Neuroprotective efficacy of intra-arterial and intravenous magnesium sulfate in a rat model of transient focal cerebral ischemia.

Abstract

Many neurovascular procedures necessitate temporary occlusion of cerebral arteries. In this situation neuroprotective drugs may increase the safety of the procedures. Magnesium may inhibit ischemic damage by anti-excitotoxic, calcium channel blocking and vasodilatory action. Some evidence suggests that intra-arterial administration might provide a much higher degree of protection than intravenous treatment. In this study the neuroprotective efficacy of intra-arterial and intravenous magnesium administration was examined in a rat model of transient focal ischemia. 34 male Sprague-Dawley rats were subjected to 90 minutes of middle cerebral artery occlusion (MCAO) by an intraluminal thread. Before ischemia, animals received an infusion of either (1) vehicle (0.9% NaCl) (2) MgSO4 intra-arterially or (3) MgSO4 intravenously. Local cortical blood flow (LCBF) was continuously measured by laser-Doppler flowmetry. Functional deficits were quantified daily, infarct volumes were assessed histologically after 7 days. There was no difference between the treatment groups concerning LCBF. Magnesium serum levels increased from approximately 1 mmol/l to approximately 1.8 mmol/l by either route of administration. Both intra-arterial and intravenous treatment improved neurological recovery and equally reduced total infarct volume by approximately 25%. The results indicate that there is no advantage of intra-arterial over intravenous magnesium administration. A comparison with previous studies suggests that even within the normal range of serum magnesium concentrations, low-normal levels may be hazardous and high-normal levels may be protective in transient focal ischemia.