| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 1999;117:406-408
© 1999 Mosby, Inc.
LETTERS TO THE EDITOR |
We read with great interest the article titled "Profound Systemic Hypothermia Inhibits the Release of Neurotransmitter Amino Acids in Spinal Cord Ischemia" by Rokkas and associates (J Thorac Cardiovasc Surg 1995;110:27-35). Although considerable information is provided, we believe it needs to be placed in the proper perspective to lead to a correct interpretation. It is unfortunate that only 2 sham animals were operated on for each experimental group (that would preclude using that information for any statistical analysis), and the data are not reported but merely mentioned in the text: "The control sham animals demonstrated stable baseline values of amino acid concentrations for at least 150 minutes. The hypothermia sham animals (hypothermia without aortic crossclamping) exhibited time-course changes in dialysate amino acid levels that were indistinguishable from the changes observed in group 2 animals (hypothermia and aortic crossclamping)." Although the general time course might have had the same trend, the values must have been different. If they were not different, that knowledge would have been helpful and informative for the readership. Had the data been reported, we believe differences would have been noticed between the clamped (group 2) and the sham (nonclamped) hypothermic animals. It is also unfortunate that the main thrust was to compare group 1 (normothermic ischemia) and group 2 (hypothermic ischemia), with less weight given to comparison against their own baselines. The baseline measurements for group 2 were taken only before cooling, which we think is inadequate unless enough sham group data are provided to assess the effects of hypothermia per se. Had enough consideration to comparison against their baselines been given, some obvious differences would have been noticed that might have helped in the proper interpretation of the data shown in Table I.
Perhaps the most important information in this article concerned the significant differences in adenosine concentrations between groups 1 and 2 during the ischemic period. However, because attention was focused on the excitatory amino acid (glutamate), the adenosine data were not properly discussed. Although Table I appears to show that the differences from the baseline values were not significant, our analysis proved otherwise. Adenosine increased more than 4-fold during normothermic ischemia, which is anticipated and in agreement with reported facts in normothermic ischemia, but it was significantly lower in the hypothermic group during ischemia, as well as during each of the reperfusion times. With such an increase in adenosine in the normothermic group, an increase in taurine is expected, because adenosine releases taurine.
1-3 Because only the baseline data for hypothermic conditions are supplied (ie, just before clamping in group 2) and because the sham group was not large enough to supply sufficient data, adequate comparison is not possible. Hypothermia will decrease the rate of all processes, taurine release included, and it would be improper to make comparisons against the baseline values measured under normothermic conditions. However, disregarding the effect of hypothermia per se on the release of the various amino acids, adenosine levels in group 2 are significantly lower than the normothermic baseline, low enough to explain at least partially why the taurine concentrations were also lower than the normothermic baseline value. The decreased adenosine and glutamate levels in group 2 during ischemia might indeed represent the protective effect of hypothermia, which prevented the degradation of adenosine triphosphate to adenosine and the ischemia-induced depolarization with its concomitant release of glutamate. It can be speculated that glutamate, 
-aminobutyric acid, and taurine metabolic production during hypothermia were decreased. Apparently taurine is a co-product formed during adenosine triphosphate degradation, which involves interaction with the homocysteine-methionine cycle producing taurine as an end co-product from decarboxylation of cysteic acid. 4,5
On the basis of the mentioned considerations, and although the authors state "the role of taurine in the spinal cord is not clear but it does not appear that taurine plays any significant role in modulating the ischemic injury," the findings of the study do not substantiate that assertion. Furthermore, the study was not designed to prove or disprove the protective effects of taurine. In their study taurine was never administered to evaluate its effects. The release of taurine is part of the natural defensive mechanism set in motion when excess adenosine is formed, such as in ischemia or trauma to any area of the central nervous system, 6,7 spinal cord included. The fact that taurine levels were found to be low does not indicate that taurine does not have a protective role. What is actually indicating is that the concomitantly used protective strategy (in this case profound levels of hypothermia) was effective in preventing the activation of mechanisms that release taurine. We even hypothesize that the levels of taurine could actually be used as an indicator of whether protection was achieved when using protective strategies not involving taurine administration. In fact, our recent experimental studies in rabbits have shown that exogenous taurine enhances the protective effects of hypothermia and confers significant protection in animals with spinal cord normothermic ischemia as well.
If the temporal course of -aminobutyric acid and glutamate in the post-rewarming phase of a large enough sham group of hypothermic animals is similar to that of group 2, the effect of hypothermia is not limited to the release of glutamate during the ischemic period only. Since it is known that mild or moderate degrees of hypothermia are effective in decreasing the release of glutamate during ischemia, it would be of interest to see whether such late effects are also observed with mild or moderate degrees of hypothermia rather than profound hypothermia.
Tadaomi-A. Miyamoto, MD
Research DepartmentKokura Memorial HospitalKitakyushu, Japan
Koho-J. Miyamoto, MD, PhD
Assistant Professor
II Department of Physiology
University of Ryukius
School of Medicine
Okinawa, Japan
12/8/95024
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
