| Summary: | 碩士 === 國立成功大學 === 醫學工程研究所碩博士班 === 93 === Cerebral stroke is a leading cause of death and disability worldwide. In general, transient focal cerebral ischemia that occurs during cerebrovascular surgery may result in irreversible cell damage and neurobehavioral dysfunction due to the release of excitotoxic neurotransmitters, influx of calcium ions into neurons, free radical generation, lipid peroxidation, and protein degradation. Much evidence implicates the influx of calcium ions via the N-methyl-D-aspartate (NMDA) receptor complex in the pathogenesis of cerebral ischemic injury. Intravenous thrombolysis within 3 hr after symptoms onset represents the first therapeutical approach that can effectively treat acute ischemic stroke. Until now, thrombolysis has not been approved for intravenous administration ＞3 hr after stroke onset because the risk of hemorrhage increases with time. However, most patients arrive at the hospital too late to receive the maximum benefit. Thus an effective neuroprotective agent is needed to protect ischemic brain after thrombolytic therapies.
Mg2+ has a variety of pharmacological actions that may be beneficial in the treatment of acute ischemic stroke. Neuroprotective mechanisms of Mg2+ include blockade of L- and N-type voltage-operated calcium channels, inhibition of excitatory neurotransmitter release, and blockade of voltage-dependent NMDA channels. These mechanisms show a dose-dependent vasodilation of intracranial arterioles and venules. Mg2+ may decrease the size of brain infarct due to increase cerebral blood flow after cerebral vasodilation. In the current study, we investigate whether delayed treatment with magnesium sulfate (MgSO4；750μmol/Kg ia) could improve electrophysiology and neurobehavioral function in the transient focal cerebral ischemia model. Improvement of functional outcome is more important than reduced brain damage with regard to stroke patients through treatment.
At 72 hr after the onset of reperfusion, the amplitude of somatosensory evoked potentials (SSEP) recorded from ischemic fore- and hindpaw cortical fields decreased to 18% and 26% of baselines in vehicle-injected rats. Respectively, the amplitude of SSEP recorded from cerebral ischemia rats treated with MgSO4 improved to 24% and 40% of baselines. In addition, MgSO4 improved sensory and motor neurobehavioral outcomes by 33% and 25%, and reduced cortical and striatal infarct sizes by 40%. In conclusion, delayed treatment with magnesium could improve electrophysiology and neurobehavioral outcomes and reduce brain damage after cerebral ischemia-reperfusion.
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