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J Thorac Cardiovasc Surg 1999;117:1039
© 1999 Mosby, Inc.


LETTERS TO THE EDITOR

Reply

Masahiro Sakurai, MD, Takeshi Hayashi, MD

Tohoku University School of Medicine
Sendai, Japan

Koji Abe, MD, PhD

Okayama University School of Medicine
Okayama, Japan

Mitsuaki Sadahiro, MD, PhD, Koichi Tabayashi, MD, PhD

Tohoku University School of Medicine
Sendai, Japan

Reply to the Editor:

In our model, systemic proximal aortic pressure revealed only a trivial and transient change, not a significant change. Hence we believe that the change in proximal pressure has no influence on the spinal cord injury.

In this model spinal temperature was 37°C. Miyamoto and Miyamoto cited a reference that spinal cord temperature was more closely correlated with esophageal temperature. However, the correlation was not in the lumbar region but in the thoracic region, since the esophagus and lumbar region are at different levels. We believe esophageal temperature does not precisely reflect the lumbar spinal cord temperature. Therefore, we measured the temperature of the rectum, which is more proximal to the spinal cord in the lumbar region.

The models described by Miyamoto and Miyamoto are quite invasive. Previous reports describing spinal cord ischemia were made using laparotomyGo Go 1,2; however, the aorta was occluded from 4 hours to 2 days after closure of the abdominal wall (the authors did not administer ketamine during the time the aorta was occluded). Therefore, their spinal ischemia model may not recover after 8 or 9 minutes of ischemia.

The word "apoptosis" describes histologic and biologic features.Go Go 3-6 However, in their letter, Miyamoto and Miyamoto have not described histologic and biologic findings in spinal cord ischemia.

12/8/96847

References

  1. Moore WM, Hollier LY. The influence of severity of spinal cord ischemia in the etiology of delayed-onset paraplegia. Ann Surg 1991;213:427-32. [Medline]
  2. Zivin JA, DeGirolarni U, Hurwitz EL. Spectrum of neurological deficits in experimental CNS ischemia: a quantitative study. Arch Neurol 1982;39:408-12. [Abstract]
  3. Nitatori T, Sato N, Waguri S, Karasawa Y, Araki H, Shibanai K, et al. Delayed neuronal death in the CA1 pyramidal cell layer of the gerbil hippocampus following transient ischemia is apoptosis. J Neurosci 1995;15:1001-11. [Abstract]
  4. Héron A, Pollard H, Dessi F, Moreau J, Lasbennes F, Ben-Ari Y, et al. Regional variability in DNA fragmentation after global ischemia evidenced by combined histological and gel electrophoresis observations in the rat brain. J Neurochem 1993;61:1973-6. [Medline]
  5. Li Y, Chopp M, Yao F, Zaloga C. Temporal profile of in situ DNA fragmentation after transient middle cerebral artery occlusion in the rat. J Cereb Blood Flow Metab 1995;15:389-97. [Medline]
  6. Arends MJ, Wyllie AH. Apoptosis: mechanisms and roles in pathology. Int Rev Exp Pathol 1991;32:223-54. [Medline]




This Article
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