Autonomic dysfunction in experimental allergic neuritis
Corresponding Author
G. Solders
Department of Clinical Neurophysiology, Huddinge University Hospital, Sweden
Department of Neurology, Huddinge University Hospital, Sweden
Göran Solders, M.D. Huddinge University Hospital S-141 86 Huddinge SwedenSearch for more papers by this authorA. Persson
Department of Clinical Neurophysiology, Huddinge University Hospital, Sweden
Search for more papers by this authorK. Kristensson
Department of Neuropathology, Huddinge University Hospital, Sweden
Search for more papers by this authorS. Hansson
Department of Neurology, Huddinge University Hospital, Sweden
Search for more papers by this authorCorresponding Author
G. Solders
Department of Clinical Neurophysiology, Huddinge University Hospital, Sweden
Department of Neurology, Huddinge University Hospital, Sweden
Göran Solders, M.D. Huddinge University Hospital S-141 86 Huddinge SwedenSearch for more papers by this authorA. Persson
Department of Clinical Neurophysiology, Huddinge University Hospital, Sweden
Search for more papers by this authorK. Kristensson
Department of Neuropathology, Huddinge University Hospital, Sweden
Search for more papers by this authorS. Hansson
Department of Neurology, Huddinge University Hospital, Sweden
Search for more papers by this authorAbstract
ABSTRACT – Beat-to-beat variation (R-R variation) in the electrocardiogram was studied in experimental allergic neuritis in the Sprague-Dawley rat. Reduced R-R variations were found in 2 of 10 animals, probably as a sign of autonomic dysfunction. The vagal nerves from these two animals, studied in vitro, showed disturbed conduction. In one animal prolonged conduction latencies to supramaximal electrical stimuli were found. Vagal nerves from controls and from animals without clinical symptoms showed normal conduction. Histologically, the vagal nerves from affected animals showed a slight inflammatory cell infiltration and signs of demyelination but there was no evidence of involvement of the brainstem vasomotor nuclei. Thus, we suggest that the autonomic dysfunction in experimental allergic neuritis, measured as reduced R-R variations, is caused by a peripheral vagal neuropathy.
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