Blood buffering in sedentary miniature horses after administration of sodium bicarbonate in single doses of varying amounts

Blood acid-base and electrolyte status was studied in four sedentary Miniature Horses treated with 200, 300, 400 and 500 mg of sodium bicarbonate (NaHCO₃) per kg of body weight (BW). Arterial blood was collected before treatment with NaHC0₃ and each hour for 5 h after treatment. All treatments resulted in an increase in blood pH, bicarbonate (HCO₃⁻) concentration and base excess (BE) by 1 h post-dosage, which continued through the 5th hour (P < .05). Treatment with 200 mg NaHC0₃/kg BW resulted in less elevated blood HCO₃⁻ concentrations (P < .03) and BE values (P < .01) when compared to the other treatments. Following dosing with NaHCO₃, plasma Na⁺ concentrations increased among all treatments but declined to initial values by 3 h post-treatment. The 200 mg NaHCO₃/kg BW dosage resulted in the smallest increases in plasma Na⁺ concentrations (P < .03). Both plasma K⁺ and Ca⁺⁺ concentrations were lower (P < .05) among all treatment groups 1 h post-dosage but returned to initial values by 5 h and 3 h posttreatment, respectively, with no differences (P >.05) among treatments. All NaHCO₃ dosages increased blood buffering capacity as indicated by increased blood pH, HCO₃⁻ concentration and BE. Maximum blood pH, HCO⁻₃ concentration and BE was reached using a dosage of 300 mg NaHCO₃/kg BW. Also, all treatments altered the plasma electrolyte concentrations.     

Influence of Medetomidine on Acid-base Balance and Urine Excretion in Goats

Raekallio M., M. Hackzell and L. Eriksson: Influence of medetomidine on acid-base balance and urine excretion in goats. Acta vet. scand. 1994,35,283-288.– Seven goats were given medetomidine 5 μg/kg as an iv bolus injection. Venous blood samples were taken repeatedly and urine was collected continuously via a catheter up to 7h after the injection.Medetomidine caused deep clinical sedation. Base excess, pH and PCO₂ in venous blood rose after medetomidine administration. There were no significant changes in plasma concentrations of sodium, calcium, magnesium, creatinine or osmolality, whereas potassium and bicarbonate concentrations increased, and phosphate and chloride decreased. Medetomidine increased plasma glucose concentration, and in 4 of 7 goats glucose could also be detected in urine. Medetomidine did not influence urine flow rate, free water clearance, bicarbonate and phosphate excretion or pH, but renal chloride, sodium, potassium, calcium, magnesium and creatinine excretion were reduced.The results suggest that the metabolic alkalosis recorded after medetomidine administration is not caused by increased renal acid excretion.     

Dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in a horse

A 3-year-old mare repeatedly had clinical signs of rhabdomyolysis on mild exertion. Serum creatine kinase and aspartate transaminase activities were high at rest. Responses to dietary sodium bicarbonate were tested through 7 alternating periods of supplementation of a basal ration of timothy hay and oats. Physical signs; venous blood pH and gases; blood glucose and lactate; serum electrolytes, enzymes, and creatinine; and urine pH were monitored before and after exercise. Dietary sodium bicarbonate raised resting venous blood pH and bicarbonate slightly and significantly increased urine pH from pH 7.46 to 8.2 (P less than 0.001). An exercise test included 5 minutes at the walk followed by 20 minutes at the trot. The exercise induced gait stiffness, muscle fasciculations, and muscle induration when the diet was not supplemented, but not when it was supplemented with sodium bicarbonate. Myoglobin was present in 16 of 21 urine samples after exercise during nonsupplemented periods, but only in 3 of 28 urine samples during supplemented periods (P less than 0.0001). Bicarbonate supplementation significantly decreased the responses of blood lactic acid, serum creatine kinase, and aspartate transaminase to exercise. Supplementation of the diet was associated with higher venous blood pH and bicarbonate ion concentrations throughout exercise. Dietary sodium bicarbonate apparently mitigated or prevented physical, chemical, and enzymatic characteristics of exertional rhabdomyolysis in this mare, possibly through its enhancement of buffering capacity in muscle tissue fluids.     

