Partial pressures of oxygen and carbon dioxide, pH, and concentrations of bicarbonate, lactate, and glucose in pleural fluid from horses

Samples of pleural fluid from 20 horses with effusive pleural diseases of various causes were evaluated; samples from 19 horses were used for the study. There were differences for pH (P = 0.001) and partial pressure of oxygen (PO2) between arterial blood and nonseptic pleural fluid (P = 0.0491), but there were no differences for pH, PO2, partial pressure of carbon dioxide (PCO2), and concentrations of bicarbonate (HCO3-), lactate, and glucose between venous blood and nonseptic pleural fluid. Paired comparisons of venous blood and nonseptic pleural fluid from the same horse indicated no differences. There were differences (P = 0.0001, each) for pH, PO2, PCO2, and concentrations of HCO3- between arterial blood and septic pleural fluid. Differences also existed for pH (P = 0.0001), PCO2 (P = 0.0003), and concentrations of HCO3- (P = 0.0001), lactate (P = 0.0051), and glucose (P = 0.0001) between venous blood and septic pleural fluid. Difference was not found for values of PO2 between venous blood and septic pleural fluid, although 4 samples of septic pleural fluid contained virtually no oxygen. Paired comparisons of venous blood and septic pleural fluid from the same horse revealed differences (P less than 0.05) for all values, except those for PO2. These alterations suggested functional and physical compartmentalization that separated septic and healthy tissue. Compartmentalization and microenvironmental factors at the site of infection should be considered when developing therapeutic strategies for horses with septic pleural disease.     

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)     

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.     

Determinants of oxygen delivery and hemoglobin saturation during incremental exercise in horses

OBJECTIVE: To determine components of the increase in oxygen consumption (VO2) and evaluate determinants of hemoglobin saturation (SO2) during incremental treadmill exercise in unfit horses. ANIMALS: 7 unfit adult mares. PROCEDURES: Horses performed 1 preliminary exercise test (EXT) and 2 experimental EXT. Arterial and mixed venous blood samples and hemodynamic measurements were taken during the last 30 seconds of each step of the GXT to measure PO2, hemoglobin concentration ([Hb]), SO2, and determinants of acid-base state (protein, electrolytes, and PCO2). RESULTS: Increased VO2 during exercise was facilitated by significant increases in cardiac output (CO), [Hb], and widening of the arteriovenous difference in O2. Arterial and venous pH, PaO2, and PvO2 decreased during exercise. Arterial PCO2, bicarbonate ([HCO3-])a, and [HCO3-] decreased significantly, whereas PVCO2 and increased. Arterial and venous sodium concentration, potassium concentration, strong ion difference, and venous lactate concentration all increased significantly during exercise. CONCLUSIONS AND CLINICAL RELEVANCE: Increases in CO, [Hb], and O2 extraction contributed equally to increased VO2 during exercise. Higher PCO2 did not provide an independent contribution to shift in the oxyhemoglobin dissociation curve (OCD) in venous blood. However, lower PaCO2 shifted the curve leftward, facilitating O2 loading. The shift of ODC resulted in minimal effect on O2 extraction because of convergence of the ODC at lower values of PO2. Decreased pH appeared responsible for the rightward shift of the ODC, which may be necessary to allow maximal O2 extraction at high blood flows achieved during exercise.     

A Comparison of Simultaneously Collected Arterial, Mixed Venous, Jugular Venous and Cephalic Venous Blood Samples in the Assessment of Blood-Gas and Acid-Base Status in the Dog

Blood samples were collected simultaneously from the pulmonary artery, jugular vein, cephalic vein, and carotid artery in awake dogs. Blood-gas and acid-base values were measured from these blood samples in normal dogs and in dogs after production of metabolic acidosis and metabolic alkalosis. The values obtained from each of the venous sites were compared with those obtained from arterial blood to determine if venous blood from various sites accurately reflected acid-base balance and could therefore be used in the clinical patient. The results of this study demonstrated significant differences between the blood from various venous sites and the arterial site for PCO2 and pH in all acid-base states. Significant differences for standard bicarbonate (SHCO3) were found only when jugular and cephalic venous blood were compared with arterial blood in dogs with a metabolic acidosis. No significant differences were found for BE when blood from the venous sites was compared with arterial blood. The values for pH, HCO3, TCO2, BE, and SHCO3 measured on blood collected at the various venous sites were found to correlate well with those obtained from arterial blood, with a correlation coefficient of 0.99 for HCO3, TCO2, BE, and SHCO3. These correlation coefficients, together with similar values in BE at all collection sites, indicate that, in the dog with normal circulatory status, blood from any venous site will accurately reflect the acid-base status of the patient.     

