“…The check to the fall and the subsequent rise of blood sugar could be said to result not from 'adrenaline' release but from the operation of the other factor or factors which, as has been seen, can on occasion restore blood sugar. It is true that the general result of animal experiment is to show that the hypoglycaemic effect of insulin is potentiated when adrenaline release is prevented (a) by denervation or demedullation of the adrenal glands in cats (Cannon et al 1924;Britton, Geiling & Calvery, 1928;Schlossberg, Sawyer & Bixby, 1933;Berg & Zucker, 1937) rabbits (Freeman et al 1934) and dogs (Houssay et al 1924;Crandall & Cherry, 1939); (b) by adrenalectomy in cats (Cannon et al 1924) dogs (Crandall & Cherry, 1939 and rabbits (Sundberg, 1923): only Stewart & Rogoff (1923) found no difference in the effects of insulin in normal and adrenalectomized rabbits, but they used doses of insulin convulsant for normal animals-in these experiments cortisone was not given; Crandall & Cherry (1939) gave occasional doses of cortical extract to their dogs; Sundberg (1923) mentions that some of his rabbits had cortical transplants; (c) after hexamethonium in dogs (Schachter, 1951) and in rabbits (Laurence & Stacey, 1952). It has therefore been generally accepted in the past that adrenaline release is responsible for, or at least assists in, restoring low blood sugar towards normal levels, although it is recognized that recovery from insulin hypoglycaemia does not require the presence of the adrenal medulla (Peters & Van Slyke, 1946).…”