Magnesium sulfate fails to reduce infarct volume following transient focal cerebral ischemia in rats

Zhu, Hongdong; Martin, Rosemary; Meloni, Bruno P.; Oltvolgyi, Csongor; Moore, Stephen; Majda, Bernadette T.; Knuckey, Neville W.

doi:10.1016/j.neures.2004.04.001

Cited by 33 publications

(14 citation statements)

References 29 publications

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“…However, other studies have failed to detect a neuroprotective effect of magnesium (22,23). The explanation about this controversial outcome includes the different doses, forms of magnesium administration, various models of cerebral ischemia, individual diversity of animals, etc.…”

Section: Discussionmentioning

confidence: 99%

“…The explanation about this controversial outcome includes the different doses, forms of magnesium administration, various models of cerebral ischemia, individual diversity of animals, etc. (22). However, magnesium was applied to brain ischemia, and it will certainly affect the intracellular magnesium.…”

Section: Discussionmentioning

confidence: 99%

“…20, 21; "not effective" in Refs. 22,23), the profile of intracellular magnesium changes during ischemia reperfusion and the possible involved mechanisms, which may be not only related to the application of magnesium but also may be explained by the pathology of cerebral ischemia, remain to be defined.…”

mentioning

confidence: 99%

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Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Zhang¹,

Zhao²,

Zhao

et al. 2011

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Zhang¹,

Zhao²,

Zhao

et al. 2011

Journal of Biological Chemistry

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“…This corresponds to basic studies, where, for example, the high intravenous MgSO 4 dose of 720 mmol/kg had no effect on the infarct volume in rats. 21,22 Intravenous Mg 2þ reaches very low concentrations in cerebrospinal fluid when it is given over a long period of time. For example, inducing an hypermagnesemia (2.1-2.5 mmol/l) in brain-injured patients could increase the amount of Mg 2þ in cerebrospinal fluid only by 15% (1.43 AE 0.13 mmol/l).…”

Section: Action Mechanism Of Mg 2þmentioning

confidence: 99%

Incidence, hemodynamic, and electrical characteristics of spreading depolarization in a swine model are affected by local but not by intravenous application of magnesium

Santos

León

Silos

et al. 2016

J Cereb Blood Flow Metab

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The aim was to characterize the effects of magnesium sulfate, using i.v. bolus and local administration, using intrinsic signal imaging, and on electrocorticographic activity during the induction and propagation of spreading depolarizations in the gyrencephalic porcine brain. Local application of magnesium sulfate led to a complete inhibition of spreading depolarizations. One hour after washing out the topical magnesium sulfate, re-incidence of the spreading depolarizations was observed in 50% of the hemispheres. Those spreading depolarizations showed attenuation in hemodynamic characteristics and speed in intrinsic optical signal imaging. The electrical amplitude decreased through electrocorticographic activity. Intravenous magnesium therapy showed no significant effects on spreading depolarization incidence and characteristics.

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“…28,29 However, in rats that do not have their body temperatures actively regulated after ischemia, the animals experience a 1-to 5-hour period of mild hypothermia; these animals do show neuroprotection, but only if magnesiumtreated (that is, the hypothermia is necessary, but not sufficient to impart the observed neuroprotective effect). 29,30 The effect is preserved, too, with delayed treatment.…”

Section: Experimental Mild Hypothermia and Magnesium Studiesmentioning

confidence: 99%

In Search of Clinical Neuroprotection After Brain Ischemia

Meloni

Campbell

Zhu

et al. 2009

Stroke

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Background and Purpose-Brain injury after stroke and other cerebral ischemic events is a leading cause of death and disability worldwide. Our purpose here is to argue in favor of combined mild hypothermia (35°C) and magnesium as an acute neuroprotective treatment to minimize ischemic brain injury. Methods and Results-Drawing on our own experimental findings with mild hypothermia and magnesium, and in light of the moderate hypothermia trials in cardiac arrest/resuscitation and magnesium trials in ischemic stroke (IMAGES, FAST-Mag), we bring attention to the advantages of mild hypothermia compared with deeper levels of hypothermia, and highlight the existing evidence for its combination with magnesium to provide an effective, safe, economical, and widely applicable neuroprotective treatment after brain ischemia. With respect to effectiveness, our own laboratory has shown that combined mild hypothermia and magnesium treatment has synergistic neuroprotective effects and reduces brain injury when administered several hours after global and focal cerebral ischemia. Conclusions-Even when delayed, combined treatment with mild hypothermia and magnesium has broad therapeutic potential as a practical neuroprotective strategy. It warrants further experimental investigation and presents a good case for assessment in clinical trials in treating human patients after brain ischemia.

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Magnesium sulfate fails to reduce infarct volume following transient focal cerebral ischemia in rats

Cited by 33 publications

References 29 publications

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Incidence, hemodynamic, and electrical characteristics of spreading depolarization in a swine model are affected by local but not by intravenous application of magnesium

In Search of Clinical Neuroprotection After Brain Ischemia

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