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Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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532<br />

Chapter | 17 Fluid, Electrolyte, and Acid-Base Balance<br />

the volume dilution procedure used. Regulation <strong>of</strong> ECF<br />

volume is a complex process in which a variety <strong>of</strong> factors<br />

interact. The ECF consists <strong>of</strong> all the fluids located outside<br />

the cells and includes the plasma (0.05 l/kg), interstitial<br />

fluid and lymph (0.15 l/kg), and the transcellular<br />

fluids ( Edelman and Leibman, 1959 ; Rose, 1984 ; Saxton<br />

and Seldin, 1986 ). The transcellular fluids, which include<br />

the fluid content <strong>of</strong> the gastrointestinal tract, are generally<br />

considered a subcomponent <strong>of</strong> the ECF. In small animal<br />

species, the fluid content <strong>of</strong> the gastrointestinal tract<br />

is relatively small ( Strombeck, 1979 ). In the large animal<br />

herbivore species, a substantial volume <strong>of</strong> fluid is normally<br />

present within the gastrointestinal tract. In the horse, this<br />

may amount to 30 to 45 l ( Carlson, 1979a ), and in cattle,<br />

the forestomach may contain as much as 30 to 60 l <strong>of</strong> fluid<br />

( Phillipson, 1977 ). During periods <strong>of</strong> water restriction and<br />

certain other forms <strong>of</strong> dehydration, this gastrointestinal fluid<br />

reservoir can be called on to help maintain effective circulating<br />

volume ( McDougall et al ., 1974 ). All <strong>of</strong> the fluids<br />

<strong>of</strong> the ECF contain sodium in approximate concentrations<br />

<strong>of</strong> 130 to 150 mEq/l H 2 O. Sodium provides the osmotic<br />

skeleton for the ECF, and the sodium content is the single<br />

most important determinant <strong>of</strong> ECF volume ( Rose, 1984 ).<br />

Sodium deficits result in decreases in ECF volume, whereas<br />

sodium excess is most <strong>of</strong>ten associated with water retention<br />

and results in edema ( McKeown, 1986 ; Rose, 1984 ).<br />

C . Intracellular Fluid Volume<br />

The ICF volume represents the fluid content within the<br />

body’s cells. This volume cannot be measured directly but<br />

is calculated as the difference between the measured TBW<br />

and the measured ECF volume. Potassium provides the<br />

osmotic skeleton for the ICF in much the same way that<br />

sodium provides the osmotic skeleton for the ECF. Because<br />

water is freely diffusible into and out <strong>of</strong> the cell, changes<br />

in the tonicity <strong>of</strong> the ECF are rapidly reflected by similar<br />

changes in ICF tonicity ( Saxton and Seldin, 1986 ). This is<br />

largely the result <strong>of</strong> the movement <strong>of</strong> water across the cell<br />

membrane with resultant changes <strong>of</strong> ICF volume. Thus,<br />

whereas plasma sodium concentration decreases in response<br />

to water retention, ICF volume increases ( Humes, 1986 ).<br />

On the other hand, with water depletion resulting in hypernatremia,<br />

ICF volume decreases ( Humes, 1986 ). Relatively<br />

little is known about the organization <strong>of</strong> intracellular water<br />

into the various subcellular compartments and organelles.<br />

IV . REGULATION OF BODY FLUIDS AND<br />

ELECTROLYTES<br />

A . Effective Circulating Volume<br />

The effective circulating volume refers to that part <strong>of</strong> the<br />

ECF that is within the vascular space and is effectively<br />

perfusing the tissues ( Rose, 1984 ). Effective circulating<br />

volume tends to vary with ECF volume, and both parameters<br />

vary with the total body sodium stores ( Rose, 1984 ).<br />

Sodium loading produces volume expansion, whereas<br />

sodium depletion leads to volume depletion.<br />

Effective circulating volume is not a quantitatively measurable<br />

entity but refers to the rate <strong>of</strong> perfusion <strong>of</strong> the capillary<br />

circulation. Effective circulating volume is maintained<br />

by varying vascular resistance, cardiac output, as well as<br />

renal sodium and water excretion ( Rose, 1984 ). Decreases<br />

in effective circulating volume result in decreased venous<br />

return, decreased cardiac output, and decreased blood pressure.<br />

Decreased volume and pressure are recognized by<br />

special volume receptors in the cardiopulmonary circulation<br />

and kidney, which trigger increased sympathetic tone<br />

resulting in increased arterial and venous constriction as<br />

well as increased cardiac contractility and heart rate. These<br />

responses tend to correct for the volume deficit by increasing<br />

cardiac output and systemic blood pressure. Volume and<br />

pressure changes associated with decreases in effective circulating<br />

volume also result in activation <strong>of</strong> the renin-angiotensin<br />

system with subsequent enhancement <strong>of</strong> aldosterone<br />

secretion by the adrenal cortex ( Brobst, 1984 ). Aldosterone<br />

acts to enhance renal sodium resorption, which is a critical<br />

factor for maintaining and eventually restoring effective circulating<br />

volume. Additional factors that influence sodium<br />

resorption in response to changes in fluid volume include<br />

alterations in glomerular filtration rate, renal hemodynamics,<br />

atrial natriuretic factor, and plasma sodium concentration.<br />

B . Antidiuretic Hormone<br />

Antidiuretic hormone (ADH) plays a primary role in the<br />

regulation <strong>of</strong> the osmolality <strong>of</strong> the body fluids. Antidiuretic<br />

hormone is synthesized in the hypothalamus, stored in the<br />

neurohypophysis, and released in response to changes in<br />

plasma osmolality. Because sodium concentration is the<br />

primary determinant <strong>of</strong> plasma osmolality, ADH-release is<br />

closely correlated to plasma sodium concentration. Special<br />

sensors in the hypothalamus recognize increases in plasma<br />

osmolality, and the normal response is increased thirst<br />

to enhance water intake and the release <strong>of</strong> ADH, which<br />

increases water reabsorption by the renal collecting tubules.<br />

Antidiuretic hormone exerts its activity on the collecting<br />

tubules by activating adenyl cyclase; this results in the generation<br />

<strong>of</strong> cyclic adenosine monophosphate (cyclic AMP)<br />

and protein kinases, which in turn alter the permeability <strong>of</strong><br />

the tubules to water ( Rose, 1984 ). Antidiuretic hormone also<br />

is released in response to decreases in effective circulating<br />

fluid volume, although the renin-angiotensin system exerts<br />

primary control over volume changes. Antidiuretic hormone<br />

acts extrarenally as an arterial vasoconstrictor, thus increasing<br />

blood pressure. Plasma osmolality decreases in response<br />

to a water load, and ADH release is inhibited. The resultant<br />

reduction in ADH-mediated reabsorption <strong>of</strong> water in the collecting<br />

tubules allows for appropriate renal excretion <strong>of</strong> the<br />

water load and a return <strong>of</strong> plasma osmolality toward normal.

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