Brain damage induced by focal interruption of blood flow can be differentiated in two pathophysiologically different categories: a hemodynamic type of injury, resulting in primary necrotic brain damage, and a molecular type of injury which leads to delayed or secondary brain injury [15]. Primary necrotic brain injury occurs when blood flow declines — and remains — below the threshold of energy failure. In anaesthetized laboratory animals, this threshold gradually increases from about 15% of control shortly after the onset of ischemia to about 30% after several hours of vascular occlusion [35].