Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.

急性頭蓋内圧亢進時の脳循環動態に関する研究 第2編 急性頭蓋内圧亢進と脳血液量の変動

久山 秀幸 岡山大学医学部脳神経外科学教室
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During conditions of increased intracranial pressure (ICP), the cerebral blood volume (CBV) is thought to be an important factor producing acute brain swelling. Because of technical problems in measuring CBV, however, the changes in CBV during increased intracranial pressure are still poorly understood. In this study, during stepwise increases in ICP in 22 unselected mongrel dogs, CBV was measured continuously by a photoelectric method and cerebral blood flow (CBF) by a heat clearance method. CO(2) reactivity was also obtained from alterations of CBV following inhalation of 10% CO(2). ICP was gradually raised by infusion of saline through a tube into the cisterna magna from a bottle of fluid which was lifted to various height, and then the ICP was returned to the control level. While ICP was below 40-70 mmHg, neither CBV nor CBF showed any changes. However, as ICP was raised further, CBV showed a continuous increase while CBF showed a continuous decrease. CO(2) reactivity was completely lost when ICP was more than 110 mmHg, at which stage increase of CBV was thought to be due to vasomotor paralysis. Finally, CBV decreased when ICP reached the level of mean arterial blood pressure. This suggests that marked intracranial hypertension might act to squeeze the blood from cerebral vessels. In contrast, the animals with a vasopressor response had an increase in CBV in advanced intracranial hypertension. From these results, it appeared that the changes in CBV were dependent on the mean arterial blood pressure at the stage where vasomotor paralysis developed. Even after restoring the raised intracranial pressure with a vasopressor response to control level, both CBV and ICP continued to increase with no recovery of CO(2) reactivity. This result indicates that acute brain swelling might be caused by arterial hypertension during markedly increased intracranial pressure.
Cerebral blood volume
Cerebral blood flow
Increased intracranial pressure
CO(2) reactivity
Vasomotor paralysis