Abstract
The pharmacological effects of xylopinine (2, 3, 10, 11-tetramethoxy-5, 6-13, 13a-tetrahydro-8-dibenzo(a-g)quinolizine) in rabbit, cat and dog have been reported elsewhere (1, 2). Xylopinine induced a long-lasting fall of blood pressure and peripheral adrenolytic and sympatholytic effects. Furthermore, the sedative and potentiating effects of xylopinine on barbiturate sleep in mice were also observed. The electroencephalographic studies of xylopinine in the current report confirm that the drug depresses the activity of the brain stem reticular activating system, the specific and non-specific thalamocortical projection systems and the hypothalamic activating system. Further, there is a possibility that xylopinine exerts its central depressive effect by virtue of its adrenolytic activity as chlorpromazine presumably does (3). Although chemical structure of xylopinine closely related with those of reserpine and tetrabenazine, xylopinine does not affect the content of brain noradrenaline (4), and its pharmacological effects are not modified by pretreatment of animals with monoamine oxidase inhibitors (1).
The electroencephalographic studies of reserpine, decaserpine and tetrabenazine have been described elsewhere (5-7). Reserpine and decaserpine produced a biphasic response in unanesthetized rabbit. The first appearance of the resting waves in the spontaneous EEG for 30 to 60 minutes was followed by the appearance of the arousal waves. The initial responses of the EEG to the drugs were likely to derive from the endogenously liberated noradrenaline. The manifestation of the resting waves in the EEG by the intravenous noradrenaline has already been demonstrated (8, 9). However, the manifestation of the arousal waves by the intravenous or intracarotid injection of catecholamine has also been shown (10, 11). These evidences support the biphasic response of catecholamine on the spontaneous EEG.
