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.

Ihe Effect of Arginine Vasopressin on Acute Ischeme Brain Edema and Its Mechanism / 第二军医大学学报

The purpose of this experiment was to study the role of arginine vasopressin (AW) in acute cerebral ischemic edema in mongolian gerbils. The results showed that intracerebroventricular injection (ICV) of AVP exacerbated the ischemic brain edema, while ICV of AW antiserum significantly decreased the ischemic brain edema. Nimodipine couldn't block this role of AW in ischemic brain edema. The cortical Na+ -K+ ATPase activity was significantly decreased, the contents of cAMP in the ischemic cortex and hypothalamus and the contents of cGMP in the hypothalamus were remarkably increased after ICV of AW. These suggest AW was involved in the pathophysiologic process of acute ischemic brain edema. And its mechanism might be the effect of AW on AW receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+ -K+ ATPase activity of brain cell membrane, then exaggerated the formation of ischemic brain edema.