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J Thorac Cardiovasc Surg 2002;124:1055-1056
© 2002 The American Association for Thoracic Surgery

Letters to the Editor

Reply

Department of Cardiovascular Surgery, Tohoku University Hospital, Sendai-City, Japan

Reply to the Editor:

We read with interest the letter by Miyamoto and Miyamoto concerning our article about the method of establishment of local spinal cord cooling and interpretation of heat shock protein (Hsp) induction. The authors proposed that as much as 2°C might be inappropriate for investigation of the hypothermic effect on brain ischemia. Some reports have shown the importance of strict management of temperature. ¹ However, we were satisfied in our early period with the utility of this model, in which a cold pack was attached to the lumbar region of the animals, because we had aimed to establish a simple, local cooling model against spinal cord ischemia. Preliminary study had provided us the spinal cord temperature, which was significantly lower than those of two other sites (rectal and esophageal [the latter data were not shown]), which meant regional hypothermia was established. ² Other types of local cooling in animal models have been reported, but few series of studies have been performed. One reason may be that those previous models are complicated to reproduce. We may need to apply a few tips for the establishment of a refined model in which the temperature of the spinal cord can be managed minutely. We did not report preischemic or postischemic hypothermia in this study; therefore, that type of research might be expected.

The authors also insisted that spinal cord ischemia for 15 minutes would not occur under an esophageal temperature of 35.8°C. Inappropriate comparison of spinal cord temperatures using different models should not be performed because the ischemic effect depends on small differences in temperature. ¹ Many investigations of brain ischemia have informed us that no absolute critical temperature has been identified that could avoid an ischemic insult through all ischemic models. We could not find any comments in the previous reports that ambient preischemic hypothermia could preserve high-energyP to support continuous Hsp synthesis in spinal cord motor neurons, as Miyamoto and Miyamoto explained. Furthermore, our study provided the effect of intraischemic hypothermia, not preischemic hypothermia.

Miyamoto and Miyamoto also commented that apoptosis and necrosis are continuum reactions unrelated to Hsp synthesis. There have been some reports describing the relations between apoptosis/necrosis and Hsp induction. ^3,4 Some kinds of Hsp families have been reported to inhibit apoptosis/necrosis. ⁵ Less than 10 minutes of ischemia was reported to result in Hsp induction. One study reported that neuronal ischemia for even 6 minutes was enough to promote Hsp induction. ⁶ Ten minutes of normothermic spinal cord ischemia also induced sustained Hsp72 synthesis, which resembled 15 minutes of ischemia under mild hypothermia using the same transient ischemic model. ⁷ The 10 minutes of ischemia did not cause neuronal damage; moreover, this ischemic period seemed to protect against the following ischemic insult, known as preconditioning. There should be a topical correlation with Hsp induction and neuronal damage that might lead to cell death.

The rewarming condition, which was thought to be constant in our animals, was not considered in our report. Rewarming conditions have not been studied in most investigations of neuronal ischemia. However, it would be interesting to research whether various rewarming durations would alter the degrees of spinal cord ischemic insult in our model, as Miyamoto and Miyamoto have already suggested.

References

1. Busto R, Dietrich WD, Globus MY, Valdes I, Scheinberg P, Ginsberg MD. Small differences in intraischemic temperature critically determine the extent of ischemic neuronal injury. J Cereb Blood Flow Metab. 1987;7:729-38.[Medline]
   
2. Motoyoshi N, Sakurai M, Hayashi T, Aoki K, Itoyama Y, Tabayashi K. Establishment of a local cooling model against spinal cord ischemia representing prolonged induction of heat shock protein. J Thorac Cardiovasc Surg. 2001;122:351-7.[Abstract/Free Full Text]
   
3. Fehrenbach E, Northoff H. Free radicals, exercise, apoptosis, and heat shock proteins. Exerc Immunol Rev. 2001;7:66-89.[Medline]
   
4. Hasegawa K, Litt L, Espanol MT, Sharp FR, Chan PH. Expression of c-fos and hsp 70 mRNA in neonatal rat cerebro slices during NMDA-induced necrosis and apoptosis. Brain Res. 1998;785:262-78.[Medline]
   
5. Sheth K, De A, Nolan B, Friel J, Duffy A, Ricciardi R, et al. Heat shock protein 27 inhibits apoptosis in human neutrophils. J Surg Res. 2001;99:129-33.[Medline]
   
6. Yagita Y, Kitagawa K, Ohtsuki T, Tanaka 5, Hon M, Matsumoto M. Induction of the HSP 110/105 family in the rat hippocampus in cerebral ischemia and ischemic tolerance. J Cereb Blood Flow Metab. 2001;21:811-9.[Medline]
   
7. Sakurai M, Hayashi T, Abe K, Aoki M, Sadahiro M, Tabayashi K. Enhancement of heat shock protein expression after transient ischemia in the preconditioned spinal cord of rabbits. J Vasc Surg. 1998;27:720-5.[Medline]
   

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): Koichi Tabayashi Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Motoyoshi, N. Articles by Tabayashi, K. Search for Related Content PubMed Articles by Motoyoshi, N. Articles by Tabayashi, K.