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Related Experiment Videos

Cyclic AMP response to epinephrine and shock.

A H McArdle, C J Chiu, E J Hinchey

    Archives of Surgery (Chicago, Ill. : 1960)
    |March 1, 1975
    PubMed
    Summary

    Hemorrhagic shock increases plasma cyclic AMP but depletes intestinal mucosal cyclic AMP and ATP. Alpha-blockade mitigates these shock-induced changes, suggesting a role for alpha-adrenergic receptors in regulating cyclic AMP during shock.

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    Area of Science:

    • Physiology
    • Biochemistry
    • Pharmacology

    Background:

    • Hormonal regulation is crucial for maintaining homeostasis.
    • Adenosine 3':5' cyclic phosphate (cyclic AMP) mediates tissue responses to hormonal signals.
    • Elevated catecholamines during hemorrhagic shock necessitate understanding cyclic AMP dynamics.

    Purpose of the Study:

    • To investigate the effects of epinephrine and hemorrhagic shock on cyclic AMP levels in plasma and canine intestinal tissue.
    • To determine the role of alpha-adrenergic receptors in mediating these changes.

    Main Methods:

    • Epinephrine infusion (constant or pulse) in normotensive dogs.
    • Induction of hemorrhagic shock in dogs.
    • Measurement of cyclic AMP and adenosine triphosphate (ATP) in plasma and intestinal mucosa.
    • Assessment of alpha-blockade effects prior to shock induction.

    Main Results:

    • Epinephrine administration increased circulating cyclic AMP, particularly in portal and hepatic venous blood, with minimal tissue changes.
    • Hemorrhagic shock significantly elevated plasma cyclic AMP while depleting mucosal cyclic AMP and ATP.
    • Alpha-blockade prior to shock prevented mucosal cyclic AMP and ATP depletion and attenuated plasma cyclic AMP elevation.

    Conclusions:

    • Hemorrhagic shock profoundly alters cyclic AMP and ATP levels in plasma and intestinal mucosa.
    • Alpha-adrenergic pathways appear to play a significant role in the observed changes in cyclic AMP during shock.
    • These findings have implications for understanding tissue vulnerability and potential therapeutic targets during shock states.

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