Chemical formula: MgSOâ‚„ Molecular mass: 120.368 g/mol PubChem compound: 24083
Magnesium is the second most abundant cation in intracellular fluid and is an essential body electrolyte. It is a cofactor in numerous enzyme systems and is involved in phosphate transfer, muscle contractility and neuronal transmission.
The precise site of action of magnesium sulfate in eclampsia is not known. Experimentally, magnesium has been shown to block the NMDA subtype of glutamate channel through which calcium enters the cell and causes neuronal damage during cerebral ischaemia. Ischaemia leads to lowering of the transmembrane potential allowing calcium ion influx across the membrane and from the endoplasmic reticulum and mitochondria. This leads to further calcium influx as membrane phospholipids are hydrolysed by activated enzymes. Magnesium blocks calcium at intracellular sites in addition to the outer lipid membrane.
Magnesium sulfate is a saline purgative.
It can be employed locally in various inflammatory conditions, due to its osmotic action.
Serum magnesium levels in the range of 1.5-2.5mmol/l cause vasodilatation in the peripheral and coronary circulation, and corresponding increases of 20-25% in cardiac output and coronary blood flow. There is little change in heart rate or blood pressure. The Atrium-His interval is slightly prolonged as a result of the electrophysiological actions of magnesium. Any direct inhibition is offset by the reflex response to a drop in peripheral vascular resistance, and the Q-T interval is unchanged, thus the function of the SAN is little altered. Within this concentration range there are no detectable effects on CNS function or neuromuscular transmission.
At a serum magnesium level of 1-3mmol/l platelet disaggregation has been reported; possibly mediated by stimulation of prostacyclin release from vascular endothelium.
When a dilute solution of magnesium sulfate is taken by mouth, the absorption of water from the intestine is reduced, and the bulky fluid contents distend the bowel. Active peristalsis is excited and evacuation of the contents of the intestine results.
Magnesium salts cause the secretion of cholecystokinin from the duodenal mucosa, it has been suggested that cholecystokinin – mediated pancreatic secretion and increased secretion and motility of the small intestine and colon may contribute to the cathartic effect.
Magnesium sulfate causes bowel evacuation normally within 2-4 hours.
The concentration of magnesium in plasma is normally tightly regulated in the range of 0.75-0.95mmol/l.
When given intravenously, Magnesium Sulfate has an immediate onset of action, and its duration of activity is about 30mins.
Small and clinically irrelevant amounts of magnesium are excreted in milk. The major excretory pathway is renal and parenteral loads are rapidly eliminated in this way. In renal impairment, there may be accumulation of magnesium. Faecal loss is very limited; small amounts are excreted in saliva and magnesium crosses the placenta.
There are no preclinical data.
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