A pharmacological analysis of autonomic pathways mediating myocardial disturbances originating in a lateral hypothalamic area of the cat.
A study was made of the mechanisms mediating autonomic changes resulting from stimulation of a site in the lateral hypothalamic area (LHA). This site, when stimulated, induced angina-like ECG disturbances similar to those observed in some cases of brain traumas. These ECG changes were often associated with other autonomic changes, such as pressor response, tachycardia (in some cases bradycardia), nictitating membrane (NM) contraction and pupillary dilatation. Most symptoms were sympathetic: they were largely abolished by spinal cord section between C1 and C2, but were not affected by vagotomy, except that bradycardia was converted to tachycardia. Adrenal catecholamines were not involved since adrenal vein ligation was without effect. Hexamethonium (5-10 mg/kg) prevented pressor response and tachycardia in most cats but only partly protected against ECG changes and NM contractions. Atropine methyl nitrate (0.2 mg/kg) abolished the remaining ECG abnormalities and NM tension. The beta-receptor antagonists, propranolol and practolol (50 micrograms/kg) completely prevented the ECG changes induced either by isoprenaline or LHA stimulation. It is concluded that the symptoms induced by LHA stimulation result from noradrenaline release in the target organs.
D000787:Angina Pectoris / Q000209:etiology; D000818:Animals; D001342:Autonomic Nervous System Diseases / Q000209:etiology*; D001794:Blood Pressure; D002415:Cats; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D007026:Hypothalamic Area, Lateral / Q000502:physiology*; D008297:Male; D009435:Synaptic Transmission