Jones H C, Andersohn R W
Department of Pharmacology and Therapeutics, University of Florida, Gainesville 32610, USA.
Exp Neurol. 1998 Nov;154(1):126-36. doi: 10.1006/exnr.1998.6934.
Infantile hydrocephalus causes injury to the developing brain and despite surgical treatment, neurological deficits persist. The H-Tx rat develops inherited hydrocephalus in late gestation. Rapid postnatal ventricular enlargement, results in severe hydrocephalus by 21 days after birth. This is accompanied by changes in cortical morphology and metabolite content that indicate possible changes in intracellular composition. This study has tested the hypothesis that tissue water and electrolyte content is altered in hydrocephalus. The objective was to gain further insight into the mechanisms leading to neuronal damage. Water and electrolyte content (Na+, Cl-, and K+) were measured in the cerebral cortex of control and hydrocephalic rats at 4, 11, and 21 days after birth, and at 21 days in rats that received alleviating shunt surgery at 4 or 11 days. At all ages, hydrocephalic tissue was significantly increased over control for cortical water, Na+, and Cl- content. Additionally, at the intermediate (11-day) and advanced (21-day) stages there were significant decreases in K+ content, consistent with previous observations of decreases in organic osmolytes and energy metabolites. This suggests that by 11 days there are intracellular changes, probably through impaired membrane homeostatic mechanisms. In shunt-treated rats, the extracellular constituents were almost normal, although a small increase over control values persisted. The decrease in intracellular K+ was not corrected in either group of shunt-treated rats. It is concluded that early hydrocephalus is characterized by extracellular edema that largely reverses with shunt treatment. Subsequently, as the hydrocephalus progresses, there is a breakdown of cell homeostasis and an irreversible loss of intracellular constituents.
婴儿脑积水会对发育中的大脑造成损伤，尽管进行了手术治疗，但神经功能缺损仍然存在。H-Tx大鼠在妊娠后期会发生遗传性脑积水。出生后脑室迅速扩大，到出生后21天会导致严重脑积水。这伴随着皮质形态和代谢物含量的变化，表明细胞内成分可能发生了改变。本研究检验了脑积水时组织水和电解质含量会发生改变这一假说。目的是进一步深入了解导致神经元损伤的机制。在出生后4天、11天和21天，以及在4天或11天接受缓解性分流手术的大鼠在21天时，测量对照大鼠和脑积水大鼠大脑皮质中的水和电解质含量（Na+、Cl-和K+）。在所有年龄段，脑积水组织的皮质水、Na+和Cl-含量均显著高于对照。此外，在中期（11天）和晚期（21天）阶段，K+含量显著降低，这与之前观察到的有机渗透质和能量代谢物减少一致。这表明到11天时存在细胞内变化，可能是通过受损的膜稳态机制。在分流治疗的大鼠中，细胞外成分几乎正常，尽管仍比对照值略有增加。两组分流治疗的大鼠细胞内K+的降低均未得到纠正。结论是早期脑积水的特征是细胞外水肿，分流治疗后大部分可逆转。随后，随着脑积水的进展，细胞内稳态被破坏，细胞内成分发生不可逆的丢失。
