Blood-gas, acid-base and haematological values in horses during an endurance ride.

The effects of prolonged strenuous exercise on arterial and venous oxygen tension, carbon dioxide tension, pH, bicarbonate, standard bicarbonate, base excess, haemoglobin, packed cell volume and total plasma protein were studied in 36 horses during a 100 km endurance ride. There were significant changes in many parameters when pre-ride values were compared with both mid-ride and end of ride values. The prominent changes were the development of dehydration and a metabolic alkalosis. At the mid-ride sampling time those horses with higher heart rates had a greater degree of metabolic alkalosis than those with lower heart rates. The first 4 horses in the race completed the ride with speeds between 322-330 m/min and demonstrated a metabolic acidosis.     

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.     

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.     

Effects of intravenous sodium bicarbonate and sodium acetate on equine acid-base status

Changes in blood gases, pH, and plasma electrolyte concentrations in response to intravenously infused sodium bicarbonate (NaHCO₃) and sodium acetate (NaCH₃CO₂) solutions (1.34 mEq/mL) in 5 light breed mares were investigated. Jugular venous blood samples were collected before and after completion of the infusions in 20-minute intervals for 200 minutes. Infusion of sodium bicarbonate and sodium acetate caused significant (P < .00l) increases in blood pH and bicarbonate ion concentration that persisted throughout the collection period. The elevation in blood pH and bicarbonate ion concentrations was greater (P < .01) for sodium bicarbonate than for sodium acetate immediately after the completion of the infusions but was not different (P > .05) thereafter. There were significant reductions (P < .01) in plasma-ionized calcium and potassium after infusion of both sodium bicarbonate and sodium acetate. This study found that significant metabolic alkalosis in horses and corresponding shifts in electrolyte concentrations can be induced by intravenous infusion of solutions of either sodium bicarbonate or sodium acetate, and they persist for at least 3 hours. These data show that the short-term elevation in pH and bicarbonate ion concentration is momentarily higher after infusion of sodium bicarbonate. This is likely due to the direct infusion of bicarbonate ions in the sodium bicarbonate treatment, such that further metabolism is not required to be effective. However, the longer-term alkalosis did not differ between isomolar solutions of sodium bicarbonate and sodium acetate.     

Experimental model of hypochloremic metabolic alkalosis caused by diversion of abomasal outflow in sheep

Hypochloremic metabolic alkalosis accompanied by hypokalemia and hyponatremia was induced experimentally in 7 adult sheep by diversion (loss) of gastric contents through an Ivan and Johnston cannula placed in the cranial part of the duodenum just distal to the pylorus. Cannula placement was easily accomplished, and cannulae were tolerated well by the sheep. Volume of effluent produced during the 60- to 120-hour period of diversion ranged from 7.7 to 14.9 L and tended to be greatest during the first 24 hours. All sheep became dehydrated, with mean PCV and plasma total protein concentration increases of 94.2 and 61.7%, respectively. Plasma chloride concentration decreased in linear fashion from a prediversion mean of 113 mEq/L (range, 111 to 117 mEq/L) to an end-point mean of 54 mEq/L (range, 45 to 65 mEq/L). Plasma sodium and potassium concentrations also decreased, though potassium concentration increased terminally. There were rapid increases in arterial blood pH and bicarbonate and base excess concentrations during the first 48 hours after diversion. However, during the final stages of diversion, sheep developed superimposed metabolic acidosis with increased plasma lactate concentration and high anion gap.     

Metabolic response of horses to a high soluble carbohydrate diet: effects of low-intensity submaximal exercise and sodium bicarbonate supplementation.

