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Ann Thorac Surg 2002;73:1360
© 2002 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku, Kitakyushu-shi, Fukuoka, 802-8555, Japan
b II Department of Physiology The University of the Ryukyus School of Medicine Okinawa, Japan 903-0215
e-mail: tkmiyamo{at}f3.dion.ne.jp
To the Editor
We congratulate Gangemi and associates [1] on their study of retrograde perfusion with phenytoin to provide ischemic spinal cord protection. Despite the protection achieved, no animal recovered fully from 45 minutes of ischemia. Had a shorter period of ischemia been studied instead of or in addition to normothermic systemic infusion of phenytoin, extrapolation of the ischemic time all animals could be protected, which is the information surgeons want, might theoretically have been possible.
There are two fundamental methodological flaws. First, phenytoin delivered retrograde may reach an ischemic spinal cord after aortic clamping, but systemic phenytoin must be allowed enough time to cross the blood-brain barrier before induction of ischemia. Second, in our opinion, spinal cord temperature measurements, like those of the brain, are absolutely necessary to properly evaluate methods of protection. For anatomico-physiological reasons, neither esophageal temperatures nor rectal temperatures reflect real-time spinal cord temperature changes during regional antegrade or retrograde perfusion.
Retrograde regional perfusion of saline or phenytoin solution (22°C) (0.8 mL · kg-1 · min-1 for 45 minutes) to the spinal cord deprived of antegrade blood flow must decrease the temperature more than 0.5°C. This is enough to separate animals that are protected from those that are not [2, 3] and partially explains the protection provided by saline solution.
To conclude that retrograde phenytoin (Na+-channel blockade with some degree of hypothermia) is protective but systemic phenytoin (NA+-channel blockade at normothermia) is not is like stating that apples are not oranges. To properly compare the two methods, two options are available: to match the esophageal or spinal cord temperature of the systemic phenytoin group to the spinal cord temperature of the retrograde phenytoin group or to dilute the phenytoin in the retrograde group with saline solution warmer than 38°C (normal rabbit rectal temperature is close to 39°C, not 22°C). Properly administered systemic phenytoin in properly cooled animals might have provided equal protection.
We [2, 3] used a similar ischemic model and surface-induced hypothermia with eucapnic ventilation (expiratory [CO2] of 5% at all temperatures) to produce an arterial carbon dioxide tension of 50 to 55 mm Hg, pH 7.23, and an arterial oxygen tension of 230 to 260 mm Hg before aortic cross-clamping. This is equivalent to pH-stat perfusion management. Before aortic clamping, esophageal temperature but not rectal temperature correlated with spinal cord temperature, and all rabbits regained complete function within 5.5 hours of reperfusion after 60 minutes of ischemia at 29.4°C; at 29.9°C, none recovered. Assuming a straight regression line between 38.3°C and 29.5°C, pH-stat hypothermia alone at 31.6°C could consistently protect the spinal cord for 45 minutes of ischemia.
Taurine, a well-known antioxidant-protective ß-amino acid [4–6], given intravenously 20 to 30 minutes before ischemia, enhances the protective effects of pH-stat hypothermia by preventing hypoxia during cooling and reperfusion injury during rewarming just as nature has done for millions of years [4]. Sixty minutes of protection against spinal cord ischemia was consistently achieved at esophageal temperatures 1.2°C higher (ie, at 30.6°C) compared with protection using hypothermia alone in rabbits [3]. Taurine may be an effective ingredient to which other drugs could be added to provide an optimal protection strategy for the central nervous system.
References
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