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.     

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.     

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.     

Blood gas and acid-base values in calves, sampled from the brachial and coccygeal arteries

Blood samples were taken from the brachial and coccygeal arteries of young calves and blood gas and acid-base values determined. There was no significant difference in pH, PO2, PCO2 or HCO3- between sites as demonstrated by a paired t-test (P greater than 0.05). Significant correlations between sites existed for individual values of PO2 (P less than 0.001), HCO3- (P less than 0.05) and pH (P less than 0.02), but not for PCO2.     

Physiological responses in swine treated with water containing sodium bicarbonate as a prophylactic for gastric ulcers

Maintenance of gastric pH above 4.0 aids the prevention of bile acid-mediated ulcerative damage to the pars esophageal tissue in pigs. One means of doing so is the addition of buffering compounds, such as sodium bicarbonate, to the water supply; however, any potential physiological effect of buffer consumption has yet to be determined. Experiment 1 tested the acute effects of buffer addition to the water supply on systemic acid-base and electrolyte balance in swine (BW 40.7 +/- 3.0 kg). Consumption of water calculated to a 200 mOsm solution with sodium bicarbonate for 24 h increased (P < 0.05) blood Na+, HCO3(-), and pCO2, although these effects were all within physiologically tolerable levels. Urine pH and Na+ excretion increased (P < 0.001) following the consumption of NaHCO3, with Na+ concentration almost threefold higher in treated pigs compared with controls. Experiment 2 determined the chronic systemic effects of buffer consumption by measuring blood and urine variables, with pigs consuming NaHCO3-treated water throughout. Water consumption increased (P < 0.001) during buffer consumption, although intake levels remained within normal ranges. Blood pH levels were not affected by long-term consumption of dietary buffer; however, blood HCO3(-) (P < 0.05), Na+, and pCO2 (P < 0.01) increased. Urine pH and urine Na+ concentration increased (P < 0.01) in buffer-treated compared with control animals. Results indicate that sodium bicarbonate can safely be added to the water supply for pigs, with no clinically relevant alterations in acid-base balance because the animals readily compensate for buffer intake.     

Effects of handling intensity and live weight on blood acid-base status in finishing pigs

The objective of this study was to determine the effect of live weight on the plasma acid-base response of pigs subjected to various handling intensities. Eighty pigs (equal numbers of barrows and gilts) were used in a completely randomized block design with a 2 x 2 x 2 factorial arrangement of the following treatments: 1) live weight (light [104 kg] vs. heavy [128 kg]), 2) handling intensity (low vs. high), and 3) gender (barrows vs. gilts). Before the handling test, pigs were weighed, venous blood samples were taken to establish baseline levels, and rectal temperature was measured. Pigs were allowed to rest for 2 h before being subjected to the handling treatments, which consisted of moving the pigs through a course (12.2 m long x 0.91 m wide), for a total of eight laps. Animals on the high-intensity treatment were moved rapidly through the course and subjected to a total of 16 single shocks (two shocks per lap) with an electric livestock goad, whereas pigs on the low-intensity treatment were moved at their own pace using a moving panel and a paddle. Rectal temperature and a venous blood sample were taken immediately after handling and at 2 h after handling. Blood plasma was assayed for pH, partial pressure of carbon dioxide (PCO2), partial pressure of oxygen (PO2), saturated oxygen (SO2), total carbon dioxide (TCO2), bicarbonate (HCO3), base excess, and lactate. Live weight had no effect on the baseline measurements. After handling, light pigs had higher (P < 0.05) blood SO2 (65.6 vs. 57.2+/-2.80%) and showed a greater (P < 0.05) increase in PO2 from baseline to post-handling than heavy pigs (15.6 vs. 8.3+/-2.63 mmHg). Post-handling, pigs on the high- compared with the low-intensity handling treatment had greater (P < 0.001) lactate (19.1 vs. 4.9+/-0.56 mmol/L) and PO2 (51.6 vs. 36.5+/-2.44 mmHg) with lower (P < 0.001) TCO2 (18.6 vs. 34.7+/-0.64 mmol/L), pH (7.02 vs. 7.36+/-0.015), HCO3 (16.7 vs. 33.0+/-0.62 mmol/L), and base excess (-14.2 vs. 7.5+/-0.75) values. There were no effects of gender on blood measurements or rectal temperatures. Results from this study highlight a major effect of pig handling intensity, a limited effect of live weight, and no effect of gender on blood acid-base responses to handling.     

