Anaemia and the brain.
Anaemia and the brain.
复制标题
DOI：
10.1097/00001503-200410000-00003
复制
发表时间：
2004-10-01
期刊：
影响因子：
--
通讯作者：
Hare, Gregory M T
中科院分区：
文献类型：
--
作者：
Hare, Gregory M T
综述目的：本文综述了贫血对大脑的生理和病理生理影响，重点讨论了贫血性脑缺氧导致贫血性脑功能障碍和脑损伤的假说。它还回顾了贫血期间观察到的脑血流量调节增加的证据，这代表了一种代偿性神经保护机制，用于优化脑氧输送，从而保护大脑免受缺氧损伤。最近发现：严重贫血或低红细胞压积与认知功能障碍、脑血管调节受损、神经损伤和死亡率增加有关，这表明大脑易受贫血性损伤的影响。血红蛋白浓度接近35 g/l时，脑组织氧张力降低，提示缺氧可能导致贫血性脑损伤。缺氧脑基因表达增加的证明，包括神经元一氧化氮合酶，可能提供一种更敏感的方法来确定贫血性脑缺氧的最低血红蛋白浓度。在血红蛋白浓度在50 - 60 g/l之间时，测量大鼠大脑皮层神经元一氧化氮合酶信使RNA和蛋白质水平的增加，表明在这些较高的血红蛋白浓度下发生脑缺氧。调节贫血性脑血管舒张和增加脑氧输送（包括一氧化氮）的机制需要进一步阐明，以确定它们在贫血期间保护大脑的作用。摘要：明确贫血性脑损伤的机制将有助于制定针对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尽量减少与贫血有关的发病率和死亡率。
PURPOSE OF REVIEW: 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.RECENT FINDINGS: 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.SUMMARY: 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.