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抄録 Succinylcholine 不動化無麻酔ネコを用いMCI−2016の脳波覚醒化作用を明らかにすべくpowerspectrum分折および各種薬剤との併用によるMCI−2016の脳波作用の検討を行なった。 MCI−2016 5および10mg/kg ivにより皮質脳波は低振幅速波化を示すが,power spectrumも明らかな右方偏位を示した。同様の傾向はmeclofenoxate 20,40mg/kg ivでも認められたが,Ca-hopantenate 200mg/kg ivではほとんど影響をはなく,imipramineは2mg/kg iVで顕著な左方偏位を示した。一方,α—methyl-pityrosine 350mg/kg ivおよびscopolamine 0.015mg/kg iv投与による徐波脳波に対しMCI−2016はそれぞれ5,10mg/kg ivの併用で拮抗傾向を示した。さらにphysostigmine 0.01mg/kg ivによる覚醒脳波の持続時間をMCI−2016はその単独で覚醒作用を示さない用量の1.5mg/kg ivで増強し,imipramineは1.5mg/kg ivで拮抗した。以上より,MCI−2016の脳波覚醒化作用は定量的にも明らかとなり,かつその作用の一部にcholine作働神経とcatecholamine作働神経の賦活様作用が関与すると推測される。
In order to make clear the activating effect of MCI-2016 on EEG, power spectrum analysis was performed and the interaction in EEG between MCI-2016 and some drugs were studied in suc-cinylcholine-immobilized cats.
MCI-2016 at doses of 5 and 10 mg/kg iv pro-duced apparent arousal pattern in cortical EEG characterized by low amplitude fast wave, and evoked the right-shift in power spectrum. In the case of meclofenoxate at doses of 20 and 40 mg/ kg iv, the shifts in power spectra were similar to that of MCI-2016, very slight changes were observed by Ca-hopantenate at a dose of 200 mg/ kg iv and typical left-shift was introduced by imipramine at a dose of 2 mg/kg iv.
MCI-2016 tended to suppress the SWS state induced by α-methyl-p-tyrosine and scopolamine at a dose of 350 mg/kg ip and 0.015 mg/kg iv, respectively.
Subsequently, the duration of arousal state in EEG induced by physostigmine at a dose of 0.01 mg/kg iv was enhanced by MCI-2016 at a dose of 1.5mg/kg iv whose injcction does not produce any arousal pattern in EEG.
The activating effect of MIC-2016 on EEG was indicated quantitatively and it is suggested that the cholinergic mechanism and the catecholami-nergic mechanism would be involved in the EEG activating effect of MCI-2016.
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