Page 453 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid and Electrolyte Disturbances In Gastrointestinal and Pancreatic Disease 441

of the enterocyte in the villus or crypt is also important: difference across the epithelium. 120 This negative poten-
þ
villus enterocytes absorb, whereas crypt enterocytes tial difference attracts K into the intestinal lumen, and
secrete. consequently the concentration of K is always higher
þ
in intestinal contents than in plasma. In the jejunum, sol-
Jejunum vent drag created by glucose and amino acid transport
40

Because of the high permeability of the jejunum, passive causes passive absorption of Cl and HCO 3 .
transport processes make a major contribution to overall
þ
Na and Cl movement in this segment of the intestinal Ileum

þ

tract. Absorption is driven by Na and Cl uptake (which The predominant form of Na absorption in the ileum is
þ
in turn drives water uptake) via two linked transporters, a neutral NaCl absorption (see Figure 18-6) with some con-
þ
þ

Na -H þ exchanger and a Cl -HCO 3 exchanger (see tribution by Na -nutrient absorption. The contents of
Figure 18-3). 40 These two transporters take up Na þ the ileum and colon are normally alkaline. 33,123 Solvent
and Cl from the gut lumen and secrete H þ and drag-mediated passive absorption of Cl and HCO 3

HCO 3 into the lumen. 40 In humans, the Cl -HCO 3 does not occur in the ileum and colon, but a Cl -
exchanger in the small intestine is the “downregulated HCO 3 exchange mechanism is present. 40 Bicarbonate
in adenoma” (DRA) gene product, which generates an is secreted by electrogenic and electroneutral processes
alkaline solution. DRA is now known to be abundantly in the duodenum, ileum, and colon. Being a metabolic
expressed in colonocytes, but not enterocytes, and product, intracellular HCO 3 can arise from intracellular

120
transports more than 2 Cl ions to 1 HCO 3 ion. metabolism,diffusion ofCO 2 or the action of transporters
þ

Transport of many hydrophilic nutrients including glu- such as the basolateral Na -HCO 3 cotransporter. 120
cose, amino acids, and some vitamins occurs against con-
centration gradients by secondary active transport across Colon
þ
the luminal membrane and by facilitated diffusion across Absorption of Na in the colon is achieved against a large
the basolateral membrane. 120 The luminal membranes electrochemical gradient (see Figure 18-6) and is princi-
of the epithelial cells in this region contain sodium- pally a result of active Na þ transport. 38 Colonic Na þ
dependent transporters for hexose sugars and amino acids absorption is also influenced by mineralocorticoids
(see Figure 18-6). Sodium enters the epithelial cell down (e.g., aldosterone). 40 Mineralocorticoids increase the
its concentration gradient and is the driving force for activity of Na þ channels in the luminal membranes of
accumulation of the nutrient intracellularly. Glucose colonic epithelial cells and may increase Na ,K -ATPase
þ
þ
and glutamine supply energy. The entry of sodium and in the basolateral membranes. The colonic epithelium
glucose promotes water absorption. Sodium then is contains K channels and is capable of active potassium
þ
extruded from the cell at the basolateral membrane by transport (see Figure 18-3). 40 Absorption of potassium
þ
þ
Na ,K -ATPase while the hexose sugar or amino acid is thought to be accomplished by means of a K -ATPase
þ
diffuses out of the cell at the basolateral membrane down with characteristics similar to those of both basolateral
a favorable concentration gradient. Therefore Na ,K - membrane Na ,K -ATPase and parietal cell H ,K -
þ
þ
þ
þ
þ
þ
ATPase drives net absorption of both Na and the sugar ATPase. 10,120 The concentration of K þ in colonic
þ
or amino acid. Proteins that function as Na -H þ contents is high because of the high potential difference
þ
exchangers are present in the luminal membranes of the generated and can approach 90 mEq/L. 38 Active K þ
þ
þ
þ
þ
enterocytes in the jejunum and allow absorbed Na to secretion is mediated by Na ,K -ATPase or by Na -

þ
be exchanged for intracellular H þ (see Figures 18-3 K -2 Cl cotransport. Aldosterone and cyclic adenosine
and 18-6). This exchange is driven by both the electro- monophosphate (cAMP) increase luminal K þ conduc-
þ
þ
chemical gradient for Na and a pH gradient that results tance and stimulate secretion of K (see Figure 18-6). 10
120
from a moderately acidic intracellular environment. As Colonic absorption is important in small-intestinal disease
Na is extruded at the basolateral membrane by Na K - because the colon may compensate for fluid losses
þ
þ
þ
ATPase, HCO 3 also moves out of the cell, resulting in associated with small-bowel dysfunction. Alternatively,

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net absorption of sodium bicarbonate. Although Na - patients with small-bowel dysfunction may have signs of
þ
nutrient absorption and Na -HCO 3 absorption occur large-bowel disease. This is thought to result from

in the jejunum as already described, solvent drag- impairment of colonic absorption or stimulation of
mediated Na absorption secondary to monosaccharide colonic secretion by products of abnormal small-intestinal
þ
þ
absorption is the major mechanism for Na absorption function, such as hydroxylated fatty acids or deconjugated
in this segment. bile acids.
Movement of K in the intestinal tract follows its elec- The primary anions in the colon are short-chain fatty
þ
trochemical gradient, and secretion generally acids, which are generated by bacterial metabolism of
þ
predominates. 120 In the small intestine, most K secre- carbohydrate and protein. 120 Some of the organic anions
tion is passive (a luminal K channel is lacking) and results are absorbed by a linked HCO 3 exchange transporter
þ
from the generation of a lumen-negative potential (see Figure 18-3). These short-chain fatty acids include