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I.はじめに
高血圧,脳動脈硬化症,脳血栓らの脳血管障害患者においては,脳血管抵抗の増大,脳血流量の減少,さらに脳酸素消費量の減少などが認められるが,近年,これらの脳血流動態を改善せしめるために,種々の脳血管拡張剤が使用されている1)〜5)。
脳血管拡張剤投与の終局の目的は,脳血流の増大により側副血行を増加させ,脳血管障害により生じた脳虚血部を縮小せしめることにある6)。同時に脳血管拡張剤投与により,血管床の増大をともない,多かれ少なかれ頭蓋内圧の上昇をきたすのも事実である。
In these years, many vasodilators have been used in cerebrovascular diseases. There are many re-ports on the effect of vasodilators on cerebral blood flow, but few have investigated the effects of vasodi-lators on intracranial pressure or cerebral hemo-dynamics in condition of intracranial hypertension.
In our experiments, we used 15 dogs and observed the effects of the potent vasodilator "Cinnarizine" (2.5mg/kg) on intracranial pressure, cerebral bloodflow and systemic arterial pressure in various levels of increased ICP produced by the intracranial ex-tradural balloon method. The local CBF was mea-sured by the double thermister and the ICP was by extradural balloon method.
In normal ICP, cerebral blood flow was increased by the administration of Cinnarizine aproximately as much as by 10% CO2 inhalation, but the effect on ICP was minimal (mean 6.6mmHg of elevation) compared with 10% CO2 inhalation (mean 18.7 mmHg of elavation). In mild intracranial hyper-tension (initial ICP was about 20mmHg), the administration of Cinnarizine induced the same increase of the cerebral blood flow as in normal ICP though the elevation of ICP was more (mean 21.3mmHg of elevation).
In moderate intracranial hypertension (initial ICP was about 30~50mmHg), the administration of Cinnarizine had no significant increase of cerebral blood flow though the effect on ICP was further increased (mean 23.5mmHg of elevation).
In marked intracranial hypertension (initial ICP was more than 80mmHg), administration of Cin-narizine induced harmful effects on the systemic circulation such as hypotension, bradycardia and arrhythmia and the changes of ICP and CBF were completely parallel with blood pressure.
According to these experimental results, we would emphasize that the initial ICP is the important factor in cerebral hemodynamics on administration of vasodilators, especially to the patients whose ICP were increased by brain edema or space taking lesion, etc.
In normal ICP, the administration of Cinnarizine induced the minimal effects on ICP compared with 10% CO2 inhalation, we discussed the following two points about the possible mechanisms of this phenomenon.
1) It would be due to the buffer action of dis-placeable fluid (CSF) to increased cerebrovascular bed.
2) It would be due to buffer action between the brain parenchyma and the vascular bed by exchang-ing water or other substances.
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