Voluntary feed intake, acid-base balance and partitioning of urinary nitrogen in lambs fed corn silage with added sodium bicarbonate or sodium sesquicarbonate

An experiment with growing lambs was designed to test the hypothesis that alterations in blood acid-base status would influence intake of corn silage. Six wethers (29 kg) were fed a diet of corn silage (36% DM, 8% CP) supplemented with 1.25% urea and .2% sulfur. At feeding time, sodium bicarbonate (NaHCO3) and sodium sesquicarbonate (NaSC) were added to the silage at levels of 0, 2% or 4% of diet DM. The treatments were arranged as a 2 x 3 factorial, and the study was conducted as a 6 x 4 incomplete latin square with four 17-d periods. Voluntary intake of OM was not different (P greater than .05) between NaHCO3 (1,008 g/d) and NaSC (1,041 g/d). There was no significant interaction between type of buffer (NaHCO3 or NaSC) and level of buffer on any of the variables measured. The progressive increase in buffer load did not alter feed intake (P greater than .05), although there was a quadratic response (P less than .05) in urine pH and a linear increase (P less than .01) in blood HCO3- 2 h after feeding. There was no evidence that lambs fed corn silage experienced metabolic acid stress. Urinary excretion of ammonia and urea were indicative of changes, although not pronounced, in ammoniuria and ureapoiesis in response to bicarbonate loading. This study implies that corn silage imposes no "acid stress" on lambs and, consequently, that there is no nutritional benefit in adding buffers to corn silage for sheep.     

Evaluation of colostral IgG1 absorption in newborn calves after treatment with alkalinizing agents.

The effects of alkalinizing agents, administered prior to feeding colostrum, on blood-gas and acid-base values and on absorption of IgG1 were determined in 40 newborn Holstein calves. Two treatments, sodium bicarbonate (3 mEq/kg of body weight, IV) and doxapram HCl (2 mg/kg, IV), were evaluated, using a randomized complete-block experimental design. These treatments resulted in significant (P less than 0.01) alteration of blood-gas and acid-base values, generally in the direction of normal values for adult cattle. Significant least squares mean effects were detected for sodium bicarbonate treatment on blood pH (+ 0.04 units, P less than 0.01), PCO2 (+ 4.1 mm of Hg, P less than 0.01), and HCO3 concentration (+ 4.4 mEq/L, P less than 0.01). Significant least squares mean effects were detected for doxapram HCl treatment on blood pH (+ 0.06 pH units, P less than 0.01) and PCO2 (-5.2 mm of Hg, P less than 0.01). Absorption of colostral IgG1 was not affected by the treatments given or by the altered blood-gas and/or acid-base status.     

The Effects of Equivalent Doses of Tromethamine or Sodium Bicarbonate in Healthy Horses

Objective—To describe the effects of tromethamine, a putative treatment for metabolic acidosis, and to compare its biochemical effects with those of sodium bicarbonate.
Design—Randomized intervention study with repeated measures.
Animals—16 healthy horses, 3 to 17 years old, weighing 391 to 684 kg.
Methods—Ten horses received 3 mEq/kg tromethamine and six received 3 mEq/kg sodium bicarbonate. Samples of venous blood and cerebrospinal fluid (CSF) were collected at intervals before and after drug administration. Heart rate and breathing rate were also recorded at intervals. Results—Median standard base excess increased significantly ( P < .05) from baseline immediately after both bicarbonate and tromethamine. These increases were not significantly different between treatments. Standard base excess returned toward baseline but remained significantly increased 3 hours after infusion of either treatment. After tromethamine, there was a significant decrease in plasma sodium concentration that lasted for at least 90 minutes. After sodium bicarbonate, no change in plasma sodium concentration was detected. Both sodium bicarbonate and tromethamine increased carbon dioxide tension in venous blood and CSF. Despite venous alkalemia, the pH of CSF decreased after both treatments.
Conclusions—Tromethamine and sodium bicarbonate have similar alkalinizing ability. Tromethamine causes hyponatremia, whereas both tromethamine and sodium bicarbonate increase carbon dioxide tension in venous blood and CSF.
Clinical Relevance—If hyponatremia, hypercarbia, and acidosis of the CSF occur after tromethamine is given to horses with existing metabolic acidosis, some of the potential advantages of tromethamine may prove theoretical rather than practical.     

