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J Thorac Cardiovasc Surg 1999;118:1156-1157
© 1999 Mosby, Inc.

LETTERS TO THE EDITOR

A word of caution in extrapolating the riluzole spinal cord injury protective effects obtained in a rabbit model under ketamine anesthesia

Tadaomi-Alfonso Miyamoto, MD

Research Department, Kokura Memorial Hospital, 1 Kifunecho, Kokurakitaku
Kitakyushushi, 802-8555, Japan

Koho-J. Miyamoto, MD, PhD

Assistant Professor, II Department of Physiology, University of Ryukius, School of Medicine
Okinawa, Japan

To the Editor:

We read with great interest the excellent article titled "Riluzole Prevents Ischemic Spinal Cord Injury Caused by Aortic Crossclamping" by Lang-Lazdunski and associates (J Thorac Cardiovasc Surg 1999;117:881-9). We do not doubt the protective effects exhibited by riluzole, and we believe this article is a significant contribution to central nervous system protection, for which the authors are to be congratulated. However, we would like to reiterate a point that was raised recently concerning an article on memantine.Go Go 1,2

The authors’ anesthetic included 50 mg/kg of ketamine. Ketamine is an N -methyl-D -aspartate antagonist and known to confer significant protection of the central nervous system against ischemia.Go Go 3,4 Since the mechanisms of action of ketamine and riluzole seem to be different, the likelihood of effects being even potentiating and not only additive are real. Thus the observed protective effects of riluzole were the result of the effects of riluzole by itself in addition to those contributed by ketamine, but their relative roles are unknown. For definitive assessment of the protective effects of riluzole alone, a group of rabbits anesthetized with nonprotective concentrations of volatile agents only, without ketamine or barbiturates, is essential before the data, concerning particularly the ischemic time, can be extrapolated to human application since ketamine is not usually used in adult human clinical practice.

WeGo 5 have found, in a similar model but without using ketamine, that neurologic functional recovery objectively evaluated 6 hours after reperfusion accurately reflects the subsequent outcome at 24 hours. We wonder whether the authors made neurologic score evaluations early after reperfusion and whether neurologic functional improvement was noticed between 24 hours and 120 hours in those observed for more than 24 hours.

References

  1. Ehrlich M, Knolle E, Ciovica R, Böck P, Turkof E, Grabenwöger M, et al. Memantine for prevention of spinal cord injury in a rabbit model. J Thorac Cardiovasc Surg 1999;117:285-91. [Abstract/Free Full Text]
  2. Miyamoto TA, Miyamoto KJ. A word of caution in extrapolating the memantine spinal cord injury protective effects obtained in a rabbit model under ketamine anesthesia [letter]. J Thorac Cardiovasc Surg 1999;118:770-1. [Free Full Text]
  3. Robinson MB, Coyle JT. Glutamate and related acidic excitatory neurotransmitters: from basic science to clinical application. FASEB J 1987;1:446-55. [Abstract]
  4. Weiss J, Goldgberg MP, Choi DW. Ketamine protects cultured neocortical neurons from hypoxic injury. Brain Res 1986;380:186-90. [Medline]
  5. Miyamoto TA, Miyamoto KJ, Ohno N. Objective assessment of CNS function within 6 hours of spinal cord ischemia in rabbits. J Anesth 1998;12:189-94.




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