Influence of sympathectomy on the lateral hypothalamic lesion syndrome

Two experiments with male Long-Evans rats examined sympathetic involvement in the lateral hypothalamic (LH) lesion syndrome. Ss were surgically or chemically sympathectomized and then given LH lesions. At 24 hrs 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 daily neonatal guanethidine (50 mg/kg) treatment. Guanethidine-sympathectomized Ss also displayed lower basal temperatures, more perilesion chromatolysis, and more severe external symptoms than 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-dextro-glucose, or body weight maintenance in recovered LH-lesioned Ss. Results suggest that sympathetic hyperactivity contributed to some aspects of the acute LH syndrome: Hyperglycemia resulted from sympathetic outflow to the abdomen, whereas hyperthermia was determined by circulating catecholamines and extra-abdominal sympathetic innervation. Findings fail to support the hypothesis that chronic increases in sympathetic tone are responsible for the reduced food intake and body weight of the LH-lesioned Ss. (47 ref)