特発性正常圧水頭症の病因的研究 : 高血圧自然発症ラットによる水頭症作製と、髄液循環動態の検索
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概要
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According to the recent papers, etiological corelation between the hypertensive cerebrovascular disease and the normal pressure hydrocephalus has been discussed. In this work three different experiments were performed to study whether the arterial hypertension and cerebrovascular disorders might be basic pathologies really to develop a hydrocephalic state or not. In the experiment I, kaolin induced obstructive hydrocephalus were produced with the spontaneously hypertensive rat (SHR) and normotensive rats ; In the SHR group, more marked ventricular dilatation was observed in contrast with in the normotensive group. In the experiment II, the pressure-volume relationship were studied by bolus saline injection method in the SHR and normotensive rats. PVI and craniospinal compliance showed no significant differences among the materials, otherwise the outflow resistance of cerebrospinal fluids in the SHR was significantly high comparing with the one in the normotensive rats. (P<0.01) In the experiment III. horseradish peroxidase (HRP) was introduced into the cisterna magna of the SHR and normotensive rats. 3,6 and 24 hours after the application of the HRP, every animals were sacrificed to examine whether in the SHR the HRP absorption from the parenchymal vessels might be supressed or not. Delayed HRP clearance from the perivascular space was observed mainly in the SHR. but this finding was also seen in the one normotensive rat. From these results of the present study, we suspect that in the SHR arterial hypertension and arterioscrelotic changes may cause the high outflow resistance of the cerebrospinal fluids of these rats and also this may cause the more marked hydrocephalus with cisternal kaoiin injection in the rat. However the morphological identification of this theory, using HRP as a tracer, were not confirmed. Concerning to the cause of this high outflow resistance of the cerebrospinal fluids in the SHR, we discussed here three different mechanism, that is transvascular CSF block by arteriosclerotic changes, functional block by arterial hypertension and block of CSF bulk flow by multiple lacunar infarcts.
- 神戸大学の論文