Effect on the Regional Cerebral Blood Flow and Biomechanical Factors in Ventricular Enlargement of Experimental Hydrocephalus

ABSTRACT

To evaluate the biomechanical changes and cerebral blood flow in hydrocephalic brain, this study was designed to determine the regional cerebral blood flow(rCBF; frontal cortex and periventricular area), the pressure volume index(PVI) and the resistance to the absorption of cerebrospinal fluid(Ro) in different stages of the kaolin-induced hydrocephalus. Fifty five 8 week-old cats, weighing 900g to 1300g were used in this experiment. The experimental animals were divided into 2 groups ; a normal control(5 cats), and kaolin-induced hydrocephalic groups(50 cats). The kaolin-induced 1,2,4,6 and 8 weeks hydrocephalic groups after intracisternal injection of the kaolin. The rCBF was measured by hydrogen clearance technique and the PVI and Ro were determined by the technique of bolus manipulation of CSF. A significant elevation of the intracranial pressure(ICP) was observed in 2 weeks after kaolin injection and peak value(ICP=10.2+/-0.9mmhg) was obtained in 4 weeks after Kaolin injection. The significant decrease in rCBF were revealed in both frontal cortex and periventricular area of kaolin-induced hydrocephalic cats. The PVI was significantly increased from the normal value 0.77+/-0.02ml to 1.60+/-0.16ml at 4 weeks after kaolin injection and increased to 2.12+/-0.34ml at 6 weeks after kaolin injection. Ro was significantly decreased from the normal value 90.6+/-1.3mmHg/ml/min to 36.8+/-4.3mmHg/ml/min at 4 weeks after kaolin injection and further decreased to 6.2+/-1.9mmHg/ml/min at 8 weeks after kaolin injection. In Hydrocephalic cats, the size of the ventricle(septum pellucidum-caudate nucleus distance) continued to increase in size up to 9.40+/-0.7mm at the 4th week. However, there was no further increase in ventricular size after the 4th week. This study indicated that kaolin-induced hydrocephalic cats led to dramatic changes in volume-buffering capacity expressed as PVI, coupled a reduction in the Ro. The absorptive defect and also loss of volume-buffering capacity are not sufficient to cause progressive ventricular enlargement. It is assuming that some microcirculatory impairment in the brain parenchyma is playing an important role which facilitates ventricular expansion with changes of biomechanical property of the brain.