Experimental neuronal protection in cerebral ischaemia part I: experimental models and pathophysiological responses

Development of neuroprotective strategies for the treatment of cerebral ischaemia depends upon knowledge of the pathophysiological responses which occur during the period of ischaemia and during reperfusion. Both in vitro and in vivo studies have been used to accumulate this base of knowledge; a brief examination of the results from the two approaches reveal that they are in general agreement and often provide complementary information. Ischaemia in the absence of reperfusion can lead to neuronal death from protein degradation and DNA breakup. Resupply of blood permits increased free radical attack but energy supply can still be limited as the cerebral circulation reacts to release of cicosanoids, and DNA repair utilizes ATP.