Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.


Honma, Yutaka
Thumnail 97_543.pdf 4.18 MB
It is widely accepted that an increase in the cerebral blood volume (CBV), secondary to loss of cerebrovascular tone, is essential for the development of acute brain swelling (ABS). Studies have shown that disruptions of metabolic and neural control of cerebrovascular tone are responsible for cerebral vasomotor paralysis, and subsequently result in ABS. However, it is not clear whether metabolic or neural control of cerebrovascular tone is predominant in producing ABS. The changes in cerebrovascular tone created by destruction of the cerebral vasomotor center of the brain-stem in animals with decreased cerebrovascular tone due to loss of metabolic control were clarified and the interaction of neural and metabolic control of cerebrovascular tone was observed. Seventy immobilized, artificially ventilated cats were divided into five groups: group I: control; group II: normocapnic hypoxia; group III: normoxic hypercapnia; group IV: increased intracranial pressure (ICP) by brain compression and group V: subarachnoid hemorrhage (SAH). The systemic arterial pressure (BP), ICP (epidural pressure) and CBV (photoelectoric method) were continuously measured. One hour after the parameters stabilized, the dorsomedial hypothalamic nucleus (DM) and the midbrain reticular formation (MB-RF) were bilaterally destroyed by a stereotaxic technique (3mA, 1min). In group I, brain-stem destruction resulted in a transient decrease in the BP (DM: -14.1±6.7mmHg, MB-RF: -10.2±4.8mmHg) and simultaneous increase in the CBV and ICP (DM: 7.6±7.0mmHg, MB-RF: 6.0±5.6mmHg) for three to four min. In groups II and IV, the ICP (group II, DM: 2.3±2.6mmHg, MB-RF: 1.6±1.2mmHg; group IV, DM: 7.5±4.0mmHg, MB-RF: 4.8±3.2mmHg) decreased after brain-stem destruction presumably due to the preceding vasodilatation caused by disruption of metabolic control. In group III, the BP decreased or increased, and changes in the CBV and ICP after brainstem destruction paralleled those of the BP. Marked hypercapnia probably yielded the maximum cerebral vasodilatation, so vasodilatory effects by brain-stem destruction were completely supressed. In group V, 12 of 15 animals showed essentially the same response patterns of the BP, CBV and ICP as group I after brain-stem destruction. The remaining three animals developed progressive intracranial hypertension up to 40, 70 and 80mmHg just as in ABS, with an increase in CBV after destruction of the brain-stem. This study suggests that in many animals, ABS is not produced by small lesions produced in the brain-stem of animals with preexisting decreased cerebrovascular tone, as in this experiment However, in pathological intracranial conditions such as severe brain-stem compression ischemia and disturbance of the cerebrospinal fluid circulation with intracranial hypertension, ABS might be provoked by destruction of the cerebral vasomotor center in the brain-stem.
acute brain swelling
cerebral vasomotor paralysis
neural factor
metabolic factor
brain-stem lesion