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Ann Thorac Surg 2000;69:750-754
© 2000 The Society of Thoracic Surgeons


Original Articles

Neuron-specific enolase increases in plasma during and immediately after extracorporeal circulation

Per Johnsson, MD, PhDa,c, Sten Blomquist, MD, PhDb,c, Carsten Lührs, MDa,c, Gunnar Malmkvist, MD, PhDb,c, Christer Alling, MD, PhDa,c, Jan-Otto Solem, MD, PhDa,c, Erik Ståhl, MD, PhDa,c

a Department of Cardiothoracic Surgery, University Hospital, Lund, Sweden
b Department of Anesthesiology, University Hospital, Lund, Sweden
c Department of Medical Chemistry, University Hospital, Lund, Sweden

Address reprint requests to Dr Blomquist, Department of Anesthesiology and Intensive Care, University Hospital, S-22185 Lund, Sweden

Background. Minor cerebral complications are common after cardiac surgery. Several biochemical markers for brain injury are under research; one of these is neuron-specific enolase (NSE). The purpose of this study was to investigate the release of this enzyme into the blood during and immediately after extracorporeal circulation and to evaluate the effect of hemolysis on this release.

Methods. Sixteen patients scheduled for elective heart surgery were included in the study. Blood samples for analysis of NSE and free hemoglobin in plasma were drawn before, during, and up to 48 hours after the end of extracorporeal circulation. The release of NSE from erythrocytes and its correlation to the release of free hemoglobin was studied by serial dilution and hemolysis in vitro.

Results. The peri- and postoperative course was uneventful in all patients. Extracorporeal circulation initiated a release of NSE that reached a maximum 6 hours after the end of perfusion. Thereafter, the levels declined with an estimated t1/2 of 30 hours. The concentration of free hemoglobin increased during the perfusion, with maximum levels at the end of perfusion, after which they fell rapidly to normal values. The in vitro study showed a strong linearity between the release of NSE and free hemoglobin after induced hemolysis.

Conclusions. The increased levels of enolase at the end of cardiopulmonary bypass can, to a major part, be explained by the release from hemolysed erythrocytes. The value of NSE as a marker for brain injury in these situations is therefore doubtful.




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