Immersion diuresis without expected suppression of vasopressin

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20–35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersionexperiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at theend of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed whenthere is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.

Hypervolemia and plasma vasopressin response during water immersion in men

To investigate changes in plasma volume (PV) and osmolality as stimuli for plasma vasopressin (PVP) suppression and diuresis, seven normal healthy men (22-48 yr) were immersed to the neck for 4 h in a sitting position in tap water (34.5 degrees C) after overnight food and fluid restriction. Mean +/- SE urine volume was 823 +/- 123 ml/4 h; fluid intake was 400 ml/4 h, and mean negative water balance was 944 ml/4 h. Urinary sodium excretion increased from 0.77 to 1.25 mosmol/min (P less than 0.05) and UNaV from 0.14 to 0.37 meq/min (P less than 0.05). During immersion, PV (T-1824) increased by 8.8% (P less than 0.05) during the first 30 min and declined linearly thereafter. Mean +/- SD serum osmolality (294 +/- 1.2 mosmol/kg H2O) and sodium (143.2 +/- 0.4 meq/l) were constant throughout immersion; PVP (2.3 +/- 0.5 pg/ml) and plasma renin activity [0.3 +/- 0.2 ng ANG I/(ml X h]) were not significantly changed. Thus, the composition of the fluid entering the vascular space maintained constant serum osmolality and PVP throughout immersion. These findings do not support the hypothesis that acute expansion of central volume and PV cause suppression of PVP. The results suggest a mechanism other than or in addition to PVP suppression as a contributory cause of the immersion diuresis.

Fluid shifts during initial phase of immersion diuresis in man

The object was to study fluid shifts in man during the 1st h of immersion diuresis. Control experiments were done on subjects lying down in air for 4 h with and without vasopressin. During immersion up to the neck, seven of nine subjects had significant diuresis and natriuresis. In the first 20 min of sitting in 33 degress C water, a hemodilution of 2% of blood volume was observed. As diuresis progressed, hemoconcentration began. When vasopressin was given just before immersion to prevent the diuresis, the hemodilution observed was greater and lasted longer. Thus the hematocrit fell by 1.7 U, plasma osmolality by 6.0 mosmol/kg, plasma proteins by 0.33 g/100 ml, and plasma sodium by 5.0 meq/l. We conclude that a hemodilution of about 4% of blood volume occurs during the early plasma of immersion and the degree of hyposmolality observed suggests that the fluid shifted was more hyposmotic than the interstitial fluid alone, possibly because some intracellular water may have shifted into the bloodstream during immersion.

Immersion diuresis in dogs

The mechanism of diuresis during the 1st h of immersion was investigated using anesthetized dogs. Four different experiments were carried out. First, left atrial transmural pressure was measured before, during, and after immersion. The data suggest that, although the left atrium may or may not be stretched depending on the conditions of immersion, the amount of diuresis is independent of the amount of left atrial stretch, and therefore a causal relationship between diuresis and left atrial stretch could not be established. Second, bilateral cervical vagotomy was carried out. Immersion diuresis sometimes occurred despite this vagotomy, suggesting that the left atrial stretch reflex was not participating in those cases. Third, negative-pressure breathing was carried out to simulate the negative transthoracic pressure associated with uncompensated immersion. The average left atrial transmural pressure did not change. A slight hemodilution and a moderate diuresis occurred. There was no correlation between changes in left atrial transmural pressure and changes in urine ouput. Fourth, blood studies were done on splenectomized dogs subjected to immersion. Hemodilution occurred and was most marked in dogs which had had their kidneys removed. The hemodilution is sufficient to explain the early phase of the immersion diuresis. The data suggest that, in anesthetized dogs, hemodilution is the probable initiator of diuresis upon immersion and that, in dogs, left atrial stretch is unrelated to diuresis during immersion or negative-pressure breathing.