Simple acid-base disorders

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.     

Magnesium Oxide Induced Metabolic Alkalosis in Cattle

A study was designed to compare the metabolic alkalosis produced in cattle from the use of an antacid (magnesium oxide) and a saline cathartic (magnesium sulphate). Six, mature, normal cattle were treated orally with a magnesium oxide (MgO) product and one week later given a comparable cathartic dose of magnesium sulphate (MgSO₄).

The mean percent dry matter content of the cattle feces changed significantly (P<0.001) following administration of both MgO (15.6-8.1) and MgSO₄ (17.0-8.7) but there was no significant difference between treatments. The mean rumen pH values changed significantly (P<0.001) following administration of both MgO (7.-8.7) and MgSO₄ (7.3-8.3) but there was no significant difference between treatments. However, use of the MgO product caused a more severe (P<0.001) metabolic alkalosis as determined by base excess values. The base excess values remained elevated for 24 hours in the MgO treated group compared to only 12 hours after MgSO₄ administration. Following MgO administration, mean hydrogen ion concentration (pH), bicarbonate ion concentration ([HCO₃-]) and base excess were 7.44, 33.3 mmol/L and +8.0 respectively compared to 7.38, 27 mmol/L and +3.0 after MgSO₄.

Since the oral use of MgO in normal cattle causes a greater and more prolonged metabolic alkalosis compared to MgSO₄, MgO is contraindicated as a cathartic in normal cattle or in cattle with abomasal abnormalities characterized by pyloric obstruction and metabolic alkalosis.

     

Effect of sodium bicarbonate infusions on ionized calcium and total calcium concentrations in serum of clinically normal cats

The effects of sodium bicarbonate (0.5 mEq/kg of body weight, 1.0 mEq/kg, 2.0 mEq/kg, and 4.0 mEq/kg) on ionized and total calcium concentrations were determined in clinically normal cats. Also, serum pH, whole blood pH, and serum albumin, serum total protein, and serum phosphorus concentrations were measured. Intravenous administration of sodium bicarbonate to awake cats decreased serum ionized calcium and serum total calcium concentrations. All dosages of sodium bicarbonate were associated with significant decreases of serum ionized calcium concentration. This effect lasted for greater than 180 minutes when cats were given 2.0 mEq/kg or 4.0 mEq/kg. When cats were given 4 mEq of sodium bicarbonate/kg, serum ionized calcium concentration was significantly decreased, compared with that when cats were given lower doses, but only at 10 minutes after infusion. After sodium bicarbonate infusion, serum total calcium concentration, measured by ion-specific electrode and colorimetry, was lower than baseline values at most of the times evaluated. Decreases in serum ionized calcium and serum total calcium concentrations can be attributed only in part to an increase in serum or whole blood pH and to a decrease in serum protein concentration. Serum total calcium concentrations measured by ion-specific electrode and by colorimetry were positively correlated, but the variability was high. Only 44% of the variability in serum ionized calcium concentration could be predicted when serum total calcium, albumin, total protein, phosphorus, and bicarbonate concentrations and pH were considered.     

Evaluation of the Total Carbon Dioxide Apparatus and pH Meter for the Determination of Acid-Base Status in Diarrheic and Healthy Calves

Three simple tests of acid-base status were evaluated for field use. Blood samples were collected from 20 diarrheic and 24 healthy calves less than six weeks of age. One sample was collected anaerobically and immediately analyzed on a blood gas analyzer. The other samples were used for measurement of blood and serum pH using a pH meter and pH paper, and for serum total carbon dioxide (TCO₂) using a TCO₂ apparatus. The TCO₂ apparatus gave the best results and would be useful in the field. TCO₂ apparatus measurements had a high correlation, r=0.91, with blood gas analyzer blood bicarbonate values. Healthy calves have a serum TCO₂ content of 30 mmol/L and bicarbonate requirements for correcting metabolic acidosis in diarrheic calves can be calculated:

Bicarbonate required (mmol) = (30-TCO₂) × Body Weight × 0.6 This can be converted to grams of sodium bicarbonate by dividing by 12.

