Fluid
balance within the body is maintained via homeostatic mechanisms (1). The body
maintains a constant state of dynamic equilibrium, fluids can shift back
and forth for redistribution upon demand, but it has a strict limit on how
much volume and concentration changes it will allow. The body tries to
maintain the exact volume in all 3 of the interior spaces.
Thirst and hunger drives helps the body regulate net
body water balance from day-to-day. Neuroendrocrine responses, renal mechanisms
and non-regulatory social behavioral factors also help regulate water balance
(2).
Water is stored in the intracellular compartment (60%)
and in the extracellular compartment (40%). The extracellular is subdivided
into the intravascular and interstitial fluid compartments. Of those 40% of the
extracellular space, 20% of the water is found in the intravascular compartment
and 80% is found in the interstitial compartment.
Movement across these compartments is regulated by
changes in Starling forces, which include oncotic (due to proteins) and
hydrostatic pressures. In the extracellular compartment, changes in sodium concentrations alter the total extracellular fluid while plasma proteins diffuse slowly across
the capillary endothelium and changes the fluid distribution: an increase in plasma proteins increases oncotic pressure and favors fluid
movement into the plasma, whereas plasma protein escape increases interstitial
fluid (3).
When there an acute plasma volume loss, capillary
fluid dynamics or Starling forces adjust to favor plasma proteins and fluid
movement out of interstitial and into vascular compartments, thereby
selectively restoring plasma volume. The reason why sodium and other electrolytes
are not as effective is because they freely diffuse across capillary
endothelium, and this is also why sodium content is more effective at changing
the total extracellular fluid (3).
The measurement of transcapillary escape of albumin
from the plasma is an important indicator of the oncotic force within the
plasma: a lower transcapillary escape of albumin is usually associated with an
increase in plasma albumin content and plasma oncotic pressure (3).
Water (and sodium)
must be constantly supplied for cardiovascular function. Plasma volume and osmolality
must be maintained within set limits. This is accomplished by the release of
hormones necessary to ingest and conserve water and sodium within the body.
An increased osmolality draws water from cells into the blood thus dehydrating specific brain osmoreceptors that stimulate drinking and release of anti-diuretic hormone (ADH or vasopressin).
ADH reduces water loss via lowered
urine volume (1).
Extracellular
dehydration (hypovolaemia) stimulates specific vascular receptors that signal brain
centres to initiate drinking and ADH release. Baro/volume receptors in the kidney stimulate the release of the enzyme renin that starts a cascade of events to produce angiotensin II (AngII), which initiates
also drinking and ADH release (1). This stimulates also aldosterone release which reduces
kidney loss of urine sodium.
Both AngII and ADH are vasoactive hormones
that could work to reduce blood vessel
diameter around the remaining blood. All these events work in concert so
that the cardiovascular system can maintain a constant perfusion pressure, especially
to the brain. Even if drinking does not take place ADH, AngII and aldosterone
are still released (1).
Normal
thirst mechanism with minimal drinking
makes vasoconstriction permanent rather than temporary, and makes the body
excrete small volumes of concentrated urine, this is why it looks darker when
you are dehydrated (see Hydration: assessing
hydration status).
In turn a normal hydration state with drinking makes
you excrete large volume of dilute urine.
Balance in the intracellular space is critical for
cell function and performance. Cells need water for organelles within them, and
for thousands of metabolic reactions that occur every second. This space is very finely tuned.
The body can also shrink the intravascular space when there’s not enough blood inside the
arteries, to maintain normal blood pressure. In case of dehydration (or
bleeding), the vascular space can use the muscles in the vessel walls to
contract, so that the total vascular space is temporarily smaller to maintain
blood pressure and blood flow for some time.
Some factors influence fluid balance, for example heat
and humidity. The body releases water through sweat to cool the
temperature, however sweat does not evaporate when the humidity is high,
so the body produces even more sweat. Low humidity is also dehydrating.
Airplane
travel can also contribute to excess fluid loss, the relative humidity in the cabin gradually
falls on high altitude and during prolonged flights (4), it's essentially 0%
humidity in a pressurized cabin. This low
humidity can cause increases in mean plasma osmolarity, mean urine
osmolarity and urine specific gravidity, indicating dehydration (5). Some
symptoms are the drying of the skin,
mucous membranes, and dry eyes present after 3-4 hours of flight (6).
However we are not losing water through sweating or exercising, but through breathing.
The kidneys play a major role in maintaining
homeostasis by helping to preserve the
constancy of the internal fluid. They excrete the products of bodily
metabolism (waste products). Each kidney has over one million microscopic
functional units known as nephrons, they are the smallest unit within
the kidney enabling it to produce its functions.
The kidney have three processes involved in forming
urine:
1.
Glomerular filtration;
2. Tubular
reabsorption;
3. Tubular
secretion.
References:
1. Thornton SN (2010). Thirst and hydration:
physiology and consequences of dysfunction. Physiol Behav 100, 15–21.
2. Michael N. Sawka,
PhD, Samuel N. Cheuvront, PhD, RD, and Robert Carter III, PhD, MPH. Human Water Needs. 2005 International Life Sciences Institute doi: 10.1301/nr.2005.jun.S30–S39
3. Nina S. Stachenfeld. Sex Hormone Effects on Body Fluid Regulation. Exerc Sport Sci Rev. 2008 Jul; 36(3): 152–159.
4. Sandor T. Travel thrombosis: Pathomechanisms and
clinical aspects. Pathophysiology. 2008;15(4):243–52.
5. Simons R, Krol J. Jet leg, pulmonary embolism, and
hypoxia. Lancet. 1996;348(9024):416.
6. Nagda NL, Hodgson M. Low relative humidity and
aircraft cabin air quality. Indoor Air. 2001;11(3):200–14.
