| pubmed-article:1371441 | pubmed:abstractText | Hyperventilation leads to an increase in slow EEG activity as well as to a decrease in alpha activity. These effects may be considered a result of reduction in cerebral blood flow due to vasoconstriction, but metabolic factors, such as alkalosis and the increased formation of cerebral lactate, may also have to be taken into account. As indomethacin decreases cerebral blood flow it is possible to study cerebral vasoconstriction, without concomitant metabolic alkalosis or cerebral lactate formation. Two parallel groups of 12 healthy male subjects (age 20-25) were studied with quantitative EEG (qEEG) and cerebral blood flow velocity as parameters. In the first group the effect of 100 mg indomethacin was studied. In the parallel group a standardized hyperventilation procedure was performed. In the indomethacin group the blood flow velocity decreased to 60% of the initial value; the qEEG showed a 0.5 Hz slowing of the alpha peak frequency (P less than 0.01) and a decrease in the power of the alpha band without any change in the delta or theta band. In the hyperventilation group the blood flow velocity decreased to 63% of the initial value and the qEEG showed a marked increase in delta and theta activity (P less than 0.01), but a non-significant change in alpha peak frequency. Indomethacin and hyperventilation caused similar degrees of vasoconstriction; however, the increase in qEEG slow wave activity, which was observed only in the hyperventilation group, is apparently related to metabolic rather than haemodynamic factors. | lld:pubmed |
