Abstract
How can we reduce the cerebrospinal damage subsequent to postcardiac arrest syndrome (PCAS) is depending on whether we could inhibit the progress of the negative spiral cascade to induce cerebral damage and improve the functional recovery. On behalf of the improvement of the BLS (Basic Life Support) and ACLS (Advanced Life Support) at the cardiopulmonary resuscitation and the progress of the blood flow interventinal therapy at cerebral infarction and combination of the brain-oriented intensive care came to be able to find the light, however brain has few reserve forces for ischmeic events and brain does not have enough defense mechanisms for ischemic events. Also, therapeutic window for the treatment is still very narrow because of its complicate mechanisms and difficult all patients to come back to normal life. To progress the brain protection and discover new treatment and drugs, it is important to investigate the mechanisms of ischemic brain damage and its pathophysiology. Especially, to analyze the mechanisms of ischemic brain damage and innovate new drugs focusing on the mitochondrial dyfunction may open new avenue. In this review, we referred to PCAS and referred a mechanism of the ischemic brain damage based on the mitochondria dysfunction and the importance of calcineurin-immunophilin signal transduction pathway to be associated with cell death.
