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Anaemia and the brain

机译：贫血和大脑

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This article reviews the physiological and pathophysiological effects of anaemia on the brain, focusing on the hypothesis that anaemia-induced cerebral hypoxia contributes to anaemic cerebral dysfunction and injury. It also reviews evidence that the regulated increase in cerebral blood flow observed during anaemia represents a compensatory neuroprotective mechanism invoked to optimize cerebral oxygen delivery, thereby protecting the brain from hypoxic injury.Severe anaemia, or low haematocrit, has been associated with cognitive dysfunction, impaired cerebral vascular regulation, neurological injury, and increased mortality, which suggests that the brain is vulnerable to anaemia-induced injury. Reduced cerebral tissue oxygen tension has been measured directly at haemoglobin concentrations near 35 g/l, suggesting that hypoxia may contribute to anaemic cerebral injury. A demonstration of increased hypoxic cerebral gene expression, including neuronal nitric oxide synthase, may provide a more sensitive means of determining the minimum haemoglobin concentration at which anaemia-induced cerebral hypoxia can be detected. The measurement of increased cerebral cortical neuronal nitric oxide synthase messenger RNA and protein levels in rats, at haemoglobin concentrations between 50 and 60 g/l, suggests that cerebral hypoxia occurred at these higher haemoglobin concentrations. Mechanisms regulating anaemic cerebral vasodilation and increased cerebral oxygen delivery, including nitric oxide, require further elucidation to establish their role in protecting the brain during anaemia.Characterization of mechanisms of anaemia-induced cerebral injury will contribute to the development of optimal therapeutic strategies for anaemic patients. Such strategies would include a clearer definition of transfusion triggers based on physiological endpoints. The overall goal of these efforts would be to minimize morbidity and mortality associated with anaemia.
机译：本文回顾了贫血对大脑的生理和病理生理影响，重点研究了贫血引起的脑缺氧导致贫血性脑功能障碍和损伤的假说。它还审查了证据，表明在贫血期间观察到的脑血流量的调节增加代表一种补偿性神经保护机制，可用于优化脑氧的输送，从而保护大脑免受缺氧损伤的影响。严重贫血或低血细胞比容与认知功能障碍有关脑血管调节，神经系统损伤和死亡率增加，这表明大脑易受贫血性损伤的影响。直接在接近35 g / l的血红蛋白浓度下测量了脑组织氧张力的降低，表明缺氧可能导致贫血性脑损伤。包括神经元一氧化氮合酶在内的缺氧性大脑基因表达增加的证明，可以提供一种更灵敏的方法来确定可以检测到贫血引起的脑缺氧的最小血红蛋白浓度。在50至60 g / l的血红蛋白浓度下对大鼠大脑皮质神经元一氧化氮合酶信使RNA和蛋白质水平升高的测量表明，在这些较高的血红蛋白浓度下发生了脑缺氧。调节贫血性脑血管舒张和增加脑供氧的机制（包括一氧化氮）需要进一步阐明，以确立其在贫血期间保护大脑的作用。贫血性脑损伤机制的特征将有助于贫血患者的最佳治疗策略。这样的策略将包括基于生理终点的更清晰的输血触发定义。这些努力的总体目标是将与贫血相关的发病率和死亡率降至最低。

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