Abstract
This chapter presents the experimental autoimmune autonomic neuropathy (EAAN) in an animal as a model. An animal model of this disorder, EAAN, can be induced in rabbits by immunization with the ganglionic acetylcholine receptor (AChR). Rabbits with EAAN manifest symptoms of autonomic failure similar to those seen in patients. Histologic and electrophysiologic studies of EAAN indicate that this autoimmune form of autonomic neuropathy is caused by an immune-mediated impairment in ganglionic synaptic transmission. EAAN recapitulates the clinical phenotype of human autoimmune autonomic neuropathy (AAN). Rabbits producing high levels of ganglionic acetylcholine receptor (AChR) antibody develop gastrointestinal dysmotility and fail to gain weight because of reduced food intake. Gastroparesis and impaired intestinal motility are evident by fluoroscopy and examination of the gut at autopsy. Severe parasympathetic dysfunction manifests as dilated and poorly responsive pupils, decreased lacrimation, reduced heart rate variability, and dilated bladder. EAAN rabbits also have reduced levels of plasma catecholamines indicating reduced sympathetic tone. As in patients with AAN, the severity of autonomic disturbances is greater in rabbits with greater antibody levels. Individual measures of autonomic function in EAAN rabbits also correlate with antibody level.
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