[Analysis of the possible mechanism for decrease of intracranial pressure following arousal stimulation].
Although decrease of intracranial pressure (ICP) and cerebral blood flow occurring following arousal from sleeping is well known phenomenon, its exact mechanism is poorly understood at the present time. The purpose of this study is to clarify its most possible mechanism, by analyzing clinical data mainly in comparison to the results obtained during hyperventilation. A small microtransducer, for ICP monitoring was placed over the dura at the time of closing of cranium and ICP was continuously recorded by ink-writing oscillograph. Systemic blood pressure, pulse and respiratory rates were continuously monitored and arterial PCO2 and pH before and after arousal stimulation were also determined. Above results are summarized as follows. There was no significant difference in time constant at decline of ICP between following arousal stimulation and hyperventilation, indicating that a response organ is the same between two groups and cerebrovascular wall is most likely as the response organ. However, since there was significant difference in time lag until initiation of decrease of ICP, the triggering mechanism for causing change of cerebrovascular tone must be different. In addition, there was no significant difference in arterial PCO2 and pH between at sleep and awake. On the basis of these results, the author concludes that rapid drop in ICP observed following arousal stimulation is due to neurogenic cerebral vasoconstriction.
D000328:Adult; D000368:Aged; D000818:Animals; D001143:Arousal / Q000502:physiology*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D004285:Dogs; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006985:Hyperventilation / Q000503:physiopathology; D007427:Intracranial Pressure; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D008875:Middle Aged; D014661:Vasoconstriction
D002245:Carbon Dioxide; D008353:Mannitol