To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
This chapter explains the mechanisms leading to neuronal cell death and the most important neuroprotective strategies. Cerebral ischaemia and/or hypoxia may occur as a consequence of shock, respiratory failure, vascular stenosis or occlusion, vasospasm, neurotrauma or cardiac arrest. Ischaemic or traumatic challenges affect both inadequate delivery of oxygen and glucose, and impairment of mitochondrial function, leading to inadequate production of ATP. Two different types of cell death may occur following brain injury: necrosis and apoptosis. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral damage after brain injury. The proposed mechanisms of anaesthetic protection include reduction of cerebral metabolism and intracranial pressure (ICP), and suppression of seizures and sympathetic discharge. Hypoxia and ischaemia are recognized as important driving forces of erythropoietin expression in the brain, suggesting that erythropoietin is part of a self-regulating physiological protection mechanism to prevent neuronal injury.