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Ann Thorac Surg 2000;69:1642-1643
© 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 Ryukyus School of Medicine, Okinawa 903-0215, Japan
To the Editor
We congratulate Higami and colleagues [1] on their article, which corroborates clinically the known evidence in animal studies: lack of efficacy of retrograde cerebral perfusion (RCP) in providing adequate oxygenation to the brain.
The alkalosis induced by alpha-stat strategies aggravates the impaired O2 delivery caused by hypothermia. The oxyhemoglobin will pass through the capillaries without unloading the O2 to the brain and the near infrared spectroscopy (NIR) might continue to sense the oxyhemoglobin resulting in spuriously high rSO2, a phenomenon that becomes more pronounced as the temperature decreases in the face of actual tissue hypoxia (Bohr effect), which may explain the time limit observed with continuous antegrade selective cerebral perfusion (SCP).
If RCP does not deliver O2 effectively, it is not different from deep hypothermic circulatory arrest (DHCA). Although the relative roles are not known, the hypoxia secondary to the Bohr effect and the arrest period activate N-methyl D-aspartate (NMDA) receptors [2], which generate nitric oxide (NO) that causes neuronal injury [3].
Alkalosis exacerbates excitotoxicity, sensitizes neurons to ischemic injury, and potentiates reperfusion injury [4], which is the scenario with DHCA using alpha-stat strategies.
Mild acidosis decreases Ca2+ influx, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures [2], as well as hippocampal neurons [5] by reducing NMDA receptor activation. Thus the mild acidosis of pH-stat management should result in less excitotoxicity and decreased NO generation.
Using eucapnic ventilation at all temperatures (equivalent to pH-stat management of cardiopulmonary bypass) the spinal cord in rabbits could be protected consistently from 1 hour of ischemia at 29.5°C induced by surface cooling [6], a significantly higher temperature than the 16° to 20°C used by the authors to protect for 70 minutes. Extrapolating the regression line in our experiments protection from 70 minutes of ischemia could be obtained at esophageal temperature of 28°C, and if the regression line remains straight, at 18° to 20°C, 120 minutes of ischemia could be protected using pH-stat management. Therefore it could be assumed reasonably safely that pH-stat hypothermic SCP without ischemia, for practical purposes, should have no time limitation.
To reliably monitor the adequacy of brain oxygenation by NIR spectroscopy during hypothermic SCP (antegrade or retrograde) the redox state of cytochrome a,a3 must be evaluated. Two issues must be addressed: (1) experimental correlation between the safe time limits of hypothermic ischemia at various temperatures under alpha-stat or pH-stat strategies and the rSO2 measured by NIR, and (2) whether NIR spectroscopy could discern the subtle hypoxia induced by the Bohr effect and metabolic abnormalities induced by hypothermia per se without ischemia under alpha-stat and pH-stat strategies. Two different rSO2 standards with two different time limits according to the pH management might result.
References
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