脳浮腫および頭蓋内圧亢進時における脳血管拡張剤プラキシレンの脳循環におよぼす影響について

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Twenty mongrel dogs were used and the effects of the vasodilator "Praxilene" (2 mg/Kg i.v.) on cerebral blood flood flow (CBF), oxygen availability (O_2a) and intracranial pressure (ICP) were srudied in acute intracranial hypertension produced by slow inflation of epidural balloon and in cerebral edema produced by epidural application of dry ice for ten minutes. The local CBF was measured by the heat clearance method with double thermister or thermocouple, while measuring O_2a by polarograph using open tip type of platinum electrode with the diameter of 50 to 270μ. ICP was measured by epidural microballoon method. In normal controls, CBF was increased for 9.6 minutes after the administration of Praxilene (2 mg/Kg i.v.) approximately as much' as that after 10% CO_2 inhalation of 4 or 5 minutes, ^ and the elevation of O_2a was paralleled to the increase of CBF. But ICP was elevated by mean 7.2 mmHg by the administration of Praxilene, while 10% CO_2 inhalation elevated ICP by mean 18.7 mmHg. Therefore, Praxilene increased CBF with less increase of ICP than 10% CO_2 inhalation. In acute intracranial hypertension by epidural balloon compression, CBF and O_2a were not increased so much by the administration of Praxilene as controls with normal ICP. When ICP was raised to the level higher than 30 to 50 mmHg, Praxilene induced further increase of ICP and the harmful effects on systemic circulation such as hypotension, arrhythmia and bradycardia. Under these condition CBF and O_2a were no longer increased. Cerebral edema was produced in five experiments. CSF pressure was measured by cisternal puncture at 24 to 48 hours after injury. It was ranged from 8 to 11 mmHg in all cases. CBF and O_2a were measured in the lesion and in the contralateral normal area. O_2a electrode was located at the same point where CBF electrode was inserted. In two of five experiments, CBF and O_2a were not increased within the lesion by the administration of Praxilene In other three experiments, CBF was increased slightly by it, but the effects of Praxilene to CBF and O_2a were abolished when ICP was elevated to the level of 25 to 30 mmHg by hydrostatic infusion of artificial CSF into the cisterna magna. However, in these condition CBF and O_2a were increased by it in the contralateral normal area. These effects would be probably due to the decrease of the vasoreactivity to the vasodilator "Praxilene" and the abnormal hemodynamics within the lesion due to the regionally increased ICP. In some cases, it was noticed that O_2a was not increased in spite of increase of CBF within the lesion by the administration of Praxilene or 10% CO_2 inhalation. This would demonstrate that there were some regions within the lesion where the increased CBF was non-nutritional. In conclusion, the effect of vasodilator "Praxilene" would not be expected in the patients with intracranial hypertension more than 30 to 50 mmHg, and in those with cerebral edema even if ICP is not elevated.
社団法人日本循環器学会の論文
1973-11-20

脳浮腫および頭蓋内圧亢進時における脳血管拡張剤プラキシレンの脳循環におよぼす影響について

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