Neuron-specific enolase in gerbil brain and serum after transient cerebral ischemia.

Abstract

The sensitivity and validity of serum neuron-specific enolase as a marker of brain injury were tested after global cerebral ischemia. Sixty-nine Mongolian gerbils were perfusion fixed after variable reperfusion after 5-minute (group 1) or 15-minute (group 2) bilateral carotid occlusion. Neuron-specific enolase was analyzed by an enzyme immunoassay in serum of control, sham-operated, and ischemic animals before euthanasia and in nonischemic gerbil brains. Brains were processed for histology, immunohistochemistry, and morphometric evaluation of ischemic neuronal damage. After cerebral ischemia, loss of neuronal immunoreactivity was closely associated with increased neuron-specific enolase serum levels, which were significantly elevated by 24 hours (group 1) or by 4 hours (group 2) of reperfusion (P < .001). Response of serum levels depended on the duration of preceding ischemia, and maximum concentrations were approximately 3-fold (group 1) or 20-fold (group 2) those of nonischemic control. Morphological damage became apparent 48 hours (group 1) or 12 hours (group 2) after ischemia, as indicated by histological and morphometric data. Significantly elevated neuron-specific enolase serum levels could be demonstrated as a consequence of ischemia-induced cytoplasmic loss of neuron-specific enolase in central nervous system neurons, corresponded quantitatively to the severity of cerebral ischemia, and were detectable before irreversible neuronal injury. Therefore, analysis of serum neuron-specific enolase is suggested to be both a valuable diagnostic tool in clinical management of the initial stages of global cerebral ischemia and a prognostic parameter during the postischemic course.