This study was carried out to assess changes in cerebrovascular tonus in acute intracranial hypertension. Incremental increases of intracranial pressure (ICP) were induced in 42 dogs by intermittent inflation of a left fronto-temporal extradural balloon until the animals showed anisocoria, whereupon the balloon was deflated. ICP was continuously monitored using a pressure indicating-balloon in the bilateral extra- or intra-dural cavities. Blood pressure was abruptly increased by administration of angiotensin II at various levels of increased ICP (IICP). The cerebrovascular tonus was calculated as the ratio of the increase in mean ICP divided by the increase in mean blood pressure and was further defined as the local vasomotor capacitance index (LVCI). CO(2) reactivity of the cerebral vessels, an electroencephalogram (EEG) and the condition of the pupils were also observed. There was no significant difference between the bilateral hemispheres in local ICP (except at a balloon volume of 3 ml) and LVCI during IICP. The LVCI was 0.085±0.056 at normal ICP, and increased exponentially with increases in ICP. The maximum LVCI was 0.89. There were significant correlations between increases in the LVCI and decreases in cerebral perfusion pressure (CPP). The LVCI began to increase when CPP was below 80 mmHg, and increased markedly to more than 0.6 when CPP was below 40 mmHg. The CO(2) reactivity of cerebral vessels was completely impaired when transtentorial herniation developed. After deflation of the balloon, LVCI did not recover in 7 of 14 dogs. In these animals, CPP remained below 80 mmHg, and the EEG and pupils never became normal.
acute intracranial hypertension
acute brain swelling
cerebral vasomotor tonus