significant and sometimes unappreciated risk of harm to mothers and babies continues to exist. Intravenous magnesium sulfate treatment has become routine practice in obstetrics, but this does not lessen the vigilance required for safe care for mothers and babies. Implementation of the recommendations provided in this article will promote patient safety and decrease the likelihood of an accidental overdose, as well as increase the chances of identifying an error before a significant adverse outcome occurs.
Adult↗
Antithrombotic effects of magnesium sulfate in in vivo experiments.
In this study, magnesium sulfate was effective in reducing the mortality of adenosine diphosphate-induced acute pulmonary thromboembolism in mice, when it was administered intravenously at doses of 100 and 200 microg/g body weight. In addition, intravenous injections of magnesium sulfate (100 and 200 microg/g) significantly prolonged bleeding time in the severed mesenteric arteries of rats by approximately 1.7- and 1.9-fold, respectively, compared with normal saline. Continuous infusion of magnesium sulfate (20 microg/g per minute) for 10 minutes also significantly increased the bleeding time by approximately 1.7-fold, and the bleeding time returned to baseline within 60 minutes of cessation of magnesium sulfate infusion. On the other hand, platelet thrombi formation was induced by irradiating mesenteric venules with filtered light in mice pretreated with intravenous fluorescein sodium. When magnesium sulfate was administered at 300 microg/g during induction of platelet plug formation with 10 microg/kg fluorescein sodium, occlusion time was not significantly prolonged, but a dose of 600 microg/g did significantly prolong the occlusion time. Furthermore, aspirin (250 microg/g) also showed a similar activity in this experiment in prolonging the occlusion time. In conclusion, these results suggest that magnesium sulfate has an effective antithrombotic activity in vivo, and treatment with magnesium sulfate may lower the risk of thromboembolic-related disorders.
Adenosine Diphosphate↗
Magnesium sulfate attenuates peroxide-induced vasoconstriction in the human placenta.
OBJECTIVE: Magnesium sulfate is used to prevent convulsions in preeclamptic women. It acts as a calcium antagonist but may also stimulate prostacyclin. Because magnesium sulfate readily crosses the placenta, we evaluated whether it might have a beneficial effect on placental blood flow. STUDY DESIGN: Isolated human placental cotyledons (n = 6) were perfused for 20-minute intervals with control Krebs-Ringer-bicarbonate buffer, 200 mumol/L t-butyl hydroperoxide, magnesium sulfate (6 mEq/L), peroxide plus magnesium sulfate, and peroxide plus magnesium sulfate plus calcium chloride (6.25 mEq/L). Peroxide perfusion was used to stimulate thromboxane to induce vasoconstriction. Fetal perfusion pressure was continually monitored. Maternal and fetal effluent samples were analyzed for thromboxane and prostacyclin by their stable metabolites, thromboxane B2 and 6-keto-prostaglandin F1 alpha. RESULTS: Compared with control Krebs-Ringer-bicarbonate buffer perfusion, peroxide perfusion significantly increased (p < 0.05) vascular resistance (12.9 +/- 1.2 vs 21.1 +/- 2.6 mm Hg.min/ml, mean +/- SE) and thromboxane B2 secretion (fetal -0.22 +/- 0.08 vs 0.73 +/- 0.11 ng/min, maternal -1.5 +/- 0.4 vs 4.4 +/- 0.7 ng/min). Subsequent perfusion with magnesium sulfate significantly attenuated (p < 0.05) peroxide-induced vasoconstriction (15.1 +/- 1.7 mm Hg.min/ml), which was reversed by the addition of calcium (19.7 +/- 2.2 mm Hg.min/ml). Magnesium sulfate partially, but significantly (p < 0.05), inhibited the peroxide-induced increase in maternal thromboxane B2 secretion (3.2 +/- 0.6 ng/min) but not fetal thromboxane B2 secretion (1.1 +/- 0.3 ng/min). Magnesium sulfate did not affect 6-keto-prostaglandin F1 alpha secretion. CONCLUSIONS: (1) Magnesium sulfate attenuates peroxide-induced vasoconstriction in the human placenta. (2) This effect is mediated by inhibition of thromboxane synthesis and antagonism of calcium.
6-Ketoprostaglandin F1 alpha↗