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首页> 外文期刊>Fluids and Barriers of the CNS >Increased CSF osmolarity reversibly induces hydrocephalus in the normal rat brain
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Increased CSF osmolarity reversibly induces hydrocephalus in the normal rat brain

机译：脑脊液渗透压升高可逆地诱导正常大鼠脑积水

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Background Hydrocephalus is a central nervous system (CNS) disorder characterized by the abnormal accumulation of cerebrospinal fluid (CSF) in cerebral ventricles, resulting in their dilatation and associated brain tissue injury. The pathogenesis of hydrocephalus remains unclear; however, recent reports suggest the possible involvement of abnormal osmotic gradients. Here we explore the kinetics associated with manipulating CSF osmolarity on ventricle volume (VV) in the normal rat brain. Methods CSF was made hyper-osmotic by introducing 10KD dextran into the lateral ventricle, either by acute injection at different concentrations or by chronic infusion at a single concentration. The induction and withdrawal kinetics of dextran infusion on VV were explored in both contexts. Results Acute intraventricular injection of dextran caused a rapid increase in VV which completely reversed within 24 hours. These kinetics are seemingly independent of CSF osmolarity across a range spanning an order of magnitude; however, the magnitude of the transient increase in VV was proportional to CSF osmolarity. By contrast, continuous intraventricular infusion of dextran at a relatively low concentration caused a more gradual increase in VV which was very slow to reverse when infusion was suspended after five days. Conclusion We conclude that hyperosmolar CSF is sufficient to produce a proportional degree of hydrocephalus in the normal rat brain, and that this phenomenon exhibits hysteresis if CSF hyperosmolarity is persistent. Thus pathologically-induced increases in CSF osmolarity may be similarly associated with certain forms of clinical hydrocephalus. An improved understanding of this phenomenon and its kinetics may facilitate the development of novel therapies for the treatment of clinical hydrocephalus.
机译：背景脑积水是一种中枢神经系统（CNS）疾病，其特征是脑室中脑脊液（CSF）异常积聚，导致其扩张和相关的脑组织损伤。脑积水的发病机制仍不清楚。但是，最近的报道表明可能涉及异常的渗透梯度。在这里，我们探索与正常大鼠脑室容积（VV）上控制脑脊液渗透压有关的动力学。方法通过将10KD葡聚糖引入侧脑室，通过不同浓度的急性注射或单一浓度的慢性输注将CSF制成高渗透性。在这两种情况下都探讨了右旋糖酐对VV的诱导和退出动力学。结果急性脑室内注射右旋糖酐导致VV快速升高，并在24小时内完全逆转。这些动力学似乎在跨一个数量级的范围内与CSF渗透压无关。但是，VV瞬时增加的幅度与CSF渗透压成正比。相比之下，连续脑室内以相对较低的浓度输注右旋糖酐会导致VV逐渐增加，当输注五天后中止时，VV的恢复非常缓慢。结论我们得出结论，高渗性CSF足以在正常大鼠脑中产生一定比例的脑积水，并且如果CSF高渗性持续存在，则该现象表现出滞后现象。因此，病理学诱发的脑脊液渗透压升高可能与某些形式的临床脑积水相似。对这种现象及其动力学的更好的理解可以促进用于治疗脑积水的新疗法的发展。

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