Four mares fed a low fiber, high soluble carbohydrate diet were used in a crossover design to evaluate the effects of dietary sodium bicarbonate (NaHCO3) supplementation during daily low-intensity submaximal working conditions. Mares were fed the diet at 1.7 times the maintenance energy requirement for mature horses at work. The horses tolerated the diet well and had no clinical abnormalities. Resting venous blood bicarbonate (HCO3), standard HCO3, and base excess (BE) concentrations significantly (P less than 0.05) increased with NaHCO3 supplementation, but no significant changes in resting venous blood pH or carbon dioxide tension (PCO2) were recorded. Venous blood HCO3, standard HCO3, BE, hemoglobin, and heart rate were significantly (P less than 0.05) increased and plasma lactate concentration was significantly (P less than 0.05) decreased in the control horses and in the horses given the NaHCO3 supplement during low-intensity submaximal exercise. There were no significant changes in venous blood pH, PCO2, or plasma protein concentration with exercise. Venous blood HCO3, standard HCO3, and BE concentrations were significantly (P less than 0.05) greater during submaximal exercise in horses given the NaHCO3 supplement. There were no significant differences in plasma lactate or total protein concentrations, blood pH, PCO2, or hemoglobin concentration between the 2 groups during exercise.     

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)     

Technical note: using calcium carbonate as an osmolar control treatment for acid-base studies in horses

The efficacy of using calcium carbonate as an osmolar control treatment for acid-base studies in horses receiving alkalizing compounds was evaluated. Six mares were nasogastrically intubated with isomolar quantities of sodium or calcium as sodium bicarbonate or calcium carbonate or with water during three treatment periods. Doses of the carbonic acid salts were 500 mg/kg sodium bicarbonate mixed with 4 L of distilled water (positive control) and 595 mg/kg calcium carbonate mixed with 2 L of distilled water to yield isoosmolar treatments. Four liters of distilled water served as the negative control. Jugular venous blood samples were drawn before intubation and at hourly intervals for 6 h after intubation. The serum electrolytes Na+ and K+, blood pH, and HCO3- were determined. The sodium bicarbonate treatment increased blood pH and HCO3- (P < 0.01) above both the water and CaCO3 treatments. No differences (P > 0.05) were found between the water and CaCO3 treatments. These data indicate that calcium carbonate may serve as a suitable osmolar control treatment for studying the effects of treatments that affect acid-base status of horses.     

Acidosis and clinical condition in asphyctic calves

In depressed calves (modified APGAR score 4-6) there is at birth an evident combined respiratory-metabolic acidosis (pH = 7.082 +/- 0.175; pCO2 = 73.3 +/- 26.8 mm Hg; BE = -10.6 +/- 7.2 mmol/l). The metabolic adaptation is completed after 6 hours, the respiratory acidosis is present up to 24 hours after delivery. In comparison to normal calves there are significant deviations in pH-values, base excess standard bicarbonate and actual bicarbonate during the whole investigation time. The carbon dioxide tensions of the depressed calves are at birth similar to those of normal calves, but in the following hours they are significantly higher. A definite relationship can be demonstrated between the 1 minute APGAR score and pH-value, base excess, standard bicarbonate and actual bicarbonate. Oxygen tension, oxygen saturation and carbon dioxide do not correlate with the clinical condition.     

Effects of xylazine on acid-base balance and arterial blood-gas tensions in goats under different environmental temperature and humidity conditions

The effects of acute exposure to 3 different temperature and humidity conditions on arterial blood-gas and acid-base balance in goats were investigated after intravenous bolus administration of xylazine at a dose of 0.1 mg/kg. Significant (P<0.05) changes in the variables occurred under all 3 environmental conditions. Decreases in pH, partial pressure of oxygen and oxyhaemoglobin saturation were observed, and the minimum values for oxygen tension and oxyhaemoglobin saturation were observed within 5 min of xylazine administration. The pH decreased to its minimum values between 5 and 15 min. Thereafter, the variables started to return towards baseline, but did not reach baseline values at the end of the 60 min observation period. Increases in the partial pressure of carbon dioxide, total carbon dioxide content, bicarbonate ion concentration, and the actual base excess were observed. The maximum increase in the carbon dioxide tension occurred within 5 min of xylazine administration. The increase in the actual base excess only became significant after 30 min in all 3 environments, and maximal increases were observed at 60 min. There were no significant differences between the variables in the 3 different environments. It was concluded that intravenous xylazine administration in goats resulted in significant changes in arterial blood-gas and acid-base balance that were associated with hypoxaemia and respiratory acidosis, followed by metabolic alkalosis that continued for the duration of the observation period. Acute exposure to different environmental temperature and humidity conditions after xylazine administration did not influence the changes in arterial blood-gas and acid-base balance.     

