Possible role of calcium entry blockers in brain protection.
Cerebral protection in its proper meaning is understood as a method to suppress electrophysiological and metabolic activity of the CNS. More generally, methods which avert injury to the brain, particularly when anticipated, can be considered as cerebral protection. Prevention of secondary brain damage following a primary ischemic or traumatic lesion is a particularly important goal of cerebral protection. The concept of secondary brain damage implies that secondary changes in principle should be prevented by inhibition of the pathomechanisms involved. The introduction of Ca2+ antagonists into the treatment of traumatic or ischemic cerebral injury is an excellent example of a powerful therapeutical method, which is developed on the basis of an understanding of the underlying pathophysiological mechanisms. Ca2+ antagonists may interfere at various levels, e.g. blood flow, cellular destruction or other forms of secondary brain damage. Intracellular Ca2+ overload appears to be a common pathway to failure of pertinent cell functions, and eventually cell death. Thus, inhibition of this process might be central for cell and, hence, cerebral tissue protection. However, the use of Ca2+ antagonists requires careful considerations of the type of drug needed and of their potential side effects.
D000818:Animals; D001921:Brain / Q000378:metabolism; D001927:Brain Diseases / Q000188:drug therapy*; D001930:Brain Injuries / Q000188:drug therapy; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D006323:Heart Arrest / Q000188:drug therapy; D006801:Humans; D002534:Hypoxia, Brain / Q000188:drug therapy; D011817:Rabbits; D051381:Rats
D002121:Calcium Channel Blockers; D002118:Calcium