This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Horn, M. Articles by Schlote, W. Search for Related Content PubMed PubMed Citation Articles by Horn, M. Articles by Schlote, W. Pubmed/NCBI databases Substance via MeSH

(Stroke. 1995;26:290-297.)
© 1995 American Heart Association, Inc.

Articles

Neuron-Specific Enolase in Gerbil Brain and Serum After Transient Cerebral Ischemia

Markus Horn, MD; Florian Seger, MD Wolfgang Schlote, MD

From the Institute of Neurology (Edinger-Institut), University of Frankfurt/Main (M.H., W.S.), and the Department of Neurosurgery, University of Würzburg (F.S.) (Germany).

Correspondence to M. Horn, MD, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, FRG.

Background and Purpose The sensitivity and validity of serum neuron-specific enolase as a marker of brain injury were tested after global cerebral ischemia.

Methods 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.

Results 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.

Conclusions 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.

Key Words: cerebral ischemia • neuronal death • neuron-specific enolase • gerbils

This article has been cited by other articles:

				K. Yamane, A. Minamoto, H. Yamashita, H. Takamura, Y. Miyamoto-Myoken, K. Yoshizato, T. Nabetani, A. Tsugita, and H. K. Mishima Proteome Analysis of Human Vitreous Proteins Mol. Cell. Proteomics, November 1, 2003; 2(11): 1177 - 1187. [Abstract] [Full Text] [PDF]

				R. Goswami, N. Kochupillai, P. A. Crock, A. Jaleel, and N. Gupta Pituitary Autoimmunity in Patients with Sheehan's Syndrome J. Clin. Endocrinol. Metab., September 1, 2002; 87(9): 4137 - 4141. [Abstract] [Full Text] [PDF]

				W. Gartner, W. Lang, F. Leutmetzer, H. Domanovits, W. Waldhausl, and L. Wagner Cerebral Expression and Serum Detectability of Secretagogin, a Recently Cloned EF-hand Ca2+ -binding Protein Cereb Cortex, December 1, 2001; 11(12): 1161 - 1169. [Abstract] [Full Text] [PDF]

				W. Schoerkhuber, H. Kittler, F. Sterz, W. Behringer, M. Holzer, M. Frossard, S. Spitzauer, and A. N. Laggner Time Course of Serum Neuron-Specific Enolase : A Predictor of Neurological Outcome in Patients Resuscitated From Cardiac Arrest Stroke, August 1, 1999; 30(8): 1598 - 1603. [Abstract] [Full Text] [PDF]

				G. Nollert, M. Nagashima, J. Bucerius, T. Shin'oka, H. G. W. Lidov, A. d. Plessis, and R. A. Jonas OXYGENATION STRATEGY AND NEUROLOGIC DAMAGE AFTER DEEP HYPOTHERMIC CIRCULATORY ARREST. II. HYPOXIC VERSUS FREE RADICAL INJURY J. Thorac. Cardiovasc. Surg., June 1, 1999; 117(6): 1172 - 1179. [Abstract] [Full Text] [PDF]

				M. T. Wunderlich, A. D. Ebert, T. Kratz, M. Goertler, S. Jost, and M. Herrmann Early Neurobehavioral Outcome After Stroke Is Related to Release of Neurobiochemical Markers of Brain Damage Stroke, June 1, 1999; 30(6): 1190 - 1195. [Abstract] [Full Text] [PDF]

				K. J. Becker, R. M. McCarron, C. Ruetzler, O. Laban, E. Sternberg, K. C. Flanders, and J. M. Hallenbeck Immunologic tolerance to myelin basic protein decreases stroke size after transient focal cerebral ischemia PNAS, September 30, 1997; 94(20): 10873 - 10878. [Abstract] [Full Text] [PDF]