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J Thorac Cardiovasc Surg 1999;118:771
© 1999 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Cardiothoracic Surgery
Mount Sinai Medical Center
One Gustave Levy Place
Box 1028
New York City, NY 10029
Reply to the Editor:
My colleagues and I thank Miyamoto and Miyamoto for their interest and comments on our recent article regarding the N-methyl-D-aspartate (NMDA) blocker memantine.
1
As we are aware of the protective effect of hypothermia on the release of excitatory amino acids, we have tried to keep the rectal temperature in a normothermic range assuming that the rectal temperature will reflect more accurate spinal cord temperature than esophageal temperature. However, we will additionally monitor esophageal temperature in future experiments.
With respect to our anesthesia protocol, a comparable experiment investigating the influence of anesthetics on neurologic recovery showed that ketamine treatment reduced acute paraplegia but increased delayed paraplegia.
2 In our study, the control group did not show a protective effect of ketamine compared with the groups treated with memantine. Volatile anesthetics and nitrous oxide are suppressive to myogenic motor-evoked responses,
3 but ketamine is recommended as a suitable supplement to opioid/nitrous oxide anesthesia in men.
4 In our experiments we used ketamine to keep the experimental conditions constant and to avoid false positive depression of motor-evoked potentials due to the influence of an anesthetic.
In regard to the different applications of memantine, we assumed that intra-arterial infusion of memantine into the clamped aortic segment would result in better protection than administering the drug systematically. We were surprised by the fact that the systemic group did better than the intra-aortic group. We concur that this phenomenon was due to the slow crossing of memantine through the blood-brain barrier.
References
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