Subacute and chronic effects of hypothalamic lesions on aldosterone and sodium excretion

¹ Section on Experimental Cardiovascular Disease, Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland, and the Section of Pathlogical Anatomy, Mayo Clinic, Rochester, Minnesota

Effects of hypothalamic lesions were studied in 10 dogs with chronic ascites produced by constriction of the thoracic inferior vena cava. During the first three postoperative days, the high rate of urinary aldosterone excretion and the marked Na retention characteristic of dogs with chronic experimental ascites were unaltered in all 10 animals. Every area of the hypothalamus was destroyed bilaterally in at least one animal. Seven of the 10 dogs survived the subacute 3-day period; two dogs died after 6 days but five animals lived for 2 weeks or longer. In these seven animals, aldosterone excretion in urine remained elevated above normal although in three animals a progressive decline occurred; sodium excretion remained low in all seven dogs surviving the subacute period. In the three animals in which aldosterone output declined, there was bilateral injury of the median eminence and adrenal atrophy. The data show that chronic hypothalamic lesions were without effect unless the median eminence was injured.

Note:
With the Surgical Assistance of Alfred Casper