Evaluation of isotonic sodium bicarbonate solution for alkalizing effects in conscious calves

After intravenous (i.v.) infusion of various volumes of 1.35%-isotonic sodium bicarbonate solution (ISB), acid-base equilibrium, blood pressure, plasma volume and biochemical parameters in healthy Holstein calves were studied. Four calves each were randomly assigned to the low-dose (LD; i.v. infusion of 5 ml/kg ISB), middle-dose (MD; i.v. infusion of 10 ml/kg ISB) and the high-dose groups (HD; i.v. infusion of 15 ml/kg ISB). Administration volumes of ISB in the LD, MD and HD groups were decided based on the first half volumes of 5, 10 and 15 mEq of base requirement by the acceptable equation. Systemic, pulmonary artery and central venous pressures, cardiac output and plasma osmotic pressure were not changed by ISB infusion and remained constant throughout the experiment for all groups. There was good correlation (r(2) = 0.950) between relative changes in base excess and infused volume of bicarbonate (y=2.491x). The coefficient of distribution for bicarbonate ions was calculated to be 0.401 (=1/2.491). Therefore, it is suggested that a value of 0.4 would be most appropriate when calculating the base requirements in calves. Therefore, the first half volumes of ISB correcting base deficits of 5, 10 and 15 mEq in calves were estimated to be 6, 12 and 18 ml/kg, respectively. On the basis of the findings in this study, ISB may be used to correct metabolic acidosis without altering the plasma osmotic pressure, hemodynamic status and respiratory function in the calves.     

Effects of intravenous hyperosmotic sodium bicarbonate on arterial and cerebrospinal fluid acid-base status and cardiovascular function in calves with experimentally induced respiratory and strong ion acidosis

The objectives of this study were to determine the effects of hyperosmotic sodium bicarbonate (HSB) administration on arterial and cerebrospinal fluid (CSF) acid-base balance and cardiovascular function in calves with experimentally induced respiratory and strong ion (metabolic) acidosis. Ten healthy male Holstein calves (30-47 kg body weight) were instrumented under halothane anesthesia to permit cardiovascular monitoring and collection of blood samples and CSE Respiratory acidosis was induced by allowing the calves to spontaneously ventilate, and strong ion acidosis was subsequently induced by i.v. administration of L-lactic acid. Calves were then randomly assigned to receive either HSB (8.4% NaHCO3; 5 ml/kg over 5 minutes, i.v.; n=5) or no treatment (controls, n=5) and monitored for 1 hour. Mixed respiratory and strong ion acidosis was accompanied by increased heart rate, cardiac index, mean arterial pressure, cardiac contractility (maximal rate of change of left ventricular pressure), and mean pulmonary artery pressure. Rapid administration of HSB immediately corrected the strong ion acidosis, transiently increased arterial partial pressure of carbon dioxide (P(CO2)), and expanded the plasma volume. The transient increase in arterial P(CO2) did not alter CSF P(CO2) or induce paradoxical CSF acidosis. Compared to untreated control calves, HSB-treated calves had higher cardiac index and contractility and a faster rate of left ventricular relaxation for 1 hour after treatment, indicating that HSB administration improved myocardial systolic function. We conclude that rapid i.v. administration of HSB provided an effective and safe method for treating strong ion acidosis in normovolemic halothane-anesthetized calves with experimentally induced respiratory and strong ion acidosis. Fear of inducing paradoxical CSF acidosis is not a valid reason for withholding HSB administration in calves with mixed respiratory and strong ion acidosis.     