     

Effects of Alkalinization and Rehydration on Plasma Potassium Concentrations in Neonatal Calves with Diarrhea

Background

Increased plasma potassium concentrations (K⁺) in neonatal calves with diarrhea are associated with acidemia and severe clinical dehydration and are therefore usually corrected by intravenous administration of fluids containing sodium bicarbonate.

Objectives

To identify clinical and laboratory variables that are associated with changes of plasma K⁺ during the course of treatment and to document the plasma potassium‐lowering effect of hypertonic (8.4%) sodium bicarbonate solutions.

Animals

Seventy‐one neonatal diarrheic calves.

Methods

Prospective cohort study. Calves were treated according to a clinical protocol using an oral electrolyte solution and commercially available packages of 8.4% sodium bicarbonate (250–750 mmol), 0.9% saline (5–10 L), and 40% dextrose (0.5 L) infusion solutions.

Results

Infusions with 8.4% sodium bicarbonate solutions in an amount of 250–750 mmol had an immediate and sustained plasma potassium‐lowering effect. One hour after the end of such infusions or the start of a sodium bicarbonate containing constant drip infusion, changes of plasma K⁺ were most closely correlated to changes of venous blood pH, plasma sodium concentrations and plasma volume (r = −0.73, −0.57, −0.53; P < .001). Changes of plasma K⁺ during the subsequent 23 hours were associated with changes of venous blood pH, clinical hydration status (enophthalmos) and serum creatinine concentrations (r = −0.71, 0.63, 0.62; P < .001).

Conclusions and Clinical Importance

This study emphasizes the importance of alkalinization and the correction of dehydration in the treatment of hyperkalemia in neonatal calves with diarrhea.     

The alkalinizing effects of metabolizable bases in the healthy calf.

The alkalinizing effect of citrate, acetate, propionate, gluconate, L and DL-lactate were compared in healthy neonatal calves. The calves were infused for a 3.5 hour period with 150 mmol/L solutions of the sodium salts of the various bases. Blood pH, base excess, and metabolite concentrations were measured and the responses compared with sodium bicarbonate and sodium chloride infusion. D-gluconate and D-lactate had poor alkalinizing abilities and accumulated in blood during infusion suggesting that they are poorly metabolized by the calf. Acetate, L-lactate and propionate had alkalinizing effects similar to bicarbonate, although those of acetate had a slightly better alkalinizing effect than L-lactate. Acetate was more effectively metabolized because blood acetate concentrations were lower than L-lactate concentrations. There was a tendency for a small improvement in metabolism of acetate and lactate with age. Sodium citrate infusion produced signs of hypocalcemia, presumably because it removed ionized calcium from the circulation. D-gluconate, D-lactate and citrate are unsuitable for use as alkalinizing agents in intravenous fluids. Propionate, acetate and L-lactate are all good alkalinizing agents in healthy calves but will not be as effective in situations where tissue metabolism is impaired.     

