[Consensus review. Pharmacological neuroprotection in cerebral ischemia: is it still a therapeutic option?].
Our increasing knowledge concerning the pathophysiology of cerebral ischemia is leading to a considerable development of drugs that at various levels block or modify the chain of biochemical processes set off as a consequence of hypoperfusion of cerebral parenchyma. In this zone of ischemic penumbra, the interaction between the neuronal ischemia cascade, the response of the glia and changes in the microcirculation, determine the evolution towards either functional recovery of the ischemic fabric or it necrosis. In various types of animal models, the majority of neuroprotective drugs have been shown to have considerable efficacy. However, this has not been translated into human clinical practice. The identification of persistence of recoverable cerebral tissue, together with the development of new designs of clinical trails better adapted to preclinical experiences and to the features of the drugs concerned, may contribute to an improved applicability of the new drugs in human clinical practice.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D002545:Brain Ischemia / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D018450:Disease Progression; D018691:Excitatory Amino Acid Antagonists / Q000627:therapeutic use; D006801:Humans; D008833:Microcirculation / Q000503:physiopathology; D009457:Neuroglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D018696:Neuroprotective Agents