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Ann Thorac Surg 2000;69:1987-1988
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku, Kitakyushu-shi, Fukuoka, 802-8555, Japan
To the Editor
We read with great interest the provocative article titled: "Spinal cord protection during aortic cross-clamping using retrograde venous perfusion" by Parrino and associates [1]. That the perfusate reaches the venules of the spinal cord and might effectively cool the spinal cord is unquestionable, but there are a few flaws or points that are important to keep in mind:
(a) Ketamine is known to have protective effects [2]. Although the protective effects of hypothermia and adenosine are undoubtful, whether the same degree of protection would be afforded in subjects not receiving ketamine is unknown. Studies to assess protective strategies of the central nervous system should be ideally performed in animals anesthetized with volatile gasses at nonprotective concentrations to avoid interpretation problems.
(b) The method claims to be effective in cooling the spinal cord in normothermic subjects without cardiopulmonary bypass, based on radiographic evidence, but no spinal cord temperatures were measured. The rectal temperatures in all groups are far from being normothermic. Rabbits normal temperature ranges from 38°C to 39.5°C, not 34°C. We doubt the same results would be obtained if baseline temperatures of 38°C to 39°C were kept. Presumably, the spinal cord temperatures in their rabbits were in the vicinity of 33°C because rectal temperatures are 0.8°C to 1.5°C higher. We have found the esophageal temperature reflects closely the spinal cord temperature, and differences as small as 0.5°C separated recovering from nonrecovering rabbits from 1 hour of spinal cord ischemia [3, 4].
(c) Although protective effects of adenosine and cold saline were apparent, none of their animals seemed to have recovered to Tarlov 5 score, and because incompletely protected animals might deteriorate later, the method cannot protect reliably 45 minutes of ischemia. In our experience, 100% of the animals’ surface cooled to 29.5°C after eucapnic ventilation (equivalent to pH-stat hypothermic perfusion) recovered completely within 5 to 6 hours of reperfusion after 60 minutes of ischemia [3, 4]. With proper perfusion pH (pCO2) management, profound or deep levels of hypothermia are not required to protect consistently 60 minutes of ischemia. Based on the regression line of our accumulated data between 38.3°C and 29.5°C, 45 minutes could be completely protected at the esophageal temperature of 31.5°C in animals cooled with eucapnic ventilation.
(d) Although the beneficial effects of adenosine were theoretically ascribed mostly to vasodilation, at the dose used, other effects besides vasodilatation must have played an equal or perhaps more important role, specifically that of taurine release [5]. Taurine is well known for its marked protective effects. In fact, when systemically administered to supplement hypothermia, 60 minutes of spinal cord ischemia was consistently protected at esophageal temperature 1.2°C higher (30.6 ± 0.15°C) than rabbits protected with hypothermia alone (29.4 ± 0.15°C), and 0.7°C higher than the rabbits in which hypothermia alone uniformly failed (29.9 ± 0.13°C) [4].
References
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