Chloride Ion in Small Animal Practice: The Forgotten Ion

The Physiology of chioride ion and its relationship to clinical disorders in small animall practice is reviewed. Chioride is the major anion in the extracellular fluid and is important in the metabolic regulation of acid-base balance. A new clinical approach is used to assess chloride ion changes after accounting for changes in free water. Using this approach chloride disorders can be divided into corrected and artifactual. Changes in free water are solely responsible for the chioride ion changes in artifactual disorders, whereas in corrected chloride disorders, chloride ion itself changes. Corrected hypochioremia is associated with increases in the strong ion differece (SID) and metabolic alkalosis and is caused by administration of solution containing a high concentration of sodium relative to chioride (e.g., Sodium bicarbonate) or the excessive loss chioride relative to sodium (e.g., vomiting of stomach contents). Administration of chioride is correction of hypochioremic metabolic alkalosis. Corrected hyperchioremia is associated with a decreased SID and metabolic acidosis and is usually the result of excessive loss of sodium relative to chloride (e.g., diarrhea), chioride retention (e.g., renal tubular acidosis), or therapy with solutions containing a high concentration of chioride relative to sodium (e.g.,0.9% sodium chloride;3–24% hypertonic saline). Treatment with sodium bicarbonate should be attempted in patients with corrected hyperchioremia and a plasma pH beiow 7.2.     

Changes in fetal mannose and other carbohydrates induced by a maternal insulin infusion in pregnant sheep

Background

The importance of non-glucose carbohydrates, especially mannose and inositol, for normal development is increasingly recognized. Whether pregnancies complicated by abnormal glucose transfer to the fetus also affect the regulation of non-glucose carbohydrates is unknown. In pregnant sheep, maternal insulin infusions were used to reduce glucose supply to the fetus for both short (2-wk) and long (8-wk) durations to test the hypothesis that a maternal insulin infusion would suppress fetal mannose and inositol concentrations. We also used direct fetal insulin infusions (1-wk hyperinsulinemic-isoglycemic clamp) to determine the relative importance of fetal glucose and insulin for regulating non-glucose carbohydrates.

Results

A maternal insulin infusion resulted in lower maternal (50%, P < 0.01) and fetal (35-45%, P < 0.01) mannose concentrations, which were highly correlated (r² = 0.69, P < 0.01). A fetal insulin infusion resulted in a 50% reduction of fetal mannose (P < 0.05). Neither maternal nor fetal plasma inositol changed with exogenous insulin infusions. Additionally, maternal insulin infusion resulted in lower fetal sorbitol and fructose (P < 0.01).

Conclusions

Chronically decreased glucose supply to the fetus as well as fetal hyperinsulinemia both reduce fetal non-glucose carbohydrates. Given the role of these carbohydrates in protein glycosylation and lipid production, more research on their metabolism in pregnancies complicated by abnormal glucose metabolism is clearly warranted.     

Effect of phenylbutazone on the haemodynamic, acid-base and eicosanoid responses of horses to sustained submaximal exertion

The systemic haemodynamic and acid-base effects of the administration of phenylbutazone (4·4 mg kg⁻¹ intravenously) to standing and running horses were investigated. Phenylbutazone, or a placebo, was administered to each of six mares either 15 minutes before, or after 30 minutes of a 60-minute submaximal exercise test which elicited heart rates approximately 55 per cent of maximal, and to the same horses at rest. The variables examined included the cardiac output, heart rate, systemic and pulmonary arterial pressures, right atrial and right ventricular pressures, and arterial and mixed venous blood gases and pH. Serum sodium, potassium and chloride concentrations, and plasma thromboxane B₂, 6-keto-prostaglandin F_1α (6-keto-PGF_1α), and prostaglandin E₂ (PGE₂) concentrations were measured in separate studies using similar protocols in the same horses. Running produced increases in heart rate, cardiac output, mean arterial and right ventricular pressure, and decreases in total peripheral resistance. The acid:base responses to exertion were characterised by respiratory alkalosis. Exertion did not significantly influence plasma 6-keto-PGF_1α or PGE₂ concentrations but plasma thromboxane B₂ concentrations were increased significantly by 60 minutes of exertion in the untreated horses. This exercise-induced increase in plasma thromboxane B₂ concentration was inhibited by the previous administration of phenylbutazone, but phenylbutazone did not produce detectable changes in systemic haemodynamic or acid-base variables in either standing or running horses.     

