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[酸碱平衡与大脑]

[Acid-base equilibrium and the brain].

作者信息

Rabary O, Boussofara M, Grimaud D

机构信息

Département d'Anesthésia-Réanimation, Hôpital Saint-Roch, Nice.

出版信息

Ann Fr Anesth Reanim. 1994;13(1):111-22. doi: 10.1016/s0750-7658(94)80194-0.

Abstract

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of hypocapnia and to avoid any deleterious effect. If hypocapnia is maintained over several days, an adaptation of CSF pH may limit the therapeutic effect on the cerebral blood flow and the intracranial pressure.

摘要

在生理条件下,大脑中的酸碱平衡调节可维持脑内pH值显著的稳定性。在全身性代谢性酸碱失衡期间,脑内pH值得到良好控制,因为血脑屏障对电解质(HCO3-和H+)的通透性缓慢且较差。脑内pH值通过呼吸驱动的调节来维持,这是由靠近延髓化学感受器的间质液pH值早期变化引发的。由于血脑屏障对CO2具有高通透性,即使在严重代谢性酸中毒和碱中毒的情况下,脑脊液pH值也能在数小时内得到纠正。相反,在通气性酸中毒和碱中毒期间,脑内pH值的变化方向和幅度与血液pH值相同。因此,相较于通气性酸碱失衡,大脑对代谢性酸碱失衡的耐受性更好。通气性酸中毒和碱中毒能够通过间质pH值的改变损害脑血流量和脑活动。在呼吸性酸中毒期间,细胞外液中的[HCO3-]会增加,通过两种主要方式来控制脑内pH值:一是在血脑屏障和血脑脊液屏障水平激活碳酸酐酶,二是胶质细胞中氯离子转运增加(HCO3-与Cl-交换)。在呼吸性碱中毒期间,细胞外液中的[HCO3-]会通过HCO3-转运的相反变化以及脑细胞乳酸合成增加而降低。用碳酸氢盐治疗代谢性酸中毒可能会在酮症酸中毒期间诱发脑内酸中毒并加重脑水肿。为治疗颅内高压而进行的适度低碳酸血症主要在脑血流量高且血管CO2反应性维持时有效。低碳酸血症可能会恢复改变的脑血流量自动调节功能。人为造成的低碳酸血症需要控制脑灌注压和脑动静脉氧差,以选择可能从这种治疗中获益的患者,选择最佳的低碳酸血症水平并避免任何有害影响。如果低碳酸血症持续数天,脑脊液pH值的适应性变化可能会限制对脑血流量和颅内压的治疗效果。

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