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J Thorac Cardiovasc Surg 1999;118:1157
© 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

Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Xavier Bichat
Paris, France^a

Institut de Pharmacologie Moleculaire et Cellulaire, CNRS UPR 411, Sophia Antipolis
06560 Valbonne, France^b

Reply to the Editor:

We thank Miyamoto and Miyamoto for their interest in our recent article. ¹ It is a fact that ketamine is a widely known N -methyl-D -aspartate receptor antagonist that has demonstrated neuroprotective properties in vitro and in vivo. ² Therefore the observed neuroprotective effect in our study is the result of ketamine and riluzole effects. Ketamine has been widely used by most investigators working with the rabbit model of spinal cord ischemia, with minor spinal cord protection afforded by this drug. ^2,3 In our study, all rabbits received the same dose of ketamine, with huge differences in neurologic recovery among experimental groups. Thus, although the potentiating effect of ketamine cannot be ruled out, it is unlikely that this drug by itself could account for the dramatic differences in neurologic recovery among experimental groups. For definitive assessment of the neuroprotective effects of riluzole, we have performed a new study with a spinal cord ischemia model in the rat. ⁴ All animals were anesthetized with halothane 1.5% only, and they received riluzole before aortic crossclamping and at the onset of reperfusion. Rats were allowed to recover for 24 (n = 15), 48 (n = 10), or 96 hours (n = 5). In this study, riluzole again prevented neuronal necrosis and apoptosis and cytoskeletal proteolysis.

Regarding neurologic recovery of rabbits, we did not observe worsening of neurologic status in riluzole-treated rabbits between 24 and 120 hours after the operation. Rabbits were scored at 6 hours, 24 hours, and then daily. Riluzole-treated rabbits typically began to recover motor and sensory function between 6 and 24 hours after the operation, whereas control rabbits did not. Neurologic scoring before 6 hours would have been inappropriate considering the anesthetic properties of riluzole. In our recent study, control rats remained severely paraplegic after the operation, whereas riluzole-treated rats began to recover at 6 hours and had either completely normal neurologic function or a mild to moderate deficit up to 96 hours postoperatively.

This result is of importance because some neuroprotective drugs can modify the early recovery but finally fail to alter the mid-term and late recovery after spinal cord ischemia. ⁵ Riluzole, however, not only has a transient effect, but also may really and consistently prevent spinal cord ischemic injury when given before aortic crossclamping.

References

1. Lang-Lazdunski L, Heurteax C, Villant N, Widmann C, Lazdunski M. Riluzole prevents ischemic spinal cord injury caused by aortic crossclamping. J Thorac Cardiovasc Surg 1999;117:881-9. [Abstract/Free Full Text]
   
2. Naslund TC, Hollier LH, Money SR, Facundus EC, Skenderis BS. Protecting the ischemic spinal cord during aortic clamping. Ann Surg 1992;215:409-16. [Medline]
   
3. Herold JA, Kron IL, Langenburg SE, Blackbourne LH, Tribble CG. Complete prevention of postischemic spinal cord injury by means of regional infusion with hypothermic saline and adenosine. J Thorac Cardiovasc Surg 1994;107:536-42. [Abstract/Free Full Text]
   
4. Lang-Lazdunski L, Heurteaux C, Mignon A, Mantz J, Hvass U, Desmonts JM, et al. Ischemic spinal cord injury induced by aortic cross-clamping: prevention by riluzole. Thirteenth meeting of the European Association of Cardio-thoracic Surgery. Glasgow: September 5-8, 1999 [poster].
   
5. Follis F, Miller K, Seremin OU, Pett S, Kessler R, Wernly J. NMDA receptor blockade and spinal cord ischemia due to aortic crossclamping in the rat model. Can J Neurol Sci 1994;21:227-32. [Medline]
   

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