Physicochemical Interpretation of Acid‐Base Abnormalities in 54 Adult Horses with Acute Severe Colitis and Diarrhea

Background

The quantitative effect of strong electrolytes, pCO₂, and plasma protein concentration in determining plasma pH and bicarbonate concentrations can be demonstrated with the physicochemical approach. Plasma anion gap (AG) and strong ion gap (SIG) are used to assess the presence or absence of unmeasured anions.

Hypotheses

The physicochemical approach is useful for detection and explanation of acid‐base disorders in horses with colitis. AG and SIG accurately predict hyperlactatemia in horses with colitis.

Animals

Fifty‐four horses with acute colitis and diarrhea.

Methods

Retrospective study . Physicochemical variables were calculated for each patient. ROC curves were generated to analyze sensitivity and specificity of AG and SIG for predicting hyperlactatemia.

Results

Physicochemical interpretation of acid‐base events indicated that strong ion metabolic acidosis was present in 39 (72%) horses. Mixed strong ion acidosis and decreased weak acid (hypoproteinemia) alkalosis was concomitantly present in 17 (30%) patients. The sensitivity and specificity of AG and SIG to predict hyperlactatemia (L‐lactate > 5 mEq/L) were 100% (95% CI, 66.4–100; P < .0001) and 84.4% (95% CI, 70.5–93.5 P < .0001). Area under the ROC curve for AG and SIG for predicting hyperlactatemia was 0.95 (95% CI, 0.86–0.99) and 0.93 (95% CI, 0.83–0.99), respectively.

Conclusion and Clinical relevance

These results emphasize the importance of strong ions and proteins in the maintenance of the acid‐base equilibria. AG and SIG were considered good predictors of clinically relevant hyperlactatemia.     

Furosemide and sodium bicarbonate-induced alkalosis in the horse and response to oral KCl or NaCl therapy

Metabolic alkalosis was induced in 10 clinically normal horses by administration of furosemide (1 mg/kg of body weight, IM) followed 4.5 hours later by sodium bicarbonate (NaHCO3; 500 g in 8 L water) via nasogastric tube. Furosemide diuresis resulted in a mean weight loss of 21.1 kg, which was associated with small, but significant, increases in venous blood pH, bicarbonate, and plasma protein concentrations (P less than 0.001), while plasma potassium, chloride, and calcium concentrations declined significantly (P less than 0.001). Oral administration of the hypertonic NaHCO3 solution resulted in clinical evidence of hypovolemia, which was accompanied by a marked increase (P less than 0.001) in plasma protein concentration. Seven of the 10 horses developed signs of neuromuscular excitability, as evidenced by muscle fasciculations, and 5 of the horses developed diaphragmatic flutter. Hypernatremia was transiently induced, but it resolved as the horses were allowed access to water. The alkalosis induced by furosemide and NaHCO3 was profound and persisted for a 24-hour period and was associated with marked hypochloremia and hypokalemia. Partial replacement of the electrolyte deficits and correction of the metabolic alkalosis was attempted, using 1,000 mEq of NaCl or KCl given as an isotonic solution via nasogastric tube. In the KCl-treated group, there was a prompt and significant decline in venous blood pH and bicarbonate concentration (P less than 0.001) accompanied by a significant increase in plasma potassium concentration (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Infusion of sodium bicarbonate in experimentally induced metabolic acidosis does not provoke cerebrospinal fluid (CSF) acidosis in calves

