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Related Experiment Videos

Neurogenic hyperacute ascites in mice.

D P Nelson, E D Robin, R J Wong

    Clinical Science (London, England : 1979)
    |September 1, 1986
    PubMed
    Summary
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    Acute head trauma in mice can cause neurogenic hyperacute ascites (NHA), a condition mediated by beta-sympathetic activity. Beta-blockade significantly reduced NHA, while beta-agonists simulated its occurrence.

    Area of Science:

    • Neuroscience
    • Physiology
    • Pharmacology

    Background:

    • Acute brain trauma can lead to rapid physiological changes.
    • Neurogenic hyperacute ascites (NHA) is a newly described consequence of head trauma.

    Purpose of the Study:

    • To investigate the mechanism of neurogenic hyperacute ascites (NHA) following acute brain trauma.
    • To determine the role of sympathetic nervous system activity in NHA.

    Main Methods:

    • Mice were subjected to controlled fatal head trauma.
    • Groups were pretreated with beta-blockers (propranolol) or alpha-blockers (phentolamine).
    • Ascites presence was evaluated, and agonist/antagonist effects were tested.

    Main Results:

    Related Experiment Videos

  • 87-100% of untreated traumatized mice developed ascites.
  • Propranolol pretreatment significantly decreased ascites prevalence.
  • Beta-agonist (isoethrane) administration induced ascites in 100% of animals.

    • Conclusions:

    • Neurogenic hyperacute ascites (NHA) appears to be mediated by central beta-sympathetic activity.
    • Beta-adrenergic blockade inhibits NHA.
    • Beta-adrenergic agonism can simulate NHA.