Influence of sympathectomy on the lateral hypothalamic lesion syndrome.
Sympathetic involvement in the lateral hypothalamic (LH) lesion syndrome was examined. Male rats were surgically or chemically sympathectomized and then given LH lesions. At 24 hr postlesion, lesion-induced hyperglycemia but not hyperthermia was attenuated by splanchnicectomy and celiac ganglionectomy. Hyperthermia but not hyperglycemia was attenuated by adrenal demedullation, adrenalectomy, and neonatal guanethidine treatment. Guanethidine-sympathectomized rats also displayed lower basal temperatures, more perilesion chromatolysis, and severer external symptoms than their controls. No form of sympathectomy affected lesion-induced gastric pathology, plasma gastrin concentrations, or body weight loss. Nor did any sympathectomy influence the recovery of ingestive behavior, daily food intake, the feeding response to 2-deoxy-D-glucose, or body weight maintenance in recovered LH-lesion subjects. These results suggest that sympathetic hyperactivity contributes to some aspects of the acute LH syndrome: Hyperglycemia results from sympathetic outflow to the abdomen, whereas hyperthermia is determined by circulating catecholamines and extraabdominal sympathetic innervation. The results fail to support the hypothesis that chronic increases in sympathetic tone are responsible for the reduced food intake and body weight of the LH-lesion rat.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001831:Body Temperature; D001835:Body Weight; D005755:Gastrins / Q000097:blood; D007026:Hypothalamic Area, Lateral; D007027:Hypothalamic Diseases / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D008297:Male; D051381:Rats; D013270:Stomach / Q000473:pathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013577:Syndrome
D001786:Blood Glucose; D005755:Gastrins; D007328:Insulin