In a crossover study, 5 calves were made acidotic by intermittent intravenous infusion of isotonic hydrochloric acid (HCl) over approximately 24 h. This was followed by rapid (4 h) or slow (24 h) correction of blood pH with isotonic sodium bicarbonate (NaHCO(3)) to determine if rapid correction of acidemia produced paradoxical cerebrospinal fluid (CSF) acidosis. Infusion of HCl produced a marked metabolic acidosis with respiratory compensation. Venous blood pH (mean ± S(x)) was 7.362 ± 0.021 and 7.116 ± 0.032, partial pressure of carbon dioxide (Pco(2), torr) 48.8 ± 1.3 and 34.8 ± 1.4, and bicarbonate (mmol/L), 27.2 ± 1.27 and 11 ± 0.96; CSF pH was 7.344 ± 0.031 and 7.240 ± 0.039, Pco(2) 42.8 ± 2.9 and 34.5 ± 1.4, and bicarbonate 23.5 ± 0.91 and 14.2 ± 1.09 for the period before the infusion of hydrochloric acid and immediately before the start of sodium bicarbonate correction, respectively. In calves treated with rapid infusion of sodium bicarbonate, correction of venous acidemia was significantly more rapid and increases in Pco(2) and bicarbonate in CSF were also more rapid. However, there was no significant difference in CSF pH. After 4 h of correction, CSF pH was 7.238 ± 0.040 and 7.256 ± 0.050, Pco(2) 44.4 ± 2.2 and 34.2 ± 2.1, and bicarbonate 17.8 ± 1.02 and 14.6 ± 1.4 for rapid and slow correction, respectively. Under the conditions of this experiment, rapid correction of acidemia did not provoke paradoxical CSF acidosis.     

Clinical evaluation of sodium bicarbonate, sodium L-lactate, and sodium acetate for the treatment of acidosis in diarrheic calves

Thirty-six dehydrated diarrheic neonatal calves were used to study the effects of various alkalinizing compounds on acid-base status, the changes in central venous pressure (CVP) in response to rapid IV infusion of large volumes of fluid, and the correlation of acid-base (base deficit) status, using a depression scoring system with physical determinants related to cardiovascular and neurologic function. Calves were allotted randomly to 4 groups (9 calves/group). Over a 4-hour period, each calf was given two 3.6-L volumes (the first 3.6 L given in the first hour) of a polyionic fluid alone (control group) or were given the polyionic fluid with sodium bicarbonate, sodium L-lactate, or sodium acetate added (50 mmol/L). Acid-base status, hematologic examination, and biochemical evaluations were made immediately before infusion of each fluid (at entry) and after 3.6, 4.8, and 7.2 L of fluid had been given. Compared with control values, bicarbonate, lactate, and acetate had significantly greater alkalinizing effects on pH (P less than 0.01) and base deficit (P less than 0.01) after 3.6, 4.8, and 7.2 L of fluid were given. Bicarbonate had the most rapid alkalinizing effect and induced greater changes in base deficit (P less than 0.01) than did acetate or lactate at each of the 3 administered fluid volumes evaluated. Acetate and lactate had similar alkalinizing effects on blood. Rehydration alone did not improve acid-base status. The CVP was elevated in 10 (28%) of the 36 calves after 1 hour of fluid (3.6 L) administration, but significant differences in body weight, PCV, and clinical condition or depression score at entry were not found between calves with elevated CVP and those with normal CVP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of acute induced metabolic alkalosis on the acid/base responses to sprint exercise of six racing greyhounds

To investigate the effect of acute induced metabolic alkalosis on the haematological, biochemical and metabolic responses to sprint exercise, six greyhound dogs with previously placed carotid artetrial catheters were raced four times over a distance of 400 metres. Each dog was raced twice after receiving oral sodium bicarbonate solution (NaHCO₃) (400 mg kg⁻¹) or lactated Ringer's solution ( ). Before, and for intervals of up to one hour after, the exercise arterial blood samples were collected for the measurement of blood gases, packed cell volume, total protein, serum biochemistry and plasma lactate. The time to complete the 400 metre sprint ranged from 32·7 seconds to 36·9 seconds. There was no significant difference in racing times between the dogs treated with NaHCO₃ and , and there was no significant difference between the plasma lactate measurements after the treatments with NaHCO₃ or . Serum chloride concentrations were significantly lower after NaHCO₃ than after LRS, and there was a trend towards a lower serum potassium concentration after NaHCO₃ treatment. Plasma lactate concentrations showed a similar increase and time course of disappearance after both LRS and NaHCO₃ treatments. There were significant changes in all the parameters measured after the exercise, but there were large variations between individual dogs and between races when the dogs were receiving the same treatment.     

