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Ann Thorac Surg 2000;70:336-337
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, Kitakyushu-City, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa, Japan
To the Editor
Kadoi and associates are to be congratulated for the paper "Effects of hypothermic and normothermic cardiopulmonary bypass on brain oxygenation" [1] corroborating clinically the use of NIRS to assess cerebral oxygenation, which we do not doubt, but needs fractionated analysis.
Although the mixed rSO2 might be an adequate monitor during normothermic bypass, only the redox state of cytochrome a,a3 reflects adequacy of brain oxygenation during hypothermia. At the risk of becoming repetitive, because a related letter to the editor is in press, for the benefit of the authors, the following could be pointed out.
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 NIRS might continue to sense the oxyhemoglobin resulting in spuriously high rSO2 values, in the face of actual tissue hypoxia (Bohr effect), a phenomenon that becomes more pronounced as the temperature decreases. Nollert and associates found the percent of oxyhemoglobin to increase as temperature decreased, but with evidence of increasing hypoxia as indicated by the redox state of cytochrome a,a3 [2].
Tseng and associates described release of glutamate during the early phases of hypothermia by alpha-stat perfusion well before circulatory arrest induction [3], which we attribute to the Bohr effect.
Hypoxia is known to induce activation of N-methyl D-aspartate (NMDA) receptors or excitotoxicity [4] and eventually nitric oxide generation, both of which may cause neuronal injury.
Alkalosis by promoting Ca2+ influx exacerbates excitotoxicity, sensitizes neurons to ischemic injury, and potentiates reperfusion injury [5] that would occurr at cardiopulmonary bypass discontinuation if a state of underperfusion relative to oxygen requirements had been prevalent during perfusion. In contrast, mild acidosis decreases Ca2+ influx, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury [4, 6] by reducing NMDA receptor activation.
The unchanged rSO2 in their hypothermic group is a manifestation of the spuriously high oxyhemoglobin content, but by no means reflects adequate brain oxygenation, unless the redox state of cytochrome a,a3 is analyzed.
Paradoxically, the authors found the rSO2 and SjvO2 to decrease 20 minutes into normothermic cardiopulmonary bypass, for which a reasonable explanation was not offered. A similar finding is described in Kawahara and associates’ study in dogs. The implications and possible mechanisms are discussed in detail in a letter to the editor addressed to Kawahara from the same institution, but succinctly, we believe it is a manifestation of dominance of the increased O2 needs of the brain, secondary to increased catecholamines during cardiopulmonary bypass that could not be met by the prevailing pressure-flow autoregulatory mechanisms, ie, the pressures used (68 mm Hg) turned out not to be sufficient to maintain a normal SjvO2 or rSO2 for which a pressure greater than 73 mm Hg was required. Thus, this finding questions the validity of the widely accepted concept that normal autoregulation mechanisms would be operating at pressures of 50 mm Hg to meet brain oxygen requirements during cardiopulmonary bypass.
References
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