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acetylstrophanthidin/ganglion cysts

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GreinarKlínískar rannsóknirEinkaleyfi
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Neural mechanisms involved in acetylstrophanthidin-induced bradycardia.

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The role of neural sites in the bradycardia produced by acetylstrophanthidin (14.1, 22.5 and 35.5 mug/kg) was studied in chloralose-anesthetized cats with efferent vagal tone blocked by atropine. The sites were: carotid sinus baroreceptors, aortic arch baroreceptors, cardiac sensory receptors,

The effects of acetylstrophanthidin on the response of the AV junction to adrenergic stimulation studied in dogs.

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The response of the AV junction to adrenergic stimulation was studied in 35 anesthetized open-chest dogs before and after the injection of acetylstrophanthidin (5mug) directly into the AV node artery. An AV junctional rhythm was obtained under control conditions by injecting norepinephrine (n = 9)

Denervation of vagal cardiopulmonary receptors by injection of kainic acid into the nodose ganglia in dogs.

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We determined if kainic acid, a neuroexcitotoxin, could be used to denervate the cell bodies of cardiopulmonary vagal sensory neurons. Kainic acid (5 microg) was injected into the nodose ganglion of five dogs. Ten to fourteen days following this procedure, these kainic acid-injected dogs were
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