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Title: Urinary excretion of water and electrolytes during open-sea saturation diving to 850 fsw. Author: Neuman TS, Goad RF, Hall D, Smith RM, Claybaugh JR, Hong SK. Journal: Undersea Biomed Res; 1979 Sep; 6(3):291-302. PubMed ID: 524529. Abstract: The dive was carried out in the open sea to a depth of 850 fsw (26.7 ATA) for 6 days (DD 1--6) in the saturated mode, with personnel transfer capsule (PTC) excursions between 0 and 150 fsw and diver excursions between 0 and 50 fsw from the saturation base. Each diver had two excursion dives on alternate days. Although each PTC excursion lasted approximately 7 h, the actual time spent in the water averaged 10.5 min per diver. For 12 divers, daily excretion of water, electrolytes, aldosterone, and antidiuretic hormone (ADH) was studied, along with plasma composition (including prolactin), before, during, and after hyperbaric exposure. A significant increase in urine flow was observed on DD2--4 (1604 ml/day predive vs. 2300 ml/day on DD 4; P less than 0.05), after which the degree of diuresis decreased to about 1800 ml/day. Urine osmolality changed inversely with urine flow, with the lowest value of 532 mOsm/kg on DD 4. During the postdive period, both urine flow and urine osmolality returned to the predive level. The endogenous creatinine clearance was maintained at about 200 liters/day throughout the dive. The fractional excretion of Na+ remained unchanged while that of K+ increased significantly during hyperbaric exposure, thus decreasing the urinary Na+/K+ ratio. The fractional excretion of total osmotic substances showed a small hyperbaric exposure. Body weight decreased progressively during the initial 4 days of pressure exposure, equalling 2.6 kg on DD 4. These findings suggest that the observed diuresis may be accompanied by a net loss of body water. Neither the plasma prolactin level nor urinary excretion of aldosterone and ADHshowed any consistent change throughout the dive. It thus appears that, although there is a small osmotic component, the observed diuresis is primarily due to the ADH-independent inhibition of fre water reabsorption from the collecting duct by means of a mechanism yet to be identified.[Abstract] [Full Text] [Related] [New Search]