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Reduction of infarct volume by magnesium after middle cerebral artery occlusion in rats
1Laboratoire de Recherches Cérébrovasculaires, CNRS UA 641, Université Paris VII, France.
Abstract:
The effects of magnesium, an endogenous inhibitor of calcium entry into neurons, upon ischemic brain damage were investigated using a well-characterized model of focal cerebral ischemia in rats. Infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride transcardiac perfusion 48 h after middle cerebral artery (MCA) occlusion. The area of ischemic damage was quantified by image analysis in coronal sections taken every 0.5 mm. MgCl2 (1 mmol/kg) was injected intraperitoneally just after MCA occlusion and again 1 h later. Posttreatment with MgCl2 (16 control and 16 treated rats) significantly reduced the cortical infarct volume. Compensation for the hyperglycemic effect of MgCl2 with insulin (17 rats) further reduced the infarct volume in the neocortex. No systemic effects of either treatment could account for the observed neuroprotection.
Insights
Magnesium treatment significantly reduced ischemic brain damage in rats after middle cerebral artery occlusion. Insulin further enhanced this neuroprotective effect by mitigating hyperglycemia.
Area of Science:
- Neuroscience
- Ischemic Stroke Research
- Neuroprotection
Background:
- Magnesium is an endogenous inhibitor of calcium entry into neurons.
- Ischemic brain damage is a significant neurological concern.
- Focal cerebral ischemia models are crucial for studying stroke mechanisms.
Purpose of the Study:
- To investigate the neuroprotective effects of magnesium on ischemic brain damage.
- To evaluate the impact of magnesium chloride (MgCl2) treatment in a rat model of focal cerebral ischemia.
- To assess the role of insulin in modulating magnesium's neuroprotective effects.
Main Methods:
- A well-characterized rat model of focal cerebral ischemia was employed.
- Middle cerebral artery (MCA) occlusion was induced to create ischemic conditions.
- Infarct volumes were quantified using 2,3,5-triphenyltetrazolium chloride staining and image analysis 48 hours post-occlusion.
- Rats received intraperitoneal injections of MgCl2 post-MCA occlusion, with some receiving insulin to control for hyperglycemia.
Main Results:
- Posttreatment with MgCl2 significantly reduced cortical infarct volume in rats.
- Insulin administration, used to compensate for MgCl2-induced hyperglycemia, further decreased neocortical infarct volume.
- No systemic side effects of MgCl2 or insulin treatments were identified as the cause of neuroprotection.
Conclusions:
- Magnesium administration demonstrates significant neuroprotective effects against ischemic brain damage.
- Insulin can enhance the neuroprotective benefits of magnesium, particularly in mitigating neocortical damage.
- Magnesium represents a potential therapeutic agent for reducing brain injury following ischemic stroke.