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J Thorac Cardiovasc Surg 2001;121:957-968
© 2001 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

The N-methyl-D-aspartate antagonist memantine has no neuroprotective effect during hypothermic circulatory arrest: A study in the chronic porcine model

Jussi Rimpiläinen, MDa, Matti Pokela, MSa, Kai Kiviluoma, MD, PhDb, Vilho Vainionpää, MD, PhDb, Jorma Hirvonen, MD, PhDc, Pasi Ohtonen, MSca, Ville Jäntti, MD, PhDd, Vesa Anttila, MDa, Hanna Heinonen, MDd, Tatu Juvonen, MD, PhDa

From the Departments of Surgery,a Anaesthesiology,b and Forensic Medicinec and the Laboratory of Clinical Neurophysiology,d University of Oulu and Oulu University Hospital, Oulu, Finland.

Supported by grants from Oulu University Hospital, Finnish Foundation for Cardiovascular Research, and Sigrid Juselius Foundation. Prof. Juvonen was also supported by Ingegerd and Viking Olov Björk Scholarship for Cardiothoracic Research.

Received for publication May 18, 2000. Revisions requested Sept 5, 2000; revisions received Sept 18, 2000. Accepted for publication Nov 6, 2000. Address for reprints: Tatu Juvonen, MD, PhD, Department of Surgery, Oulu University Hospital, FIN 90220 Oulu, Finland (E-mail: tatu.juvonen{at}oulu.fi).

Background: Glutamate excitotoxicity has an important role in the development of brain injury after prolonged hypothermic circulatory arrest. The goal of the present study was to determine the potential efficacy of memantine, an N-methyl-D-aspartate receptor antagonist, to mitigate cerebral injury after hypothermic circulatory arrest.
Methods: Twenty pigs (23-33 kg) were randomly assigned to receive memantine (5 mg/kg) or placebo in a blinded fashion before a 75-minute period of hypothermic circulatory arrest at 20°C. Hemodynamic, electroencephalographic, and metabolic monitoring were carried out. The intracerebral concentrations of glucose, lactate, glutamate, and glycerol were measured by means of enzymatic methods on a microdialysis analyzer. Daily behavioral assessment was performed until the animals died or were put to death on day 7. Histologic analysis of the brain was carried out in all animals.
Results: In the memantine group, 5 of 10 animals survived 7 days compared with 9 of 10 in the placebo group. The median behavioral score at day 7 was 3.5 in the memantine group and 7.5 in the placebo group (P > .2). Among the surviving animals, medians were 9.0 and 8.0 on day 7 (P > .2), respectively. The medians of recovered electroencephalographic bursts were equal in both groups. The median of total histopathologic score was 16 in the memantine group and 14 in the placebo group (P > .2). There was a negative correlation between glutamate levels and electroencephalographic burst recovery ({tau} = –0.377, P = .043). A positive correlation was found between the highest individual glutamate value and histopathologic score ({tau} = 0.336, P = .045).
Conclusions: The present study demonstrates that memantine has no neuroprotective effect after hypothermic circulatory arrest in the pig. In addition, we have shown the accuracy of cerebral glutamate measurements to predict histopathologic injury after hypothermic ischemia.




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