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The Effect of Cerebral Ischemia on Learning and Retention in Dogs

Jack M. Zimmerman, MD; Harold C. Nielson, PhD; Thomas C. King, MD; Jerry C. Colliver, PhD
JAMA. 1966;197(2):126-128. doi:10.1001/jama.1966.03110020114035.
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With available techniques of cardiac resuscitation it is often possible to restore spontaneous cardiac action in patients with cardiac arrest. However, many patients in whom cardiac activity is restored have neurological sequelae as a consequence of the arrest. It has been demonstrated that hypothermia,1,2 and possibly the osmotic diuretics,3 used after a period of total cerebral ischemia, modify the severity of neurological damage. Investigation of agents which might be useful for this purpose has been hampered by the fact that it is difficult to detect less than massive brain damage in the dog. Brockman and Jude4 have shown that dogs subjected to ten minutes of complete cerebral ischemia by cross clamping the ascending aorta reveal no neurological deficit on gross examination whereas animals subjected to longer periods of occlusion died without awakening from anesthesia. The present report describes a means by which subtle changes in neurological status


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