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KMID : 0352519840210010155
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Korea Univercity Medical Journal
1984 Volume.21 No. 1 p.155 ~ p.165
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Influence of Clonidine on the Change Induced by Morphine of Tissue Catecholamine Content in Mice
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Abstract
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It has been well known that noradrenaline neurones appear to be involved in both morphine and clonidine analgesia, and there are many evidences that the effects of the two drugs ,on brain noradrenaline-turnover are inhibitory. But the functional role of brain noradrenaline in the suppressive effect of clonidine on the development of opioid withdrawal signs has not yet been clarified.
The present study was therefore undertaken in order to ascertain whether brain noradrenaline is responsible for clonidine-induced suppression of development of development of opioid withdrawal signs or cross-tolerance to morphine and clonidine, and so, seventeen hours after the last of 12 injections of increasing doses of both morphine and clonidine over 6 days according to the modified Paalzow´s and Weinstcck´s methods of the development of tolerance to the two drugs of morphine and clonidine on brain and heart catecholamine contents were estimated in male mice.
The results obtained were summarized as follows:
1. Morphine (20mg/kg i.p.) slightly increased brain catecholamine content and significantly increased heart catecholamine content.
The morphine-induced increase of brain catecholamine content was not altered all along the 7 day treatment of it, but the morphine-induced increase of heart catecholamine con-tent was augmented after the 4 day treatment of it and the augmentation showed a moderate decline after the 7 day treatment.
2. Clonidine (50opg/kg i.p.) significantly increased both brain and heart catecholamine con-tents.
The clonidine-induced increase of brain catecholamine content was not altered all along the 7 day treatment of it, but the clonidine-induced increase of heart catecholamine con-tent was slightly augmented after the 4 day treatment of it and then recovered to the
initial level.
3. The combined effect of morphine and clonidine on the both brain and heart catecholamine contents was additive, and the additive combined-effect was not altered all along the 7 day treatment of the two drugs.
The above results suggest that the tolerance development of morphine and the clonidineinduced suppression of opioid withdrawal signs may be mediated through other neuronal systems as well as noradrenergic system
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