Ann Thorac Surg 1997;64:1286
© 1997 The Society of Thoracic Surgeons
Discussion
Discussion
See also page 1279.
DR WILLIAM A. BAUMGARTNER (Baltimore, MD): That was a very nice presentation and an excellent model from a group that has been looking at this issue for a long time.
I have two questions. Obviously the program committee put these papers back to back for a reason, and I think they have great similarities. Because you saw a difference in apoptotic cells in different areas of the spinal cord, I would like to know if you have some thoughts as to why there is this distribution.
Doctor Kouchoukos's laboratory in the past has done some work similar to ours looking at this concept of glutamate excitotoxicity, which has one of its founders in your institution. And I wonder if you have done any further work to try to elucidate the mechanism of the cause of necrosis or apoptosis and whether it is similar to what occurs in the brain, mediated by nitric oxide.
DR KANELLOPOULOS: Doctor Baumgartner, thank you very much for your comments. A difference in the distribution of necrotic and apoptotic neurons within the spinal cord gray matter was found in our study. We believe that there are two plausible explanations for the observed distributions of the necrotic neurons and the apoptotic neurons. One is that differences in the severity of the insult sustained by cells may lead to different types of cell death. After proximal aortic occlusion, the degree of reduction in the regional blood flow is probably different between various areas of the gray matter in a given spinal cord segment. This has been shown in a rat spinal cord ischemia model. In addition, anatomic studies in rats and humans have indicated that because of the specific architecture of the spinal cord vascular system, the periphery of the gray matter may receive more collateral blood flow compared with the center during a period of aortic occlusion. Neurons in central areas of the gray matter, such as the intermediate zone and the adjacent dorsal horns, may sustain a more severe ischemic insult, lose their capacity to maintain their homeostasis, swell up, and disintegrate; that is, die by necrosis. Neurons in peripheral areas of the gray matter, such as the head of the dorsal horns, may sustain a less severe ischemic insult that allows them to maintain a certain level of homeostasis. Nevertheless, in some of these neurons the apoptotic cascade may be triggered probably leading to their death.
Alternatively, differences in the phenotype of neurons may preferentially lead to necrosis or to apoptosis after ischemia. In this respect, it is interesting that neurons in the head of the dorsal horn have the highest concentration of glutamate receptors in the plasma membrane. Glutamate receptor activation might therefore be involved in the apoptotic process in ischemic neurons. This idea would be in agreement with the experimental data from your group on the role of glutamate excitotoxicity and oxidative injury in the development of neuronal apoptosis in the brain after deep hypothermic circulatory arrest.
Related Article
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Neuronal Cell Death in the Ischemic Spinal Cord: The Effect of Methylprednisolone
- Georgios K. Kanellopoulos, Hiroyuki Kato, Yingji Wu, Dimitrios Dougenis, Mary Mackey, Chung Y. Hsu, and Nicholas T. Kouchoukos
Ann. Thorac. Surg. 1997 64: 1279-1285.
[Abstract]
[Full Text]
