Reduced cardiac vagal excitability in hyperthyroidism.
A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate. In the present work we investigated whether reduced vagal influence could contribute to the tachycardia in hyperthyroidism. Vagal excitability was studied in ten hyperthyroid patients. Prolongation of R-R interval in response to carotid baroreceptor stimulation by neck suction was found to be less in the hyperthyroid state compared to the control state after therapy. The extent of nocturnal bradycardia and the vagal excitatory response to the central effect of low dose atropin was significantly reduced in hyperthyroid patients compared to euthyroid controls. We concluded that in the hyperthyroid state cardiac vagal motoneurones were in low excitability state, and speculated that the inhibition might have resulted from thyroid hormone action on CNS structures integrating autonomic function and behaviour.
Kollai
B
B
II. Department of Internal Medicine, Balassa Janos Hospital, Budapest, Hungary.
Kollai
M
M
D000328:Adult; D001285:Atropine / Q000494:pharmacology; D001919:Bradycardia / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000294:innervation* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D011311:Pressoreceptors / Q000502:physiology; D014630:Vagus Nerve / Q000187:drug effects / Q000503:physiopathology*
D001285:Atropine