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低钠血症时脑细胞体积调节:性别、年龄、血管加压素及缺氧的作用

Brain cell volume regulation in hyponatremia: role of sex, age, vasopressin, and hypoxia.

作者信息

Ayus Juan Carlos, Achinger Steven G, Arieff Allen

机构信息

Renal Consultants of Houston, 2412 Westgate Street, Houston, TX 77019, USA.

出版信息

Am J Physiol Renal Physiol. 2008 Sep;295(3):F619-24. doi: 10.1152/ajprenal.00502.2007. Epub 2008 Apr 30.

DOI:10.1152/ajprenal.00502.2007
PMID:18448591
Abstract

Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors--discrepancy between skull size and brain size--are important in the genesis of brain damage. In adults, certain hormones--estrogen and vasopressin (usually elevated in cases of hyponatremia)--have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na(+)-K(+)-ATPase system to extrude cellular Na(+). In menstruant women, estrogen + vasopressin inhibits the Na(+)-K(+)-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po(2) and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones.

摘要

低钠血症是住院患者中最常见的电解质异常。出现症状时(低钠性脑病),总体发病率为34%。最易发生死亡或永久性脑损伤的人群是青春期前儿童和月经期女性。大脑无法适应低钠血症会导致脑损伤。可损害大脑适应能力的主要因素包括缺氧和肽类激素。在儿童中,身体因素——颅骨大小与脑大小的差异——在脑损伤的发生中起重要作用。在成年人中,某些激素——雌激素和血管加压素(在低钠血症病例中通常升高)——已被证明会损害大脑适应能力,降低脑血流量和氧利用率。最初,低钠血症会导致水流入大脑,主要通过神经胶质细胞,并且很大程度上是通过水通道蛋白(AQP)4。水因此被分流到星形胶质细胞中,星形胶质细胞肿胀,很大程度上保持神经元细胞体积。大脑对肿胀的初始反应是适应,利用钠钾ATP酶系统排出细胞内的钠离子。在月经期女性中,雌激素 + 血管加压素会抑制钠钾ATP酶系统并降低脑氧利用率,损害大脑适应能力。脑水肿会压迫呼吸中枢,还会迫使血液流出大脑,既降低动脉血氧分压又降低氧利用率。低氧血症会进一步损害大脑适应能力。当大脑适应能力受损时,低钠性脑病会导致脑损伤,这是脑缺氧和肽类激素共同作用的结果。

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