Effect of Methylprednisolone on Ischemic Damage and Neurologic Deficit in Focal Cerebral Infarction in the Rat.
- Author:
Chun Kun PARK
1
;
Shin Soo JUN
;
Dal Soo KIM
;
Joon Ki KANG
;
Chang Rak CHOI
Author Information
1. Department of Neurosurgery, Catholic University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Focal cerebral infarction;
Methylprednisolone;
Neurologic deficits;
Serum glucose;
Latic acidosis
- MeSH:
Acidosis, Lactic;
Animals;
Blood Glucose;
Brain Injuries;
Brain Ischemia;
Central Nervous System;
Cerebral Infarction*;
Infarction;
Infarction, Middle Cerebral Artery;
Lipid Peroxidation;
Methylprednisolone*;
Neurologic Manifestations*;
Neuroprotective Agents;
Oxygen;
Rats*;
Spinal Cord
- From:Journal of Korean Neurosurgical Society
1994;23(7):775-782
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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 group : 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(30 mg/kg of bolus followed by 5 mg/kg/h of maintenance dose) immediately after MCA coolusion 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+/-32.5 mm3 ; P>0.1). Methylprednisolone did not improve neurologic deficits either. The present study demonstrates that high doses of methylprednisolone does not exert any bebeficial effect on the volume of ischemic damage in acute cerebral infarction, and secondary consequences of glucocorticoid-elevated serum glucose levels which may act to exacerbate ischemic lactic acidosis could be one of the mechanism of this negative effect.
