Liang Danny, Bhatta Sergei, Gerzanich Volodymyr, Simard J Marc
Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, Maryland 21201-1595, USA.
Neurosurg Focus. 2007 May 15;22(5):E2. doi: 10.3171/foc.2007.22.5.3.
Cerebral edema is caused by a variety of pathological conditions that affect the brain. It is associated with two separate pathophysiological processes with distinct molecular and physiological antecedents: those related to cytotoxic (cellular) edema of neurons and astrocytes, and those related to transcapillary flux of Na+ and other ions, water, and serum macromolecules. In this review, the authors focus exclusively on the first of these two processes. Cytotoxic edema results from unchecked or uncompensated influx of cations, mainly Na+, through cation channels. The authors review the different cation channels that have been implicated in the formation of cytotoxic edema of astrocytes and neurons in different pathological states. A better understanding of these molecular mechanisms holds the promise of improved treatments of cerebral edema and of the secondary injury produced by this pathological process.
脑水肿由多种影响大脑的病理状况引起。它与两个独立的病理生理过程相关，这两个过程有着不同的分子和生理前因：一个与神经元和星形胶质细胞的细胞毒性（细胞性）水肿有关，另一个与Na⁺及其他离子、水和血清大分子的跨毛细血管通量有关。在本综述中，作者仅关注这两个过程中的第一个。细胞毒性水肿是由于阳离子（主要是Na⁺）通过阳离子通道不受控制或未得到补偿的内流所致。作者综述了在不同病理状态下与星形胶质细胞和神经元细胞毒性水肿形成有关的不同阳离子通道。更好地理解这些分子机制有望改善脑水肿的治疗以及由该病理过程产生的继发性损伤的治疗。
