Effects of Intrathecal Magnesium Administration on Neurologic Outcomes in a Porcine Model of Asphyxial Cardiac Arrest

Magnesium mitigates several mechanisms involved in secondary brain injury after cardiac arrest. Because systemically administered magnesium crosses the blood-brain barrier poorly, it may be unsuitable for early post-cardiac arrest neuroprotection. We tested whether intrathecal magnesium (IT-Mg), which bypasses the blood-brain barrier, improves neurologic outcomes in a porcine model of asphyxial cardiac arrest.

Twenty-four pigs underwent asphyxial cardiac arrest and cardiopulmonary resuscitation. Thirty minutes after return of spontaneous circulation, the IT-Mg group received 75 mg of magnesium via cranial intrathecal catheters; the control group received no IT-Mg treatment. Animals were observed for up to 72 hours post return of spontaneous circulation.

Survival duration and cumulative survival did not differ significantly between groups. In controls, the mean amplitude-integrated electroencephalography amplitude remained depressed for 24 hours, whereas it increased in the IT-Mg group (group×time interaction P<0.001). Compared with controls, the IT-Mg group demonstrated superior neurologic function (lower overall performance category, group effect P=0.039; lower neurologic deficit score, group effect P=0.013) and reduced histologic injury (lower temporal cortical [P=0.038] and total [P=0.041] histologic damage scores).

Intrathecal administration of magnesium after return of spontaneous circulation mitigated histologic injury and improved neurologic function in a porcine model of asphyxial cardiac arrest.