protection to individuals during cold exposure and therefore have potential military application in specific settings.
Body fluid balance is normally held within a fairly narrow range by a wide range of control measures. Exposure to cold stress, however, typically leads to dehydration, with a cold-induced diuresis (CID) as a major, long recognized contributing factor that is accompanied by reduced blood and plasma volumes (see review by Freund and Sawka, Chapter 9 in this volume). Other contributing causes to dehydration in the cold include losses of body water through respiration and through sweating, as well as through a diminished intake of fluids.
The mechanisms of origin of cold-induced diuresis (CID) are not yet entirely clear. It is known that CID can be blocked by administration of antidiuretic hormone (ADH or vasopressin) (Bader et al., 1952; Eliot et al., 1949). Despite early evidence for lowered concentrations of this hormone in plasma of individuals exposed to cold, subsequent research failed to confirm its suspected etiologic role in CID (Lennquist et al., 1974). Later, cold-induced increases in blood pressure, leading to a diminished renal tubular reabsorption of sodium and water became a popular mechanistic explanation for CID (Wallenberg and Granberg, 1976). More recently, studies in humans have shown that repeated immersions in cold water produced an equal diuretic response each time; however, the hypertensive component was lost with the acclimation to cold water immersion (Muza et al., 1988; Young et al., 1987). Currently, the movement of water to the body core caused by cold-induced peripheral vasoconstriction is the most attractive explanation for CID. Hydration status and body posture (Wallenberg and Granberg, 1976) also appear to be confounding factors.
Losses of respiratory water may also contribute to cold-induced dehydration. Water vapor pressure of cold air is considerably less than under thermoneutral conditions, so additional water can be lost when exhaling fully