Intravenous administration of magnesium is only neuroprotective following transient global ischemia when present with post-ischemic mild hypothermia

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

doi:10.1016/j.brainres.2004.03.073

Cited by 56 publications

(32 citation statements)

References 27 publications

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“…201 It has antiarrhythmic properties, and some animal data indicate that magnesium provides added neuroprotection in combination with hypothermia. 202 Magnesium sulfate (5 g) can be infused over 5 hours, which covers the period of hypothermia induction. The shivering threshold can also be reduced by warming the skin; the shivering threshold is reduced by 1°C for every 4°C increase in skin temperature.…”

Section: Therapeutic Hypothermiamentioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,233

398

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Section: Therapeutic Hypothermiamentioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,233

398

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“…It is well recognized that temperature in recovering animals is influenced by multiple factors, including method of temperature measurement, anesthetic regimen and injury model [6,8,27,28]. Furthermore, the neuroprotective potential of a number of pharmacologic agents such as MK-801, NBQX or Magnesium has been linked to temperature [29][30][31]. Therefore, interactions with brain injury induced spontaneous hypothermia and investigational neuroprotective drugs must be considered.…”

Section: Discussionmentioning

confidence: 99%

Experimental Hyperthermia during Cardiac Arrest and CPR Is Associated with Severe Spontaneous Hypothermia in Mice

Noppens¹,

Kofler²,

Traystman³

2012

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Background: Since genetically engineered mice are becoming more and more available, these animals become of high interest to study physiologic and pathophysiologic pathways of brain ischemia. The aim of this study was to examine body temperature (Tb), physical activity variation and neurohistopathology in mice exposed to normothermic and hyperthermic cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Methods: Male C57Bl/6 mice weighing 22 -27 g were implanted intraperitoneally with a radio telemeter and subjected to 10 min cardiac arrest followed by cardiopulmonary resuscitation. Normothermia (37.5˚C) or hyperthermia (39.0˚C) was induced by controlling peri-cranial temperature during the arrest period. Results: Hyperthermia during the arrest resulted in a Tb decrease during early recovery to a nadir of 28˚C ± 0.8˚C (mean ± SE) and partially recovered to 34.4˚C ± 1˚C 36 hrs after CA/CPR. With normothermia during the arrest, Tb depression was less pronounced (nadir of 32.3˚C ± 0.3˚C) and recovered to physiologic levels within 24 hrs. Coupling of physical activity and body temperature was absent in all animals after CA/CPR. Neuronal injury in the caudoputamen was greater in the hyperthermia group. Conclusions: This study demonstrates that CA/CPR eliminates normal connectivity between body temperature and physical activity and induces long-lasting hypothermia, the depth of which is related to severity of brain injury. Long term temperature monitoring is required in survival murine experiments, if body temperature is a study variable.

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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. Commencing 2 hours after global ischemia, a 24-hour duration of controlled mild hypothermia (35°C) alone was neuroprotective, but when combined with a 48-hour intravenous infusion of magnesium the level of protection was almost doubled (improved from 43% to 76%; Figure 1).…”

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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Intravenous administration of magnesium is only neuroprotective following transient global ischemia when present with post-ischemic mild hypothermia

Cited by 56 publications

References 27 publications

Post–Cardiac Arrest Syndrome

Post–Cardiac Arrest Syndrome

Experimental Hyperthermia during Cardiac Arrest and CPR Is Associated with Severe Spontaneous Hypothermia in Mice

In Search of Clinical Neuroprotection After Brain Ischemia

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