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The effect on ruminal motility of NH4- or Na-acetate and Na- or K-lactate of various pH and doses infused into the jugular vein (i.v.) or carotid artery (i.a.) was studied in sheep with ruminal fistula I.v. infusion of NH4-acetate whenever it was accompanied by a considerable increase of the blood NH4 level potently inhibited the amplitude and frequency of ruminal contractions. I. a. administration produced more rapid and more apparent responses and a slightly elevated venous ammonia concentration than did the i.v. infusion. Thus the augmented blood ammonia level not only affected the smooth muscles and peripheral nerve endings but also inhibited the vegetative centres of the central nervous system. Infusion of Na-acetate and Na- or K-lactate solutions induced compensated acidosis or alkalosis which reduced the amplitude of ruminal contractions and produced respiratory disturbances. The latter were more apparent in alkalosis. In uncompensated acidosis or alkalosis, ruminal motility was permanently inhibited or abolished. The results appear to show that in not properly fed ruminants the frequently observed and long lasting compensated acidosis or alkalosis might influence the activity of the vegetative centres thus further metabolic disturbances and impaired gastrointestinal activity might follow the shifts in acid-base equilibrium.

Alkalemia (pH greater than 7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3- greater than 24 mEq/L, PCO2 greater than 30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis (PCO2 less than 30 mm of Hg, HCO3- less than 24 mEq/L); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dogs had double or triple acid-base abnormalities. Dogs with metabolic alkalosis had a preponderance of clinical signs associated with gastrointestinal disorders (10 dogs). Overzealous administration of sodium bicarbonate or diuretics, in addition to anorexia, polyuria, or hyperbilirubinemia may have contributed to metabolic alkalosis in 8 of the dogs. Most of the dogs in this group had low serum K+ and Cl- values. Two dogs with metabolic alkalosis had PCO2 values greater than 60 mm of Hg, and 1 of these had arterial hypoxemia (PaO2 less than 80 mm of Hg). Treatments included replacement of fluid and electrolytes (Na+, K+, and Cl-), and surgery as indicated (8 dogs). Six dogs with respiratory alkalosis had a variety of airway, pulmonary, or cardiac disorders, and 3 of these had arterial hypoxemia. Two other dogs were excessively ventilated during surgery, and 1 dog had apparent postoperative pain that may have contributed to the respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Underlying principle for fluid therapy is the knowledge about distribution of body water (60% of body weight) into compartments: intra- and extracellular fluid (ICF, ECF) cover respectively one half, one sixth of the latter fills the intravascular system. According to the concentration of ions and molecules in the lost fluids, dehydration is classified into hypertone, hypotone and isotone. Clinical assessment and laboratory examination (PCV, hemoglobin, total protein, urine analysis, electrolyte and blood gas evaluation) are crucial features for determination of dehydration rate, acid-base and electrolyte imbalances. Derangements of body-fluid and electrolyte metabolism and their treatment are discussed. The quantity of fluids necessary for rehydration of the patient is calculated on the basis of clinical findings. Overhydration risk has to be considered more seriously in cats than dogs. Intravenous, subcutaneous, oral and intraperitoneal infusions are feasible. A survey to technical aspects and required instruments is presented in conclusion.

Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. Mixed acid-base disturbances may be suspected on the basis of findings obtained from the medical history, physical examination, serum electrolytes and chemistries, and anion gap. The history, physical examination, and serum biochemical profile may reveal disease processes commonly associated with acid-base disturbances. Changes in serum total CO2, serum potassium and chloride concentrations, or increased anion gap may provide clues to the existence of acid-base disorders. Blood gas analysis is usually required to confirm mixed acid-base disorders. To identify mixed acid-base disorders, blood gas analysis is used to identify primary acid-base disturbance and determine if an appropriate compensatory response has developed. Inappropriate compensatory responses (inadequate or excessive) are evidence of a mixed respiratory and metabolic disorder. The anion gap is also of value in detecting mixed acid-base disturbances. In high anion gap metabolic acidosis, the change in the anion gap should approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding an elevated anion gap, regardless of serum bicarbonate concentration, suggests metabolic acidosis. In some instances, elevated anion gap is the only evidence of metabolic acidosis. In patients with hyperchloremic metabolic acidosis, increases in the serum chloride concentration should approximate the reduction in the serum bicarbonate concentration. Significant alterations from this relationship also indicate that a mixed metabolic disorder may be present. In treatment of mixed acid-base disorders, careful consideration should be given to the potential impact of therapeutically altering one acid-base disorder without correcting others.

