PMID: 6399342Jan 1, 1984Paper

Interactions of Mg and K on cerebral vessels--aspects in view of stroke. Review of present status and new findings

Magnesium
B T Altura, B M Altura

Abstract

Considerable experimental evidence has accumulated to indicate that brain ischemia or stroke-like events will lead to rapid losses of brain potassium, magnesium, ATP, creatine phosphate and glucose. These events are usually followed by an uptake of sodium and calcium ions. Increased uptake or excess Ca2+ uptake in neuronal cells is thought to be the prime cause of neuronal death in the brain. Mg2+ deficiency is known to produce a host of neurological disturbances in man; experimentally, Mg2+ deficiency leads to excess uptake of Ca2+ in the brain. Strokes and transient ischemic attacks also are known to be associated with neurological disturbances and ionic changes in the brain. Stroke patients have been reported to exhibit deficits in serum and CSF [Mg]. Acute Mg or K deficiency can produce cerebrovasospasm, at least experimentally. The lower the extracellular concentration of either Mg2+ or K+, the greater the magnitude of cerebral arterial contraction. These cerebrovascular contractions induced by lowering either the [Mg2+]0 or [K+]0 cannot be antagonized or attenuated by known pharmacologic antagonists. The cerebrovasospasms produced upon lowering [Mg2+]0 can be modulated by [K+]0 and vice versa; e.g. the lower the [K+]0, th...Continue Reading

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