Contemporary approach to acid-base balance and its disorders in dogs and cats

The issue of the acid-base balance (ABB) parameters and their disorders in pets is rarely raised and analysed, though it affects almost 30% of veterinary clinics patients. Traditionally, ABB is described by the Henderson-Hasselbach equation, where blood pH is the resultant of HCO3- and pCO2 concentrations. Changes in blood pH caused by an original increase or decrease in pCO2 are called respiratory acidosis or alkalosis, respectively. Metabolic acidosis or alkalosis are characterized by an original increase or decrease in HCO3- concentration in the blood. When comparing concentration of main cations with this of main anions in the blood serum, the apparent absence of anions, i.e., anion gap (AG), is observed. The AG value is used in the diagnostics of metabolic acidosis. In 1980s Stewart noted, that the analysis of: pCO2, difference between concentrations of strong cations and anions in serum (SID) and total concentration of nonvolatile weak acids (Atot), provides a reliable insight into the body ABB. The Stewart model analyses relationships between pH change and movement of ions across membranes. Six basic types of ABB disorders are distinguished. Respiratory acidosis and alkalosis, strong ion acidosis, strong ion alkalosis, nonvolatile buffer ion acidosis and nonvolatile buffer ion alkalosis. The Stewart model provides the concept of strong ions gap (SIG), which is an apparent difference between concentrations of all strong cations and all strong anions. Its diagnostic value is greater than AG, because it includes concentration of albumin and phosphate. The therapy of ABB disorders consists, first of all, of diagnosis and treatment of the main disease. However, it is sometimes necessary to administer sodium bicarbonate (NaHCO3) or tromethamine (THAM).     

Effect of chronic hypocortisolaemia on plasma cortisol concentrations during intravenous infusions of hydrocortisone sodium succinate in dogs

Intravenous infusions of hydrocortisone sodium succinate (HSS) were given at 0·625 mg kg⁻¹ hour⁻¹ and 0·312 mg kg⁻¹ hour⁻¹ to six dogs. Plasma cortisol concentrations were measured by radioimmunoassay at 0, 15, 30, 45 and 60 minutes and then every 30 minutes for a further five hours. Chronic hypocortisolaemia was induced and maintained with mitotane and the HSS infusions were repeated after 31 and 50 days. No statistically significant difference was observed in the plasma cortisol concentrations after either period of hypocortisolaemia, but the plasma cortisol concentrations tended to be higher in most of the dogs.     

Endocrine Profile Comparisons of Fat Versus Moderately Conditioned Mares Following Parturition

The influence of progesterone, luteinizing hormone (LH), and estrogen on the mare's estrous cycle has been well researched and documented, but other endocrine profiles have not received as much attention. To evaluate endocrine concentrations in fat-conditioned (body condition score [BCS] of 7–8) versus moderately conditioned mares (BCS of 5–6), 24 mares were allotted to and maintained in respective groups from late gestation until pregnancy was confirmed after breeding on the second postpartum estrus. Serum concentrations of thyroxine (T₄), insulin-like growth factor-1 (IGF-1), and leptin were assayed to characterize circulating blood concentrations. Additionally, LH and progesterone serum concentrations were assayed to evaluate the estrous cycle status of the mares. Leptin and progesterone concentrations were not different (P > .05) between the groups. Nevertheless, serum concentrations of T₄ were higher (P < .01) and IGF-1 concentrations lower (P < .01) in moderately conditioned as compared with fat-conditioned mares during times of ovulation and the interovulatory period. Furthermore, serum concentrations of LH were found to be different between the groups only when the estrous cycle approached the second ovulation (P < .0001). Results of this study suggest that mares maintained in a BCS of 5 or greater are similar in terms of reproductive efficiency. Although the circulating serum concentrations of T₄ and IGF-1 are different after parturition, their influence does not affect reproductive capabilities of mares with a BCS of 5 or greater.