Ascites and renal dysfunction are often associated with decreased liver function and reflect the complex abnormalities of water, protein, electrolyte, and acid-base metabolism that may complicate severe liver disease. This article discusses the pathophysiology and management of ascites, polydipsia and polyuria, decreased renal function, and acid-base and electrolyte alterations that can complicate liver disease.

In 23 cats, urinary obstruction of 24 to 48 hours' duration caused marked azotemia, hyperphosphatemia, hyperkalemia, and metabolic acidosis. The metabolic acidosis was a consistent finding and was severe in all cats (venous pH, 7.11 +/- 0.09). Serum sodium and chloride were normal. Glycosuria was found in 17 (74%) of the cats. There was no clear difference in blood pH, serum chemical values, or electrolyte concentrations between cats obstructed 24 hours and those obstructed 48 hours or longer. At a mean of 8.4 hours after relief of obstruction, acid-base status was corrected to normal, using fluid replacement and sodium bicarbonate therapy. Blood urea nitrogen serum creatinine, and serum inorganic phosphorus improved significantly (P less than 0.01) at a mean of 19.5 hours after treatment. Variation in azotemia after fluid replacement suggested variable decreases in glomerular filtration rate after relief of obstruction. Hypokalemia occasionally developed after relief of obstruction during the postobstructive diuresis. It was concluded that fluid and electrolyte therapy must be regulated in response to the postobstructive diuresis, to ensure proper medical management.

Liver disease may cause a variety of clinical signs, including depression, anorexia, weakness, weight loss, vomiting, diarrhea, fever, abdominal pain, jaundice, ascites and CNS signs. Treatment is aimed at eliminating the cause, providing supportive care, and preventing secondary complications. Rest facilitates liver regeneration. Hypokalemia, respiratory alkalosis and hypoglycemia may complicate liver disease. Fluids should be given IV rather than SC to severely dehydrated animals. Preferred solutions include Ringer's and half-strength saline with 2.5% dextrose. Solutions containing lactate should not be used. Dietary management includes feeding adequate amounts of protein of high biologic value, carbohydrates, fat, vitamins and minerals.

Experimental uremia created by obstructing the urethra of 7 cross-bred bulls was associated with significant (P less than 0.05) increases in PCV, blood urea nitrogen concentration, arterial and venous pH and PCO2, arterial bicarbonate, and base excess. Total serum protein concentration decreased nonsignificantly. Arterial PO2 reduced significantly during later stages of uremia. Arterial and venous oxygen saturation, arteriovenous oxygen difference, oxygen extraction ratio, and arteriovenous pH difference were not affected significantly. Uremia was characterized by progressive metabolic alkalosis with, as a compensation, hypercapnia, and arterial hypoxemia. There was no evidence of systemic shunting of blood except in 1 animal.

The case records of 102 cows with abomasal volvulus and 71 cows with right-side displacement of the abomasum (RDA) were examined to determine whether the preoperative base-excess concentration of the extracellular fluid could be used both as a prognostic indicator for post-operative recovery in cattle with abomasal volvulus and as an aid in differentiating between abomasal volvulus and RDA. The survival rate of cows with abomasal volvulus decreased as the base excess concentration decreased (P = 0.08); the lowest survival rate was observed in cows with base excess less than or equal to -0.1 mEq/L. There was a significant difference (0.01 less than P less than 0.025) among base excess ranges between abomasal volvulus and RDA. All cows with preoperative base-excess concentrations less than or equal to -5.0 mEq/L had abomasal volvulus, rather than RDA.

