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Ann Thorac Surg 2000;69:1988-1989
© 2000 The Society of Thoracic Surgeons
a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia Health Sciences Center, Box 181-95, Charlottesville, VA 22908, USA
e-mail: cgt2e{at}virginia.edu
To the Editor
Our manuscript describing the use of retrograde venous perfusion to protect the spinal cord during periods of surgically induced ischemia [1] has prompted a great deal of discussion, as evidenced by Dr Miyamoto’s letter. We are happy to address the concerns that he raises.
In his first comment, Dr Miyamoto makes the point that the use of ketamine as an anesthetic agent may have provided some degree of neuroprotection beyond that which we ascribed to the hypothermia and adenosine perfusion. That may or may not have been the case, as there are conflicting data in the literature regarding the effects of ketamine on the ischemic CNS [2]. Even if ketamine did provide some degree of protection, this would not alter our conclusions, as the same dose of ketamine was given to all animals in all groups.
In his second point, Dr Miyamoto correctly indicates that we did not collect spinal fluid temperature data in our animals. However, we did report the rectal temperatures of animals after the procedure in Table 2 of the manuscript [1]. He suggests that our results might have been different had our animals been maintained at a higher temperature. This may be true, but as our data show, there was no significant difference between the rectal temperatures of the animals in the four groups (p = 0.86). The magnitude of temperature change was a constant among all four groups, yet the control group emerged as nearly completely paraplegic while the best experimental group was near normal. Decreased body temperature does not seem to have been protective.
Doctor Miyamoto also correctly points out that in our best group, Tarlov scores did not return to normal. We did not present these data in an effort to precisely define the ultimate protection technique. Rather, we intended to demonstrate that this technique, retrograde venous perfusion, was effective. Clearly, there is more work to be done in this model, and in any case, perfection in a rabbit model may not mean much. Large animal work, in models more analogous to human anatomy and physiology, is necessary.
Lastly, Dr Miyamoto suggests that adenosine-induced taurine release may have played a protective role. This is certainly possible, although we have no evidence to support this conclusion in this experiment. As was the case with ketamine, there are conflicting data regarding the relationship of adenosine to taurine release [3, 4]. Furthermore, there are other reports suggesting that in the spinal cord, under hypothermic conditions, no neurotransmitters are released into the extracellular space [5]. Thus, the role of adenosine-stimulated taurine release is difficult to assess in this model.
We appreciate Dr Miyamoto’s interest in our manuscript, and the opportunity to respond to his comments.
References
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