J Thorac Cardiovasc Surg 2006;131:1212-1213
© 2006 The American Association for Thoracic Surgery
Apoptosis in ischemic spinal cord injury
A.K. Koray,
Atike Tekeli,
Selim Isbir
Marmara University Faculty of Medicine, Department of Cardiovascular Surgery, Istanbul, Turkey
To the Editor:
We read the article of Suzuki and associates
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titled "Experimental study on the protective effects of edaravone against ischemic spinal cord injury" with great interest. They studied the effect of a free radical scavenger named "edaravone" in a rabbit model of transient aortic occlusion and claimed its protective effect on the ischemia-reperfusion injury of spinal cord by suppressing the level of reactive oxygen species (ROS). We congratulate Suzuki and associates for their excellent study. We think that the introduction of microdialysis method to determine the production of ROS in the neuronal tissue after transient ischemia for the first time in the literature by the authors is a great contribution to our current knowledge.
Recently, data has accumulated that programmed cell death or apoptosis of motor neurons in spinal cord after transient ischemia is an outstanding mechanism of postoperative paraplegia or paraparesis.
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The neuronal injury following transient aortic occlusion occurs in 2 phases, namely, early and delayed. Ischemic insult in spinal cord activates apoptosis by plasma membrane death receptor pathway, activation of caspase enzymes, and release of cytochrome c from mitochondria. Although blood flow to the spinal cord is restored during reperfusion, the motor neurons that seem to survive ischemic insult may undergo delayed selective death, particularly 7 days after the procedure.
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Despite that the etiology of delayed selective neuronal death has been proposed to be the activation of Akt protein, Grp78, and caspase 12 proteins, further studies should be warranted. In the present study, the authors claimed the protective effect of edaravone on spinal cord injury according to the histologic examination and levels of ROS. However, it is known that these neurons might be apoptotic despite the normal cellular architecture seen on the hematoxylin and eosin (H & E) staining. The authors did not focus on apoptotic mechanisms and demonstrated only necrotic (ghost) neurons with H & E staining without considering the neurons undergoing apoptosis. In this regard, we believe that addition of the neuronal apoptosis would increase the statistical power of this study.
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References
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- Suzuki K, Kazui T, Terada H, Umemura K, Ikeda Y, Bashar AH, Yamashita K, et al. Experimental study on the protective effects of edaravone against ischemic spinal cord injury. J Thorac Cardiovasc Surg 2005;130:1586-1592.[Abstract/Free Full Text]
- Isbir CS, Ak K, Kurtkaya O, Zeybek U, Akgun S, Scheitauer BW, Sav A, et al. Ischemic preconditioning and nicotinamide in spinal cord protection in an experimental model of transient aortic occlusion. Eur J Cardiothorac Surg 2003;23:1028-1033.[Abstract/Free Full Text]
- Sakurai M, Takahashi G, Abe K, Horinouchi T, Itoyama Y, Tabayashi K. Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits. J Thorac Cardiovasc Surg 2005;130:640-645.[Abstract/Free Full Text]
- Sakurai M, Nagata T, Abe K, Horinouchi T, Itoyama Y, Tabayashi K. Survival and death-promoting events after transient spinal cord ischemia in rabbits. induction of Akt and caspase3 in motor neurons. J Thorac Cardiovasc Surg 2003;125:370-377.[Abstract/Free Full Text]
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Reply to the Editor
- Kazuchika Suzuki, Teruhisa Kazui, and Abul Hasan Muhammad Bashar
J. Thorac. Cardiovasc. Surg. 2006 131: 1213.
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