Experimental cerebral ischemia and magnesium.
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.
Lin
Jing-Ying
JY
Department of Medical Technology, Chung-Tai Institute of Health Sciences and Technology.
Yang
Dar-Yu
DY
Cheng
Fu-Chou
FC
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D006801:Humans; D008274:Magnesium / Q000008:administration & dosage* / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D013997:Time Factors
D016194:Receptors, N-Methyl-D-Aspartate; D000251:Adenosine Triphosphatases; D008274:Magnesium