Abstract

I assessed the effect of therapeutic hypothermia on the activity in cerebrospinal fluid of creatine kinase (EC 2.7.3.2) and its brain isoenzyme (CK-BB), lactate dehydrogenase (EC 1.1.1.27), and aspartate aminotransferase (EC 2.6.1.1.) as markers of cerebral damage in patients with transient anoxic-ischemic brain injury. Moderate hypothermia (30-32 degrees C) lasting more than 24 h resulted in disproportionately greater activity of creatine kinase during the post-insult period than in patients not treated with hypothermia but having similar insults and outcome (p less than .01 for survivors, and p less than .005 for nonsurvivors). No differences were observed for the thermostable enzymes lactate dehydrogenase and aspartate aminotransferase, which demonstrates that the effect of hypothermia must be taken into account when thermolabile enzymes are used as sole markers of brain damage in such patients.

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