Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats.
Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats.
复制标题
实验性猫脑积水。
作者：
K. Shapiro;F. Takei;A. Fried;I. Kohn
在高岭土诱导的猫脑积水的颅骨-硬脑膜切除模型中，使用推注操作脑脊液（CSF）的压力-容积指数（PVI）技术来研究与脑积水相关的生物力学变化。在脑积水猫和时间匹配的对照猫中，在急性和3至5周后测定稳态颅内压（ICP）、PVI和对CSF吸收的抵抗力。脑积水猫的稳态ICP为11.0 +/- 2.1 mmHg（+/-标准差），而慢性对照组为10.8 +/- 2.2 mmHg（p> 0.1）。慢性脑积水组和慢性对照组的ICP均显著高于（p <0.001）急性硬脑膜切除术后（平均ICP 8.5 +/- 1.2 mm Hg）。硬膜开放后即刻，平均PVI为3.6 ± 0.2 ml（平均值的±标准误）;随着时间的推移，慢性对照组的PVI降至1.3 ± 0.1 ml（p <0.001），但脑积水组的PVI仍升高至3.5 ± 0.4 ml（p <0.001）。硬脑膜打开后即刻的CSF吸收阻力为9.1 +/- 1.4 mm Hg/ml/min，脑积水猫增加至28.8 +/- 4.5 mm Hg/ml/min（p <0.001）;在对照猫的慢性测量中，其进一步增加至82.3 +/- 9.2 mm Hg/ml/min（p <0.001）。所有脑积水猫的脑室大小为中度至重度扩大，对照组正常。这些结果表明，高岭土诱导的猫脑积水的改变脑容器模型的生物力学概况类似于脑积水婴儿中所描述的。如对照组所示，单纯吸收缺陷不足以引起进行性心室扩大。容量缓冲能力的增加与CSF吸收阻力的适度增加相结合，促进了脑室中的容量储存。
In a craniectomy-durectomy model of kaolin-induced feline hydrocephalus, the pressure-volume index (PVI) technique of bolus manipulations of cerebrospinal fluid (CSF) was used to study the biomechanical changes associated with hydrocephalus. Steady-state intracranial pressure (ICP), PVI, and the resistance to the absorption of CSF were determined acutely and 3 to 5 weeks later in hydrocephalic cats and time-matched control cats. Steady-state ICP was 11.0 +/- 2.1 mm Hg (+/- standard deviation) in the hydrocephalic cats, compared to 10.8 +/- 2.2 mm Hg in the chronic control group (p greater than 0.1). The ICP in both the chronic hydrocephalic and chronic control groups was significantly higher (p less than 0.001) than after acute durectomy (mean ICP 8.5 +/- 1.2 mm Hg). Immediately after dural opening, the mean PVI was 3.6 +/- 0.2 ml (+/- standard error of the mean); over time, it decreased to 1.3 +/- 0.1 ml in the chronic control group (p less than 0.001), but remained elevated in the hydrocephalic group at 3.5 +/- 0.4 ml (p less than 0.001). Resistance to CSF absorption was 9.1 +/- 1.4 mm Hg/ml/min immediately after dural opening and increased to 28.8 +/- 4.5 mm Hg/ml/min (p less than 0.001) in the hydrocephalic cats; it increased even further in the chronic measurements in control cats, to 82.3 +/- 9.2 mm Hg/ml/min (p less than 0.001). Ventricular size was moderate to severely enlarged in all hydrocephalic cats, and normal in the control group. These results indicate that the biomechanical profile of the altered brain container model of kaolin-induced feline hydrocephalus resembles that described in hydrocephalic infants. As shown in the control subjects, an absorptive defect alone is not sufficient to cause progressive ventricular enlargement. Increased volume-buffering capacity coupled with a moderate increase of CSF absorption resistance facilitates volume storage in the ventricles.