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Ann Thorac Surg 2000;70:690
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, 1-1 Kufune-cho, Kokura-kitaku, Kitakyushi-shi, Fukuoka 802-8555, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa 903-0215, Japan
To the Editor
Watanabe and colleagues [1] are to be congratulated for their recent article "Optimal Blood Flow for Cooled Brain at 20°C." However, there are some flaws in their methodology. First, there was no normothermic control group. Second, how were 60-minute data obtained? The methodology required that the brain be sliced, but perfusion at 20° was supposedly maintained for 120 minutes.
The arterial carbon dioxide tension of 52.6 ± 9.9 mm Hg that they used is barely enough hypercarbia for 29°C to 30°C. Therefore, basically their management was alpha-stat below that temperature range.
Given the normal intracellular pH of 7.3, the described baseline intracellular pH of 7.2 was already abnormal. It is attributable to the hypoxic (Bohr effect) metabolic derangement occurring during induction of alpha-stat hypothermia. Experiments involving deep hypothermic circulatory arrest suggest that well before the establishment of arrest, the development of hypoxia is evident by near-infrared spectroscopy (redox state of cytochrome a,a3) [2] or by glutamate release and activation of N-methyl-D-aspartate (NMDA) receptors with nitric oxide generation [3]. Deprivation of oxygen (O2) or glucose leads to release of glutamate and activation of NMDA receptors [4] and thereby causes Na+ and Ca2+ influx.
Dissolved O2, which is pH independent, explains the maintenance of a cerebral cortex intracellular pH greater than 7.2, though abnormal without further deterioration, for 2 hours at a stable temperature of 20°C. Dissolved O2, however, cannot supply the increasing needs of rewarming or decrease NMDA receptor activation.
Using data from rewarmed patients undergoing aortic arch operations, Higami and associates [5] calculated a safe time limit of 70 minutes for antegrade, selective cerebral perfusion at 16° to 20°C. Their time was considerably shorter than the 120 minutes used by Watanabe and coauthors, it was assumed it would be followed by normal recovery after rewarming. However, that was not tested.
The alpha-stat alkalosis during rewarming promotes Ca2+ influx, and this exacerbates hypoxic/ischemic injury. On the other hand, mild acidosis reduces NMDA receptor activation, thus decreasing Na+ and Ca2+ influx, glutamate neurotoxicity, and neuronal injury caused by oxygen or glucose deprivation [6].
Failure to utilize glucose occurs after rewarming after 60 minutes of 20°C alpha-stat hypothermic perfusion at a mean blood pressure of 60 mm Hg without circulatory arrest.
Theoretically dissolved O2 in plasma starts to play an important role as an O2 source in the brain at temperatures lower than 18°C. However, it is mainly hemoglobin and therefore pH dependent at temperatures higher than 20°C. Patient temperatures do not fall from 38°C to 20°C or rise from 20°C to 38°C instantaneously. Oxygen availability during cooling and rewarming is as important as that during a stable temperature of 20°C, and this was the only facet studied.
Preservation of cerebral blood flow and metabolism to 27°C without an increase in embolic capillary occlusion by pH-stat strategies has been proved. Nature has coped with hypoxia effectively for millions of years by using the O2-carrying capacity of hemoglobin, which is far greater than that of plasma, by eucapnic ventilation (hypercarbic acidosis, which is equivalent to pH-stat management) [7]. This prevents the Bohr effect from occurring and allows full realization of the protective effects of hypothermia other than metabolic suppression, namely, inhibition of excitatory amino acid release and hyperpolarization secondary to increase of Na+ efflux. The increased O2 availability of pH-stat hypothermic strategies may thus allow perfusion at even lower blood pressures and flows than alpha-stat management and actually decrease the chances of microembolization.
References
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