Renal tubular acidosis in horses (1980-1999)

Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.     

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.     

Effect of sodium bicarbonate infusion on serum osmolality, electrolyte concentrations, and blood gas tensions in cats.

The effects of single IV injections of sodium bicarbonate (0.5 mEq/kg of body weight, 1 mEq/kg, 2 mEq/kg, and 4 mEq/kg) on serum osmolality, serum sodium, chloride, and potassium concentrations, and venous blood gas tensions in 6 healthy cats were monitored for 180 minutes. Serum osmolality increased and remained significantly (P less than 0.05) increased for 120 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium was increased significantly (P less than 0.05) for 30 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium decreased and remained significantly (P less than 0.05) decreased for 120 minutes in cats given 1 g of 20% mannitol/kg, and serum osmolality was significantly (P less than 0.05) decreased at 30 and 60 minutes. Serum chloride decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and was significantly decreased for 30 minutes in cats given 2 mEq and 4 mEq of sodium bicarbonate/kg. Serum chloride decreased and remained significantly (P less than 0.05) decreased for 30 minutes in cats given 1 g of 20% mannitol/kg. Serum sodium and serum osmolality did not change significantly (P less than 0.05) in cats given 4 ml of 0.9% sodium chloride/kg. Serum potassium decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and for 120 minutes in cats given 2 mEq/kg or 4 mEq/kg. There was a significantly (P less than 0.05) greater decrease in serum potassium that lasted for 30 minutes after given sodium bicarbonate at the dosage of 4 mEq/kg, compared with other dosages given.(ABSTRACT TRUNCATED AT 250 WORDS)     

Investigations on the association of D-lactate blood concentrations with the outcome of therapy of acidosis, and with posture and demeanour in young calves with diarrhoea

The objective of this prospective study was to elucidate whether amounts of bicarbonate needed for correction of acidosis and normalization of clinical signs are influenced by blood D-lactate concentrations in calves with diarrhoea. In 73 calves up to 3 weeks old with acute diarrhoea and base excess values below -10 mmol/l correction of acidosis was carried out within 3.5-h by intravenous administration of an amount of sodium bicarbonate which was calculated using the formula: HCO (mmol) = body mass (kg) x base deficit (mmol/l) x 0.6 (l/kg). Clinical signs, venous base excess, and plasma D-lactate concentrations were monitored immediately following admission, following correction of acidosis at 4 h and 24 h after admission. The base excess and plasma D-lactate concentrations throughout the study were -17.8 +/- 4.0, -0.4 +/- 0.4, -3.0 +/- 5.5 mmol/l (base excess), and 10.0 +/- 4.9, 9.8 +/- 4.8, 5.4 +/- 3.4 mmol/l (D-lactate) for the three times of examination. Metabolic acidosis was not corrected in more than half of the calves (n = 43) by the calculated amount of bicarbonate, whereas the risk of failure to correct acidosis increases with D-lactate concentrations. The study shows that calves with elevated D-lactate concentrations do not need additional specific therapy, as D-lactate concentrations regularly fall following correction of acidosis and restitution of body fluid volume, for reasons that remain unclear. However, calves with distinct changes in posture and demeanour need higher doses of bicarbonate than calculated with the factor of 0.6 in the formula mentioned above probably because of D-hyperlactataemia.     

Effects of induced alkalosis on performance in thoroughbreds during a 1,600-m race.

