Responses of Adrenal Corticosteroid Secretion to

that hemorrhage leads to depletion of adrenal ascorbic acid through a mechanism dependent on the pituitary and presumably involving the re-lease of ACTH (1). Hume and Nelson pre-sented evidence that hemorrhage was effective in increasing secretion of 17-hydroxycorticosteroids (17-OHCS) and that this effect was dependent upon the pituitary (2). Subsequent reports have confirmed (3-5) or failed to confirm (6, 7) these observations without, however, extending our un-derstanding of the mechanism by which hemor-rhage stimulates release of ACTH and secretion of 17-OHCS. The present experiments repre-sent a first attempt to define these mechanisms. Methods Eighty-two experiments were performed in 49 adult mongrel dogs weighing from 12 to 20 kg anesthetized with pentobarbital, 30 mg per kg. On the day before the experiment each animal's right lumboadrenal vein was cannulated by the method of Hume and Nelson (2). Thirteen dogs were nephrectomized bilaterally at the same time. In 11 animals, silk or cotton ligatures were passed about the carotid arteries low in the neck and then passed through double-lumen plastic cannulas to form chokers, as described previously (8); in four of these dogs, both vertebral arteries were ligated at this time. In 15 animals, inflatable cuffs were passed about the thoracic descending aorta; five of these animals were nephrectomized. All chokers and cuffs were brought out through closed incisions, so that constriction of the isolated vessel could be accomplished subsequently without further surgical manipulation. After all dogs had been anesthetized on the day of the experiment, they underwent cannulation of a femoral vein and one o