The effect was established of an Eimeria adenoeides infection in turkey-poults on the body temperature and the acid-alkaline balance. Used were a total of 100 turkey-poults at the age of 3 weeks, divided into two groups of 50 each. The birds of the first group were kept as controls, and those of the second group were infected at the rate of 80 000-90 000 oocysts of the Eimeria adenoeides species. During the time of the most strongly manifested clinical symptoms (on the 6th and 7th day) part of the turkey-poults of the second group that exhibited signs of agony were taken away to form a third group. It was found that the body temperature dropped during the time of the most strongly expressed clinical symptoms. An ABL-3 unit (Radiometer, Denmark) was used to record the following blood indices: pH value of blood, PCO2 in mm Hg, PO2 in mm Hg, HCO3 in mmol/l, and BE in mmol/l. It was judged by the values of these indices that up to the fifth day following infection there set in a compensated metabolic acidosis, while on the sixth and the seventh day the metabolic acidosis was already decompensated.

In 4 cases of metabolic alkalosis with paradoxic aciduria in cattle, generalized muscle weakness was the predominant feature. In 3 of the 4 cases, prolonged anorexia preceded development of muscle weakness and aciduria. Plasma electrolyte concentrations varied but, in 3 of 4 cases, a transient decrease in plasma potassium concentration was detected. In the 3 cases in which prolonged therapy with sodium chloride, potassium chloride, and dextrose was offered, resolution of aciduria was rapid, followed by correction of metabolic alkalosis and return of muscle strength.

During one year we studied the acid-base state in the milking cows trying to solve the relationship between the secretion disorders and feeding. THe results confirm that exist a link between the acid-base state and the disorders. These disorders are connected to problems of alimentation. In our experiments it had been possible to observe a change in pH of blood versus alkalosis.

This article reviews what are considered the basic concepts of gas transport, blood gases, and acid-base physiology is most mammalian species. Techniques for the appropriate collection of blood samples for blood gas and acid-base determinations in the newborn foal are described. Guidelines for interpretation of these values in the normal foal and those animals undergoing respiratory and metabolic derangements are provided.

Effects of subclinical metabolic acid-base disturbances, caused by dietary fixed ion imbalances on kinetics of calcium (Ca) metabolism were examined in eucalcemic caprine does (period 1) and does during simulated lactational Ca loss (period 2). In both experiments, Ca balance data and serial blood, fecal and urine samples were collected after an iv injection of 45Ca. In period 2, lactational Ca loss was simulated by continuous infusion of ethylene glycol-bis (beta-amino ethyl ether)N,N,N'N'-tetraacetic acid (EGTA) to standardize the loss of Ca among goats. The data were fit to a four-compartment model of Ca metabolism. In period 1, fixed anion excess, [sodium + potassium - chloride] = -2 meq/100 g diet dry matter (ANEX) increased urinary Ca excretion relative to fixed cation excess, [sodium + potassium - chloride] = 71 meq/100 g diet dry matter (CATEX). Consequently, rates of Ca absorption and resorption were elevated in goats made acidotic by dietary fixed anion excess. During period 2 (EGTA infusion), urinary Ca loss was elevated to similar levels in goats fed ANEX and CATEX, but Ca absorption remained higher in goats fed ANEX. Consequently, size of the exchangeable Ca pool, accretion rate and balance across bone were higher in these goats. Fixed anion excesses (found in corn silage and grains) cause subclinical metabolic acidosis, which elevates rates of Ca absorption but does not affect size of the exchangeable Ca pool. Fixed cation excesses (associated with diets containing alfalfa and buffers) cause subclinical metabolic alkalosis, which diminishes Ca absorption and urinary Ca excretion. Acidosis-induced hypercalciuria is the metabolic cost of maintaining high prepartum Ca absorption rates and high flux of Ca through the exchangeable Ca pool that may aid in adjustment to sudden Ca losses at parturition.

The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.