Current concepts in brain resuscitation.
In spite of the tremendous amount of effort and money put forth to reduce morbidity and mortality associated with global cerebral ischemia, the outlook for patients suffering an ischemic insult remains dismal. The lack of a sufficient substrate supply during the period of ischemia as well as the production of toxic metabolites in response to ischemia have been incriminated as key factors causing brain damage. As discussed in this article, modes of therapy have included efforts to minimize the duration of ischemia (eg, effective cardiopulmonary resuscitation, hemodilution, heparinization, calcium antagonists) and decrease the production of toxic metabolites (eg, barbiturates, calcium antagonists). Although the barbiturates have also been proposed to decrease the metabolic needs during ischemia, they have no therapeutic value for global cerebral ischemia. The initial evaluation of the calcium antagonists has been more promising.
D000818:Animals; D001463:Barbiturates / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000209:etiology / Q000628:therapy*; D002118:Calcium / Q000032:analysis; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D005045:Etomidate / Q000627:therapeutic use; D005227:Fatty Acids / Q000032:analysis; D005609:Free Radicals; D006323:Heart Arrest / Q000150:complications; D006438:Hemodilution; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007773:Lactates / Q000032:analysis; D008928:Mitochondria / Q000032:analysis; D012151:Resuscitation
D001463:Barbiturates; D002121:Calcium Channel Blockers; D005227:Fatty Acids; D005609:Free Radicals; D007773:Lactates; D006493:Heparin; D002118:Calcium; D005045:Etomidate