頭蓋内占拠性病変による急性頭蓋内圧亢進の研究-とくに急性頭蓋内圧亢進時の局所脳血管緊張の部位的変化について-

Regional CO(2) reactivity of different areas were observed during acute intracranial hypertension produced by extradural balloon compression in dogs. Regional CBF was measured by as heat clearance method with two thermocouple probes, 1) in the parietal area adjacent to the balloon and the contralateral parietal area, 2) in the adjacent parietal area and the ipsilateral occipital area remote from the balloon, 3) in the adjacent two areas, parietal and temporal, of the damaged hemisphere. ICP was measured by an epidural microballoon method and a fiber optic pressure switch (Ladd co.). The findings were as follows. 1. Regional CO(2) reactivity was impaired first in the area adjacent to the balloon, later in the remote area, and lastly in the contralateral area. 2. The impairment of regional CO(2) reactivity of the parietal area adjacent to the balloon and the contralateral parietal area could be classified into the following 5 stages. Stage 1: (ICP less than 20 mmHg) ICP and rCBF of both sides were increased by CO(2) inhalation. Stage 2: (ICP ca. 30 mmHg) ICP was increased more. In the contralateral area, rCBF was increased, but in the adjacent area, the increment of rCBF by CO(2) inhalation was diminished. Stage 3: (ICP ca. 45 mmHg) ICP was increased. In the contralateral area, rCBF was increased, but in the adjacent area, rCBF was decreased by CO(2) inhalation (paradoxical response i.e. intracerebral steal syndrome or intracerebral squeeze phenomenon). Stage 4: (ICP ca. 75 mmHg) ICP was increased, but rCBF on both sides was not increased by CO(2) inhalation. Stage 5: (ICP more than 100 mmHg) ICP and rCBF on both sides were not increased by CO(2) inhalation. 3. This dissociation of regional CO(2) reactivity in various areas would be caused by intracranial pressure gradients, and the consequent difference in local tissue metabolites.