Therapeutic Effect of Postischemic Selective Brain Cooling on Ischemic Brain Damage and Edema in focal Cerebral Infarction

The present study investigates the effect of temporary selective brain cooling(SBC) on ischemic brain damage and edema on permanent middle cerebral artery(MCA) occlusion in the rat. Eighteen adult male Sprague-Dawley rats weighing 300-400g were used under halothane anesthesia. The brain temperature was monitored in the left caudate nucleus through a burr hole in the middle of the left coronal suture. All animals underwent left MCA occlusion via subtemporal approach. During the surgery, the physiological variables including mean arterial blood pressure were monitored continuously. Three groups of animals were studied: group 1. Normothermic brain themperature control(n=6) ; group 2, brain cooling for 30min(n=6) ; and group 3, brain cooling for 60min(n=6). In all groups, rectal temperature was maintaind 36.5 degrees C~37 degrees C, and in groups 2 and 3, brain temperature was lowered to less than 34 degrees C by active cooling. 15 min following MCA occlusion. After the brain cooling treatment, anesthesia was discontinued, and the animals were returned to the cage. Twenty-four hours following MCA occlusion, the rats were sacrificed. The volume of ischemic damage and edema was obtained by frozen section technique. There were no significant differences in all physiological parameters between normothermic and hypothermic animals, except the brain temperature. Postischemic SBC for either 30 or 60min significantly reduced the volume of infarction in the cerebral hemisphrere by 14%(p<0.05) or by 27%(p<0.01) respectively and also attenuated neurologic deficits observed at 24 hour postocclusion. However the volume of ischemic brain edema was not significantly reduced and the ratio of volume of brain edema/infarction increased signficantly in groups 2(p<0.05) and 3(p<0.05) compared with group 1. The present study demonstrates that postischemic temporary BSC can attenuate hemispheric infarction in a permanent focal cerebral ichemia model in the rat. However, ischemic brain edema appears not to be attenuated at all. The mechanisms of hypothermic protection and its clinical application are discussed.

Brain SPECT with Tc-99m HMPAO as a Diagnostic Tool for Brain Death

In the evaluation of brain function, clinical examination is used for the brain stem, and EEG for the other part of the brain. However, EEG may be falsely silent in some cases due to medical treatment and technical artifact, and not used easily at postoperative state due to opertion wound contamination. We studied the findings of Tc-99m HMPAO Brain SPECT in 9 cases, who were diagnosed as brain death by currently accepted criteria. With normal cerebral perfusion, the radionuclide activity is primarily intracranial, whereas with brain death it is limited to the scalp. Tc-99m HMPAO cerebral perfusion scintigraphy was, non-invasive and reliable method for the diagnosis of the cerebral circulation, safely before apnea test.

Effect of Methylprednisolone on Ischemic Damage and Neurologic Deficit in Focal Cerebral Infarction in the Rat

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 : p0.1). 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.