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I.はじめに
水頭症の病態に関して検査方法や研究の進歩に伴つて,髄液循環障害,とくに髄液吸収障害の病態が明らかにされつつある。現在水頭症の治療には有効な手段としてshunt手術が広く行われており,他方では髄液産生の機序解明の成果の上にたつて,産生量を減少させるようなacetazolamide10),furosemid10,17),さらに最近では脳室内脈絡叢での髄液産生過程で特異的に作用する酵素ATPase (Adenosine triphosphatase)のblockerであるcardiac glycosidesなどによる水頭症治療の試みも行われるようになつた。
Vatesら18)は髄液産生の過程でNa-K dependentATPase系中とくにdigitalis sensitive Na-K activatedATPaseが脈絡叢から脳室内へNa+イオンの能動的分泌に関与することを実証した。これと前後してNa-Kdependent ATPaseのinhibitorとして知られるstro—phantinの髄液産生抑制効果についての基礎的研究1,3,5,13,18),および臨床応用例11)についての報告が多く現われはじめた。しかし,水頭症治療面への適用をはかる場合,その効果的な投与法,用量,副作用,またその際の脳循環,頭蓋内圧動態について,現在解明されるべき点を残している。
In order to examine the effect of digitalis sensi-tive Na-K dependent ATPase on cerebrospinal fluid (CSF) dynamics, strophantin-K (0.046-0.125 mg/kg-body weight) was intravenously administered, prior to the formation of acute experimental communicating hydrocephalus in adult cats.
Changes in ventricular fluid pressure (P1) and brain tissue pressure (P2) were continuously recorded following intraventricular injection of small amountof soot suspension. Other parameters included brain water content of hemispheric white matter, cerebral blood flow (CBF) by 133Xe-clearance method and electroencephalography (EEG).
Experimental results were summarized as follows :
1) The increases in intracranial pressure in the strophantin-K treated animals appeared to be apparently mild, as compared with the untreated probably due to the inhibited CSF formation. Rises of pressure were particularly restricted in the initial phase of the experiment.
2) No difference in pressure levels between P1 and P2 was observed. There were also minimal increases in brain water content during the de-velopment of the experimental hydrocephalus. This may indicate that the driving force for forming hydrocephalus is weakened by the administration of strophantin-K.
3) Decreases in CBF were remained relatively higher above 60% of the control.
From the present findings, the authors expressed that intravenously administered strophantin-K may be available in the treatment of communicating hydrocephalus, especially in the acute stage of rises in intracranial pressure, despite of the re-quirement of the promoted investigation on dose, effect on cerebral metabolism and side effects for clinical application.
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