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J Thorac Cardiovasc Surg 2003;125:1177-1178
© 2003 The American Association for Thoracic Surgery
Letters to the Editor |
Department of Cardiovascular Surgery, Tohoku University Graduate, School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan
To the Editor:
We read with interest the article by Perdrizet and associates
1 titled "Preoperative stress conditioning prevents paralysis after experimental aortic surgery: increased heat shock protein content is associated with ischemic tolerance of the spinal cord." It is already known that induction of heat shock proteins (HSPs) by whole body hyperthermia can reduce ischemia reperfusion injury,
2 and we agree that hyperthermic pretreatment could induce tolerance against a severe spinal cord ischemic insult. However, we have one question. It has not been demonstrated that HSP72 is induced in motor neurons or glial cells. Manzerra and Brown
3 demonstrated that the heat shock response occurred in glial cells, not in motor neurons, of rabbits after administration of a hyperthermia-inducing drug. On the other hand, Xia and coworkers
4 demonstrated that whole-body hyperthermia induced HSP72 in motor neurons of the rat spinal cord. It is possible to speculate that glial cells may be a preferential target for the hyperthermia-inducing drug, or there may be differences in stress responses between rabbit and rat spinal cord. However, our previous reports have demonstrated that preconditioning with 10 minutes of ischemia enhanced and prolonged the HSP72 gene expression and protein levels in motor neurons, sparing the neuronal cells from the subsequent lethal ischemia.
5 Our result revealed that HSP72 messenger RNA and protein were induced as a "molecular chaperon" in motor neurons after ischemia. Therefore authors should demonstrate temporal profiles of HSP72 in histochemical study or in situ hybridization study.
References
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