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Ann Thorac Surg 2000;70:1764-1765
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku,, Kitakyushu-shi, Fukuoka 802-8555, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa, Japan
To the Editor
Ergin and colleagues are to be congratulated for their article [1]. Temporary neurological dysfunction is reminiscent of neurologic dysfunction observed in the early days of cardiac surgery with surface-induced or even cardiopulmonary bypass perfusion-induced hypothermia, and must be unquestionably an entirely different entity from embolic complications.
Anoxic or hypoxic injury, alone or aggravated by the reperfusion injury, must be the basis of temporary neurologic dysfunction. Involvement of the most hypoxia-sensitive brain area, the hippocampus, supports this view. We concur with Reichs reply to our letter to the editor, which appeared in J Thorac Cardiovasc Surg, Sept 1999 [2], concerning the initial portion of this study, that "the older population is different from young patients ... [and] is indeed more vulnerable to hypoxia or ischemia."
This vulnerability makes avoiding deleterious effects of protective strategies that much important. Nollert and associates demonstrated development of hypoxia during the early phases of hypothermia well before the induction of hypothermic circulatory arrest in spite of increased oxyhemoglobin indicative of increased hemoglobin O2 affinity by near infra-red spectroscopy [3]. Prevention of alpha-stat alkalosis and impaired O2 delivery-induced hypoxia (Bohr effect), occurring before the dissolved O2 role becomes relatively more important than that of hemoglobin as the source of O2 to the brain, below 18°C, is a crucial issue. Such hypoxia can be effectively averted by the acidosis of pH-stat strategies.
The increased chances of microembolization of normothermic hypercarbia should not be extrapolated to hypothermic circulatory arrest, which by necessity involves a period of ischemia followed by reperfusion. Flow-metabolism coupling is not disrupted during pH-stat hypothermic perfusion, nor is there evidence of increased embolic capillary occlusion by hypothermic pH-strategies at least down to 27°C [4]. We believe that, unless massive, the deleterious effects of gaseous microembolization, if it occurs, would be transient and relatively harmless if no prior hypoxia had taken place. Proper protective measures must be taken when flow is reestablished following reabsorption to avoid alkalosis-promoted Ca++ influx and too rapid or excessive bypass rewarming. The mild acidosis of pH-stat should also minimize reperfusion injury. Theoretically, microembolization and hyperoxic lipid peroxidation could be minimized by decreasing O2 flow in the oxygenator as discussed in the letter to the editor regarding McCulloughs article [5].
Nature has conferred newborns of all animal species (humans included) the ability to tolerate longer hypoxic periods than adults by providing their central nervous systems with higher contents of taurine [6].
Taurine given systemically enhances the protective effects of hypothermia [7]. Being an amino acid naturally involved with protective mechanisms, it should be effective in the older population as well without untoward effects. We believe the time has come to recognize the wisdom of nature and give pH-stat strategies and taurine a second look. Their concomitant use should maximize other protective strategies including that of memantine [8], riluzole [9], or nitric oxide generation inhibitors and may effectively cancel age as a risk factor for temporary neurological dysfunction after DHCA.
References
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