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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Teruhisa Kazui Abul Hasan Muhammad Bashar Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Suzuki, K. Articles by Bashar, A. H. M. Search for Related Content PubMed Articles by Suzuki, K. Articles by Bashar, A. H. M. Related Collections Related Article

J Thorac Cardiovasc Surg 2006;131:1213
© 2006 The American Association for Thoracic Surgery

Letter to the Editor

Reply to the Editor

The First Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan

We thank Dr AK for his insightful comments on our recently published article. Paraplegia or paraparesis occurring in the late postoperative period is well described in the literature. The mechanism of this delayed spinal deficit is presumed to be related with apoptosis. Sakurai and colleagues ¹ evaluated the relationship between delayed paraplegia and apoptosis using immunohistochemical techniques. In their experimental study, the transient spinal ischemic time was 15 minutes. Two days after the reperfusion, the mean Johnson score was 4.9 ± 0.894, and 3 of the 5 rabbits had normal hind-limb function. In our study, ² we applied a spinal ischemic time of 30 minutes. Two days after the reperfusion, all rabbits in the control group were completely paraplegic with a Johnson score of 0. The focus of our investigation was to assess whether prophylactic administration of edaravone could suppress necrosis and not apoptosis of the spinal cord. Consequently, a longer spinal ischemic time was employed and only hematoxylin-eosin staining was used for histopathologic evaluation. As suggested by AK, motor neurons that appear intact on hematoxylin and eosin staining as a result of the prophylactic administration of edaravone might suffer delayed apoptosis-related injury. Because we did not use any marker for apoptosis in our study, we are not in a position to comment on this. However, we agree with Dr AK that further studies need to be undertaken to clarify this issue. We are indeed planning to embark on a protocol that involves the use of markers of apoptosis in a model of shorter spinal ischemic time and longer duration of observation.

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1. 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]
   
2. Suzuki K, Kazui T, Terada H, Umemura K, Ikeda Y, Bashar AHM, 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]
   

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Teruhisa Kazui Abul Hasan Muhammad Bashar Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Suzuki, K. Articles by Bashar, A. H. M. Search for Related Content PubMed Articles by Suzuki, K. Articles by Bashar, A. H. M. Related Collections Related Article