Calcium entry blockers in cerebral resuscitation.
This paper reviews postischemic events which might influence the neurologic injury following cerebral ischemia. The influence of diverse calcium entry blockers (CEB) on postischemic cerebral blood flow (CBF) and neurologic outcome is presented. The role of intracellular calcium (Ca) accumulation in neuronal injury is discussed. Although a number of diverse experiments appear in the literature using several, different types of CEB, e.g., nimodipine, lidoflazine, flunarizine and nicardipine, they appear to have different cerebral effects. There is no solid consistent evidence that CEB prevent Ca loading following cerebral ischemia. At least one CEB appears promising, namely, nimodipine. Since the mechanisms of action of CEB in cerebral ischemia remain obscure, further studies appear necessary and warranted.
Sakabe
T
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Department of Anesthesiology, Yamaguchi University Hospital, Japan.
D000818:Animals; D002545:Brain Ischemia / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000009:adverse effects*; D002560:Cerebrovascular Circulation; D009474:Neurons / Q000473:pathology
D002121:Calcium Channel Blockers; D002118:Calcium