Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.

In 11 untreated and 6 oestrogen-treated Turner's syndrome patients, the changes in the serum growth hormone level were studied following the induction of hypoglycaemia with insulin. The growth hormone was measured with a radioimmune assay technique. The growth hormone peak value measured in healthy females was 54.32 +/- 17.17, in untreated Turner's syndrome was 14.90 +/- 3.71, and in oestrogen-treated Turner patients was 33.38 +/- 9.22 microU/ml (average +/- standard error). On the basis of the results, a role is attributed to the decreased growth hormone reserve in the low growth of Tuner's syndrome patients.

Experiments are reported to determine whether in the rat decreased content of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system influences the oliguric phase which develops following destruction of the pituitary stalk. It was found that if on the day following destruction of the stalk the animals were neurohypophysectomized, the oliguric phase did not develop. The transitory water retention also did not occur when the stalk was destroyed in rats deprived of water for 8 days before the operation. No oliguric phase developed in totally hypophysectomized rats, or in those which had been neurohypophysectomized.The evidence obtained seemed to indicate that in the development of transient water retention following destruction of the hypophysial stalk, ADH released from the degenerating hypothalamo-neurohypophysial system has an important role.

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