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  • Book
    Peter C. Belafsky, Maggie A. Kuhn.
    Summary: The Clinician's Guide to Swallowing Fluoroscopy is a comprehensive resource for all dysphagia clinicians. This beautifully-illustrated text is intended for SLP, ENT, radiology, GI, and rehabilitation specialists interested in swallowing and addresses the need for an up-to-date, all-inclusive reference. Topics covered include radiation safety and protection, fluoroscopic oral, pharygeal, and esophageal phase protocols and abnormalities, and objective measures of timing and displacement.

    Contents:
    1. Radiation Safety
    2. The Videofluoroscopic Swallow Study Technique and Protocol
    3. The Videofluoroscopic Esophagram Technique and Protocol
    4. Normal Oral and Pharyngeal Phase Fluoroscopy
    5. Normal Pharyngoesophageal Segment Fluoroscopy
    6. Normal Esophageal Fluoroscopy
    7. Objective Measures on Videofluoroscopic Swallow Studies
    8. Fluoroscopy and Dysphagia Outcome Measures
    9. Abnormal Oral and Pharyngeal Phase Fluoroscopy
    10. Abnormal Pharyngoesophageal Segment Fluoroscopy
    11. Abnormal Esophageal Fluoroscopy.
    Digital Access Springer 2014
  • Article
    Jacoby JH, Bryce GF.
    Arch Int Pharmacodyn Ther. 1978 Oct;235(2):254-70.
    Serotonin (5HT) (5 mg/kg-25 mg/kg; i.p.) induced a dose-related increase of plasma glucagon (IRG) (using 30K antibody) 3 to 60 min after administration to overnight fasted rats. Blood glucose (BS) also increased as early as 10 min post-injection whereas plasma insulin (IRI) increased in a non dose-related (30 min to onset) manner. Adreno-demedullation prevented the rise of BS and IRI, but not IRG. Pretreatment with reserpine (5 mg/kg; i.p.; 24 hr earlier) did not prevent the actions of 5HT. Pretreatment with the alpha-adrenergic antagonist phentolamine (3 mg/kg-6 mg/kg; i.p.) reduced but did not prevent the subsequent rise of IRG, whereas beta-adrenergic blockade with propranolol (5 mg/kg-10 mg/kg; i.p.) was without effect. Phentolamine and the lower dose of propranolol (5 mg/kg) reduced the 5HT-induced hyperglycemia; whereas the higher dose (10 mg/kg) prevented the hyperglycemia. Phentolamine potentiated and propranolol prevented (5 mg/kg) or reversed (10 mg/kg) the 5HT-induced IRI rise. Pretreatment with the 5HT-antagonist, methysergide, prevented all the effects of 5HT. Precursor loading with 5HTP (5 mg/kg-50 mg/kg; i.p.) also resulted in a dose-related increase of IRG and a slight increase of IRI. Blockade of the conversion of 5HTP to 5HT with Ro-4-4602 (an L-aromatic acid decarboxylase inhibitor) blocked the subsequent rise of IRG. These results suggest that the 5HT-induced changes in BS and IRI may be secondary to a release of epinephrine and/or norepinephrine, but that the effects of 5HT on the release of IRG cannot be explained solely by this mechanism.
    Digital Access Access Options