Klarica M, Oresković D, Bozić B, Vukić M, Butković V, Bulat M
Department of Pharmacology and Croatian Institute for Brain Research, School of Medicine University of Zagreb, Salata 11, Zagreb, HR 10 000, Croatia.
Neuroscience. 2009 Feb 18;158(4):1397-405. doi: 10.1016/j.neuroscience.2008.11.041. Epub 2008 Dec 7.
It is generally assumed that cerebrospinal fluid (CSF) is secreted in the brain ventricles, and so after an acute blockage of the aqueduct of Sylvius an increase in the ventricular CSF pressure and dilation of isolated ventricles may be expected. We have tested this hypothesis in cats. After blocking the aqueduct, we measured the CSF pressure in both isolated ventricles and the cisterna magna, and performed radiographic monitoring of the cross-sectional area of the lateral ventricle. The complete aqueductal blockage was achieved by implanting a plastic cannula into the aqueduct of Sylvius through a small tunnel in the vermis of the cerebellum in the chloralose-anesthetized cats. After the reconstitution of the occipital bone, the CSF pressure was measured in the isolated ventricles via a plastic cannula implanted in the aqueduct of Sylvius and in the cisterna magna via a stainless steel cannula. During the following 2 h, the CSF pressures in the isolated ventricles and cisterna magna were identical to those in control conditions. We also monitored the ventricular cross-sectional area by means of radiography for 2 h after the aqueductal blockage and failed to observe any significant changes. When mock CSF was infused into isolated ventricles to imitate the CSF secretion, the gradient of pressure between the ventricle and cisterna magna developed, and disappeared as soon as the infusion was terminated. However, when mock CSF was infused into the cisterna magna at various rates, the resulting increased subarachnoid CSF pressure was accurately transmitted across the brain parenchyma into the CSF of isolated ventricles. The lack of the increase in the CSF pressure and ventricular dilation during 2 h of aqueductal blockage suggests that aqueductal obstruction by itself does not lead to development of hypertensive acute hydrocephalus in cats.
一般认为脑脊液(CSF)是在脑室中分泌的,因此在中脑导水管急性阻塞后,预计脑室脑脊液压力会升高,孤立的脑室会扩张。我们在猫身上验证了这一假设。阻塞导水管后,我们测量了孤立脑室和小脑延髓池中的脑脊液压力,并对侧脑室的横截面积进行了影像学监测。通过在水合氯醛麻醉的猫的小脑蚓部的一个小通道中将一根塑料套管植入中脑导水管,实现了完全的导水管阻塞。枕骨重建后,通过植入中脑导水管的塑料套管测量孤立脑室中的脑脊液压力,并通过不锈钢套管测量小脑延髓池中的脑脊液压力。在接下来的2小时内,孤立脑室和小脑延髓池中的脑脊液压力与对照条件下的压力相同。我们还在导水管阻塞后通过影像学监测了2小时的脑室横截面积,未观察到任何显著变化。当向孤立脑室注入模拟脑脊液以模拟脑脊液分泌时,脑室和小脑延髓池之间的压力梯度形成,并在注入终止后立即消失。然而,当以不同速率向小脑延髓池注入模拟脑脊液时,由此产生并升高的蛛网膜下腔脑脊液压力会准确地穿过脑实质传递到孤立脑室的脑脊液中。导水管阻塞2小时期间脑脊液压力未升高且脑室未扩张,这表明导水管阻塞本身不会导致猫发生高血压性急性脑积水。