Magnesium Sulfate

Magnesium is the second most abundant intracellular cation, and it serves as a cofactor in more than 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Among other magnesium salts with clinical uses, magnesium chloride, magnesium gluconate, magnesium lactate, and magnesium oxide provide oral supplementation for patients with magnesium deficiency due to malnutrition, restricted diet, alcoholism, or magnesium-depleting drugs. Magnesium oxide can also be used as an antacid or laxative.

Magnesium sulfate is the most common clinically used magnesium salt and can be administered orally or parenterally. It is used orally as a laxative and parenterally as a neuromuscular depressant or to treat hypomagnesemia. Oral magnesium sulfate is a saline laxative, used primarily to empty the bowel before surgery or procedures. Magnesium sulfate is also a useful cathartic in combination with charcoal to treat acute drug overdose. Parenteral magnesium sulfate is primarily used to prevent and control seizures in preeclampsia and eclampsia. Parenteral magnesium sulfate is also used to control seizures due to epilepsy, glomerulonephritis, or hypothyroidism. Parenteral magnesium may also be used cardiac glycoside-induced arrhythmias. The 2000 ECC/AHA guidelines conclude that IV magnesium during cardiopulmonary resuscitation is effective only for the treatment of patients with hypomagnesemic states or polymorphic ventricular tachycardia. IV magnesium is not recommended in cardiac arrest except in suspected hypomagnesemic states or tachycardia. Magnesium sulfate was officially approved by the FDA in 1939.

Mechanism of Action

Magnesium acts as an enzyme cofactor during phosphate transfer reactions that use ATP and other nucleotides as substrates. Magnesium ions contribute to the normal function of the ATP-dependent sodium-potassium "pump" in muscle membranes. Without magnesium, this pump is compromised. Hypomagnesemia is believed to be an important aspect of hypokalemia, so drugs that cause hypokalemia, such as cisplatin, amphotericin B, and loop diuretics, also cause hypomagnesemia. Correcting this condition supports the treatment of hypokalemia by improving the efficacy of the pump. This mechanism also may explain how IV magnesium sulfate treats cardiac glycoside-induced arrhythmias, although magnesium may exert therapeutic effects unrelated to the sodium-potassium pump.

Magnesium is also required for the binding of intracellular macromolecules to organelles and mRNA to ribosomes. As a laxative, magnesium sulfate exerts action in the small intestine, including a hyperosmotic effect and stimulation of stretch receptors and peristalsis through retention of water. Other evidence indicates, however, that hyperosmolarity does not occur and that cholecystokinin release or decreased transit time are more likely mechanisms.

The mechanism of the antacid effects of magnesium oxide involves reaction with water. In the presence of water, magnesium oxide is converted to magnesium hydroxide which rapidly reacts with gastric acid to form water and magnesium chloride.

As an anticonvulsant, magnesium sulfate depresses the CNS and blocks peripheral neuromuscular transmission. This is achieved through inhibition of acetylcholine release by motor nerve impulses. Magnesium is a peripheral vasodilator and an inhibitor of platelet function.

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