Oxygen free radical-mediated lipid peroxidation has been implicated in the pathophysiology of various central nervous system injuries. Therapeutic use of methylprednisolone, a potent steroid and lipid peroxidation inhibitor, has been suggested in
spinal
cord and brain injuries. However, its neuroprotective effect against ischemic cell injury in cerebral ischemia still remains controversial. The present study was conducted to evaluate anti-ischemic effects of methylprednisolone in a middle
cerebral
artery occlusion model in rats.
The experimental animals were divided into two groups : The first group was vehicle-treated control (n=6), and the other was drug-treated group (n=6). In the drug-treated group, the animals received high doses of methylprednisolone (30mg/kg of
bolus
followed by 5mg/kg/h of maintenance dose) immediately after MCA occlusion until 24 hours post occlusion.
Methylprednisolone did not exert any influence upon the physiological parameters during the surgery. However, the serum glucose level increased significantly during the survival period in the drug-treated animals (at 2 and 24 hours post occlusion
:
p<0.05. paired t-test), while the serum glucose level decreased significantly in the vehicle-treated controls. Methylprednisolone did not reduce the volume of infarction, compared with the controls, in the cerebral hemisphere (307.2±52.7 vs.
302.3±32.5mm3 ; P>0.1). Methylprednisolone did not improve neurologic deficits either.
The present study demonstrates that high doses of methylprednisolone does not exert any beneficial effect on the volume of ischemic damage in acute cerebral infarction, and secondary consequences of glucocorticoid-elcvated serum glucose levels
which may
act to exacerbate ischemic lactic acidosis could be one of the mechanisms of this negative effect.
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