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    44-46 Water metabolism

    44-46 Water metabolism

    Water metabolism

    WATER METABOLISM

     

    ID44. Extracellular water. (%)

    ID45. Cellular water. (%)

    ID46. Total water. (%)

    Water is the most abundant molecule in the human body that undergoes continuous recycling. Numerous functions have been recognized for body water, including its function as a solvent, as a means to remove metabolic heat, and as a regulator of cell volume and overall function. Tight control mechanisms have evolved for precise control of fluid balance (less than 1%) by a physiologic control system located in the hypothalamus, indicative of its biological importance. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake.247

    Water movement in the gastrointestinal tract is regulated by osmotic gradients and is linked to ionic movements. Specifically, absorption of water is linked primarily to the movement of sodium ions, whereas secretion is linked to the movement of chloride ions.238

    The distribution of the total body water in mammals between the intracellular compartment and the extracellular compartment, which is, in turn, subdivided into interstitial fluid and smaller components, such as the blood plasma, the cerebrospinal fluid (CSF) and lymph:241

           

    A general problem in the study of water as a nutrient is that there is a scarcity of studies examining the effect of long-term water deficiency and its complications in the human body. Acute mild dehydration (a 4% change in body weight) provokes unfavourable effects on cardiovascular function as plasma volume drops. These effects include an increase in stroke volume and a concomitant increase in heart rate, to maintain constant cardiac output.239

    In the periphery, dehydration decreases skin blood flow and sweating, thus compromising thermoregulation and increasing body core temperature.240 However, these levels of water deficiency are fixed rapidly by a decrease in body water loss and the stimulation of thirst. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone arginine vasopressin (AVP). Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 μU per ml have major effects on urine osmolality and renal water handling.247

    Elevated water.

    Most nutrients display toxicity if their intake exceeds a critical threshold that represents the tolerable upper intake level. For water, no such threshold has ever been established, assuming that the functioning kidney removes the excess fluid. However, in some circumstances, massive fluid intake may indeed provoke toxicity. In psychiatric patients, particularly those with schizophrenia, polydipsia (excess intake of fluids) occurs frequently and may lead to dilutional hyponatremia, a condition also known as water intoxication. Although this kind of hyponatremia is usually associated with an inability to excrete water because of kidney and/or antidiuretic hormone disturbances, some patients are reported to drink such a large fluid volume that they exceed the ability of the kidney to excrete water.242 This kind of hyponatremia leads to brain edema, causing neurological symptoms such as nausea, vomiting, delirium, ataxia, seizures, and coma, which in turn worsen the psychiatric symptoms of these patients.243 Water intoxication with hyponatremia may also appear in many other clinical conditions accompanied by a primary defect in the renal excretion of free water and a subsequent expansion of extracellular fluid, but these cases are not related to fluid consumption.244

    An interesting condition of water intoxication is exertional hyponatremia, occurring in some athletes during long ultra-endurance events (>3 hours). This type of water toxicity is associated with a fluid intake during exercise that exceeds fluid losses via the sweat without a concomitant replacement of sodium lost.245 Decreased free water clearance from the kidney, because of redistribution of cardiac output to the active muscle and the skin capillary bed, as well as inappropriate secretion of antidiuretic hormone may contribute to this kind of water toxicity.246 However, no adverse effects have been reported as a result of chronically high intakes of fluids when intake approximates losses.

    Important note: The extracellular water in the software USPIH does not include CSF and plasma. Therefore, total water (ID46) may not be equal to the sum of intracellular (ID45) and extracellular (ID44) fluid from the list.

    238.   Martínez-Augustin O, et al. Molecular bases of impaired water and ion movements in inflammatory bowel diseases. Inflamm Bowel Dis. 2009 Jan;15(1):114-27. doi: 10.1002/ibd.20579

    239.   González-Alonso J, et al. Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J Appl Physiol (1985). 1997 Apr;82(4):1229-36. doi: 10.1152/jappl.1997.82.4.1229

    240.   G. C. Pitts, R. E. Johnson, and F. C. Consolazio. WORK IN THE HEAT AS AFFECTED BY INTAKE OF WATER, SALT AND GLUCOSE. 1944, https://doi.org/10.1152/ajplegacy.1944.142.2.253

    241.   Khmelevsky YuV, Usatenko OK. Basic Biochemical Human Constants in the Norm and Pathology. Kiyv, 1984, [in Russian]

    242.   LANGGARD H, SMITH WO. Self-induced water intoxication without predisposing illness. N Engl J Med. 1962 Feb 22;266:378-81. doi: 10.1056/NEJM196202222660803

    243.   de Leon J, Verghese C, Tracy JI, Josiassen RC, Simpson GM. Polydipsia and water intoxication in psychiatric patients: a review of the epidemiological literature. Biol Psychiatry. 1994 Mar 15;35(6):408-19. doi: 10.1016/0006-3223(94)90008-6

    244.   Weitzman RE, Kleeman CR. The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. West J Med. 1980 Jan;132(1):16-38

    245.   Costas A. Anastasiou, et al. Sodium Replacement and Plasma Sodium Drop During Exercise in the Heat When Fluid Intake Matches Fluid Loss. J Athl Train (2009) 44 (2): 117–123. https://doi.org/10.4085/1062-6050-44.2.117

    246.   Armstrong LE, Casa DJ, Watson G. Exertional hyponatremia. Curr Sports Med Rep. 2006 Sep;5(5):221-2. doi: 10.1097/01.csmr.0000306418.01167.46.

    247.   Richard E. Weitzman , et al. The Clinical Physiology of Water Metabolism. Part I: The Physiologic Regulation of Arginine Vasopressin Secretion and Thirst. West J Med. 1979 Nov; 131(5): 373–400.

     

     

    Published on 26 April 2024