There is considerable debate regarding the ergogenic effects of sodium bicarbonate (NaHCO3) on racing performance in horses. Anecdotal evidence suggests that NaHCO3 improves performance by increasing the buffering capacity of the blood and delaying the onset of hydrogen ion-induced fatigue. In a cross-over study, 16 Thoroughbred racehorses were given an aqueous solution of NaHCO3 (0.4 g/kg in 1 litre H2O) or a control treatment (1 litre H2O) before a 1600-m race. Treatments were administered 3 h before the race, which was the time to peak buffering capacity (2.5-3.0 h) determined in a separate study. Before the race, there was a significant increase in venous HCO3- and pH in the NaHCO3-treated horses. After the race, there was a significant increase in venous blood pH and lactate in the NaHCO3-treated horses. Collectively, the data suggest an improved buffering capacity of the blood after NaHCO3 treatment. However, there was no change in race times or venous partial pressure of carbon dioxide. Therefore, the administration of NaHCO3 provided no ergogenic benefit to horses competing in a 1,600-m race.     

Influence of Fasting on Canine Arterial and Venous Blood Gas and Acid-Base Measurements

Arterial and venous blood gas profiles were obtained from 33 clinically normal adult dogs of two breeds (German Shepherd Dog and English Pointer) 4 and 24 hours after eating. Fresh drinking water was available. All dogs were fed a nutritionally complete and balanced dry diet. Blood gas parameters measured included pH, pCO₂, pO₂, bicarbonate, base excess, total carbon dioxide, oxygen content, and oxygen saturation.
Statistically significant differences (P < 0.01) were found between sampling intervals (4 and 24 hours postprandial) for pCO₂, bicarbonate, total carbon dioxide, and base excess, for arterial and venous blood samples.
Statistically significant differences (P < 0.01) were found between arterial and venous blood for all parameters, at both sampling intervals.
No statistically significant interactions (P > 0.05) were found between sample type (arterial or venous) and sampling interval.
Correlations between arterial and venous samples were generally (but not exclusively) higher than correlations between sampling intervals. Breed differences were also noted.     

绵羊实验性乳酸酸中毒研究——Ⅱ.血气和阴离子隙对乳酸酸中毒的诊断价值

12只2～(?)岁健康绵羊被分为Ⅰ组(3只)、Ⅱ组(?)只)和Ⅲ组(3只),分别按2.5,5.0,10.0g/kg瘤胃内注入50%D-L消旋体乳酸溶液.Ⅱ组羊在恢复期因过度代偿而导致代谢性碱中毒。各实验绵羊血液pH值与HCO3-、BEB、TCO2、BEECF和SB成正相关,可作为绵羊乳酸酸中毒的可靠诊断依据。计算AG能反映绵羊酸中毒的程度。绵羊瘤胃内注入乳酸10.0g/kg体重,AG升高到35mmol/L时,绵羊处于休克状态,AG35mmol/L可作为乳酸酸中毒预后不良的监测指标。     

Effect of sodium bicarbonate on racing Standardbreds

Twenty-two Standardbred horses in race training were used in a crossover experiment to determine the effect of oral sodium bicarbonate (NaHCO3) administration on performance and metabolic responses to a 1.6-km (1-mile) race. Horses were paired and one horse in each pair was treated with either NaHCO3 (300 mg/kg BW) or a placebo, 2.5 h before they raced against each other. Each horse was scheduled to compete in two races, approximately 1 wk apart, one on each treatment. Horses always raced in the same pairs. Fourteen horses successfully completed both races. Jugular blood samples were obtained 1.5 h after treatment (rest), immediately before racing, 5 min post-race and 15 min post-race. In six horses, blood samples also were obtained 30 min post-race. Race times averaged 1.1 s faster after NaHCO3 treatment (P less than .1). Sodium bicarbonate treatment also elevated blood pH (P less than .05). In the horses sampled 15 and 30 min post-race, blood lactate disappearance was faster with the NaHCO3 treatment (P less than .05). The NaHCO3 may delay the fatigue precipitated by i.m. acidosis. Because other factors may limit performance (musculoskeletal soundness, cardiovascular and respiratory ability), NaHCO3 would not be expected to enhance the performance of all horses. However, the effect of NaHCO3 on lactate clearance may have implications for all intensively worked horses; because lactate and the associated hydrogen ions are believed to cause muscle damage and soreness, any mechanism to increase their removal rate could benefit the equine athlete.