The regulation of antidiuretic hormone release in man: I. Effects of change in position and ambient temperature on blood ADH levels.

It has been postulated that alterations in the intravascular distribution of blood affect antidiuretic hormone (ADH) secretion in man. The studies reported here were designed to alter blood distribution by thermal and by positional change to test this thesis.HUMAN BLOOD ADH LEVELS HAVE BEEN SHOWN TO VARY WITH POSITION: a mean value of 0.4 +/- 0.6 (SD) muU/ml was obtained while the subject was supine, a value of 1.4 +/- 0.7 muU/ml while sitting, and 3.1 +/- 1.5 muU/ml while standing. In 79 control subjects, sitting comfortably for 30 min in a normal environment, a blood ADH level of 1.65 +/- 0.63 muU/ml was found. It is suggested that subjects assume this position during experiments in which blood is drawn for measurement of ADH levels.In eight seated subjects the ADH level rose from 1.6 +/- 0.4 to 5.2 +/- 0.8 muU/ml after a 2 hr exposure at 50 degrees C and fell to 1.0 +/- 0.26 muU/ml within 15 min at 26 degrees C.Six subjects with a mean ADH level of 2.2 +/- 0.58 muU/ml sat quietly in the cold (13 degrees C) for 1 hr, and the ADH level fell to 1.2 +/- 0.36 muU/ml. After 15 min at 26 degrees C, the level rose to 3.1 +/- 0.78 muU/ml. The serum sodium and osmolal concentrations remained constant during all studies.Water, sodium, and total solute excretion decreased during exposure to the heat, whereas the urine to plasma (U/P) osmolal ratio increased. During cold exposure, water, sodium, and total solute excretion increased, and there was a decrease in the U/P osmolal ratio.These data are interpreted as indicating that changes in activity of intrathoracic stretch receptors, in response to redistribution of blood, alter ADH secretion independently of changes in serum osmolality. The rapidity of change of blood ADH concentration indicates a great sensitivity and a prime functional role for the "volume receptors" in the regulation of ADH secretion.

Inflammatory meningeal masses of unexplained origin. An ultrastructural and immunological study.

Two patients with inflammatory meningeal masses were studied. Lesions in both patients showed varying proportions of meningothelial and inflammatory components. The non-neoplastic nature of the inflammation was confirmed in one case by lymphocyte surface marker study, which showed T and B cells in one to four ratio, and by immunohistochemistry, which revealed polyclonal plasma cells. The abundant histiocytes contained muramidase and often enclosed intact lymphocytes or plasma cells within their cytoplasm, i.e., emperipolesis. Their surfaces bore slender interdigitating pseudopodia, intercellular junctions, and subplasmalemmal linear densities. The derivation of these histiocytes is uncertain: mononuclear phagocytes, meningothelial cells, and multipotential meningeal cells are all possible progenitors. A comparison with eleven similar reported cases reveals a tendency for inflammatory meningeal masses to occur in the young, as well as a predilection for posterior fossa involvement. They resemble the extranodal lesions of sinus histiocytosis with massive lymphadenopathy, as well as plasma cell granulomas or inflammatory pseudotumors of lung and other tissues. However, it is possible that these lesions represent a variant of meningioma in which an unusual immunological response has been evoked.

Neurologic signs in senescence.

We examined 2,029 volunteers 50 to 93 years of age in a cross-sectional study of nine bedside neurologic tests to determine the frequency of "abnormal" responses in uncomplicated aging (senescence). Rates of abnormal responses remained constant until age 70 years, after which they increased significantly. The number of abnormal signs per subject also increased, especially over 70 years of age. These results provide normative data against which these signs may be compared when applied as a clinical screening battery for diffuse cerebral dysfunction.