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  • 1
    Electronic Resource
    Electronic Resource
    Inhibition by cholinergic agonists of the prolactin release induced by morphine (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 308 (1979), S. 249-254 
    Details
    ISSN: 1432-1912
    Keywords: Prolactin ; Morphine ; Pilocarpine ; β-Endorphin ; Catecholamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cholinergic agonists, pilocarpine, physostigmine and nicotine, inhibited the prolactin release induced by morphine in male rats in vivo. Pilocarpine also inhibited the release of prolactin induced by β-endorphin or metoclopramide without affecting the basal and haloperidol-stimulated serum prolactin levels. The inhibitory effect of pilocarpine on the morphine-stimulated release of prolactin was antagonized by concurrent administration of atropine but not by atropine methylnitrate or by mecamylamine, while the inhibition by nicotine was antagonized by mecanylamine but not by atropine. The stimulation of prolactin release by morphine and its reversal by pilocarpine were observed after the administration of haloperidol or α-methyltyrosine. These results suggest that the central cholinergic system exerts an inhibitory influence on the prolactin release induced by morphine or β-endorphin and the cholinergic inhibition is not mediated via catecholaminergic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501389
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Influence of hypoxia on mitochondrial function and energy status in CCl4-induced cirrhotic rat liver (1989)
    Springer
    Research in experimental medicine 189 (1989), S. 153-161 
    Details
    ISSN: 1433-8580
    Keywords: Rat ; Liver cirrhosis ; Hypoxia ; Redox state ; Mitochondrial oxidative phosphorylative activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of hypoxia on hepatic mitochondrial function and energy status was studied in normal and carbon tetrachloride (CCl4)-induced cirrhotic rats. Under hypoxemia of 50 mm Hg-PaO2, hepatic energy status was suppressed both in normal and cirrhotic rats. After the reversal of hypoxia, it was completely restored in normal rats concomitant with a rapid elevation of hepatic mitochondrial redox state (overshoot phenomenon) and increase in the mitochondrial oxidative phosphorylative activity. By contrast, in cirrhotic rats, such an enhancement of mitochondrial function was not observed. It was clarified that cirrhotic liver mitochondria have little capacity to respond to the hypoxic stress. A lower resistance to hypoxic episode in cirrhotics might be attributable to the absence of mitochondrial enhancement which is a compensatory mechanism for the deranged energy metabolism of the liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852163
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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