Abstract
Cerebral ischemia engages multiple terminal pathways involving the loss of ionic homeostasis, and acute and delayed neuronal damage. Several studies have focused on the derangement of energy metabolism and calcium, but not on magnesium. Hypomagnesium or low dietary magnesium intake may increase the risk of stroke and other cardiovascular diseases. The neuroprotective effects of magnesium have been attributed to a variety of effects on pathophysiologic mechanisms during and after cerebral ischemia, such as antagonizing calcium-mediated metabolic processes, inhibition of the N-methyl-D-aspartate (NMDA) receptors and relaxing vascular smooth muscles. Systemically administered magnesium provides beneficial effects in both clinical patients and cerebral ischemic animal models. Magnesium, as one of the therapeutic agents in stroke treatment, has the advantages of being inexpensive, widely available, and causing few side effects. The optimal doses for the treatment of cerebral ischemia both in animal models and in humans have not been defined yet. Thus, we attempted to evaluate the effects of magnesium on experimental cerebral ischemia.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
