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Related Experiment Videos

The hyperglycaemic effect of morphine.

W Feldberg, S V Shaligram

    British Journal of Pharmacology
    |December 1, 1972
    PubMed
    Summary
    This summary is machine-generated.

    Morphine causes hyperglycemia and other effects in cats, which can be altered by other substances. These actions may originate from deeper brain structures rather than the ventricles themselves.

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    Area of Science:

    • Neuropharmacology
    • Endocrinology
    • Animal Models

    Background:

    • Morphine's central nervous system effects are well-documented.
    • The specific mechanisms underlying morphine-induced hyperglycemia and associated behaviors require further elucidation.
    • Investigating the interaction of morphine with other neurochemicals can provide insights into its complex actions.

    Purpose of the Study:

    • To investigate the effects of intraventricular morphine administration in unanesthetized cats.
    • To examine the influence of noradrenaline, adrenaline, 5-hydroxytryptamine (5-HT), reserpine, and pentobarbitone sodium on morphine-induced effects.
    • To explore the potential central nervous system sites of action for morphine's hyperglycemic effect.

    Main Methods:

    • Administration of morphine sulfate (0.75 mg) into the lateral cerebral ventricle of unanesthetized cats.

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  • Intravenous administration of morphine for dose comparison.
  • Intraventricular administration of noradrenaline, adrenaline, 5-HT, reserpine, and pentobarbitone sodium.
  • Observation and recording of behavioral and physiological responses, including hyperglycemia, shivering, pupillary dilatation, and excitation.

    • Main Results:

    • Intraventricular morphine induced hyperglycemia, shivering, pupillary dilatation, excitation, and analgesia.
    • Noradrenaline, adrenaline, and 5-HT attenuated morphine-induced hyperglycemia, with adrenaline showing the strongest effect.
    • Reserpine potentiated morphine's effects, while pentobarbitone sodium initially depressed and then enhanced hyperglycemia.
    • Morphine's hyperglycemic action likely involves caudal neuro-axis structures, not ventricular walls.

    Conclusions:

    • Morphine exerts significant central effects, including hyperglycemia, mediated through specific neurochemical pathways.
    • Exogenous neurotransmitters and drugs differentially modulate morphine's actions.
    • The study suggests that morphine's hyperglycemic effects are mediated by deeper brain structures rather than direct action on the ventricular walls.