996
UNIT 4
Maintenance of the Body
26
Hypotonic Hydration
Declining ECF osmolality sets several compensatory mecha-
nisms into motion. ADH release is inhibited, and as a result,
less water is reabsorbed and excess water is quickly flushed
from the body in urine. But, when there is renal insufficiency
or we drink an extraordinary amount of water very quickly, a
type of cellular
overhydration
called
hypotonic hydration
may
occur. In either case, the ECF is diluted—its sodium content is
normal, but excess water is present. For this reason, the hall-
mark of hypotonic hydration is
hyponatremia
(low ECF Na
1
concentration), which promotes net osmosis into tissue cells,
causing them to swell as they become abnormally hydrated
(Figure 26.7b).
Hypotonic hydration leads to severe metabolic disturbances
evidenced by nausea, vomiting, muscular cramping, and cere-
bral edema. It is particularly damaging to neurons. Uncorrected
cerebral edema quickly leads to disorientation, convulsions,
coma, and death. Indeed, several marathon runners have died
of overhydration a±er drinking too much water. Sudden and
severe hyponatremia is treated by administering intravenous
hypertonic saline to reverse the osmotic gradient and “pull” wa-
ter out of the cells.
Edema
Edema
(ĕ-de
9
mah; “a swelling”) is an atypical accumulation of
fluid in the interstitial space, leading to tissue (but not cell) swell-
ing. Unlike hypotonic hydration, which increases the amount of
fluid in all compartments due to an imbalance between water
intake and output, edema is an increase in volume of
only
the IF.
It may be caused by any event that steps up the flow of fluid out
of the blood or hinders its return.
Factors that accelerate fluid loss from the blood include
increases in capillary hydrostatic pressure and permeability.
Increased capillary hydrostatic pressure can result from incom-
petent venous valves, localized blood vessel blockage, conges-
tive heart failure, or high blood volume. Whatever the cause,
the abnormally high capillary hydrostatic pressure intensifies
filtration at the capillary beds.
Increased capillary permeability is usually due to an ongo-
ing inflammatory response. Recall from p. 767 that inflamma-
tory chemicals cause local capillaries to become very porous,
allowing large amounts of exudate (containing not only clotting
proteins but also other plasma proteins, nutrients, and immune
elements) to form.
Edema caused by hindered fluid return to the blood usually
reflects an imbalance in the colloid osmotic pressures on the
two sides of the capillary membranes. For example,
hypopro-
teinemia
(hi
0
po-pro
0
te-ĭ-ne
9
me-ah), a condition of unusually
low levels of plasma proteins, results in tissue edema because
protein-deficient plasma has an abnormally low colloid osmotic
pressure. Fluids are forced out of the capillary beds at the arte-
rial ends by blood pressure as usual, but fail to return to the
blood at the venous ends. As a result, the interstitial spaces be-
come congested with fluid. Hypoproteinemia may result from
protein malnutrition, liver disease, or
glomerulonephritis
(in
Stimulates
Stimulates
Releases
Targets
Effects
Results in
ECF osmolality
Na
+
concentration
in plasma
Osmoreceptors
in hypothalamus
Antidiuretic
hormone (ADH)
Collecting ducts
of kidneys
ECF osmolality
Plasma volume
Negative
feedback
inhibits
Posterior pituitary
Water reabsorption
Scant urine
ADH
Inhibits
Stimulates
Plasma volume
(5 –10%),
BP
Baroreceptors
in atria and
large vessels
Figure 26.6
Mechanisms and consequences of ADH release.
(Vasoconstrictor effects of ADH are not shown.)
from the cells into the ECF
(Figure 26.7a)
. Tis water movement
equalizes the osmolality of the extracellular and intracellular flu-
ids even though the total fluid volume has been reduced.
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