Effects of hyperosmolar ionic and low osmolar non-ionic contrast media on acid base, blood gas and electrolyte status in dogs

The dogs in groups I, II and III in equal numbers received diatrizoate, iohexol and ioxilan at a dose of 700 mgI/kg intravenously (i.v.) as a bolus, respectively. Blood samples were collected prior to contrast media (CM) administration and thereafter at 3, 15, 30, 60, 90 and 180 min to evaluate acid-base, venous blood gas status (pH, PCO2, PO2, HCO, BE, O2) and electrolytes (Na+, Ca++, K+). Values of pH, PCO2, BE, HCO, Na+ and K+ remained unchanged or within non-significant fluctuations compared with the baseline values. PO2 was significantly different from the baseline values in group 1 up to 90 min after administration, significant alterations were found for O2 saturation in group 1 up to 90 min, and in group II at 3, 60 and 180 min; and for Ca++ in group 1 at all time points except at 90 min, and groups II and II at 3 and 15 min post administration. It was concluded that none of the CM are considered to cause long-lasting and major effects on acid-base, blood gas and electrolyte status.     

Quantitative analysis of acid-base balance in show jumpers before and after exercise

The acid-base status of venous blood was studied in 17 show jumpers before and after exercise using both a traditional and a quantitative approach. Partial pressure of carbon dioxide (PCO(2)), pH, haemoglobin, and plasma concentrations of sodium (Na(+)), chloride (Cl(-)), potasium (K(+)), ionized calcium (Ca(2+)), total proteins, albumin, lactate and phosphorus were measured in jugular venous blood samples obtained before and immediately after finishing a show jumping competition. Bicarbonate, anion gap and globulin concentration were calculated from the measured parameters. 'Quantitative analysis' of acid-base balance was performed utilising values for three independent variables: PCO(2), strong ion difference [SID = (Na(+)+ K(+)+ Ca(2+)) - (Cl(-)+ Lact)] and total concentration of weak acids [A(T)= Alb (1 paragraph sign23 pH - 6 paragraph sign31) + Pi (0 paragraph sign309 pH - 0 paragraph sign469) 10/30 paragraph sign97]; plasma concentrations of hydrogen ion ([H(+)]) were also calculated from these variables using Stewart's equation. No significant changes in blood pH were detected after the show jumping competition. Exercise resulted in a significant increase in lactate, Na(+), K(+), haemoglobin, total proteins, albumin, globulin and anion gap, and a decrease in bicarbonate, Cl(-)and Ca(2+). PCO(2)decreased after exercise while SID and A(T)increased. A significant correlation between measured and calculated [H(+)] was found both before and after exercise. However, individual [H(+)] values were not accurately predicted from Stewart's equation. In conclusion, even though pH did not change, significant modifications in the acid-base balance of horses have been found after a show jumping competition. In addition, quantitative analysis has been shown to provide an adequate interpretation of acid-base status in show jumpers before and after exercise.     

Effect of dietary starch, fat, and bicarbonate content on exercise responses and serum creatine kinase activity in equine recurrent exertional rhabdomyolysis

To determine the effect of dietary starch, bicarbonate, and fat content on metabolic responses and serum creatine kinase (CK) activity in exercising Thoroughbreds with recurrent exertional rhabdomyolysis (RER), 5 RER horses were fed 3 isocaloric diets (28.8 Mcal/d [120.5 MJ/d]) for 3 weeks in a crossover design and exercised for 30 minutes on a treadmill 5 days/wk. On the last day of each diet, an incremental standardized exercise test (SET) was performed. The starch diet contained 40% digestible energy (DE) as starch and 5% as fat: the bicarbonate-starch diet was identical but was supplemented with sodium bicarbonate (4.2% of the pellet): and the fat diet provided 7% DE as starch and 20% as fat. Serum CK activity before the SET was similar among the diets. Serum CK activity (log transformed) after submaximal exercise differed dramatically among the diets and was greatest on the bicarbonate-starch diet (6.51 +/- 1.5) and lowest on the fat diet (5.71 +/- 0.6). Appreciable differences were observed in the severity of RER among individual horses. Postexercise plasma pH, bicarbonate concentration, and lactate concentration did not differ among the diets. Resting heart rates before the SET were markedly lower on the fat diet than on the starch diet. Muscle lactate and glycogen concentrations before and after the SET did not differ markedly among the diets. A high-fat, low-starch diet results in dramatically lower postexercise CK activity in severely affected RER horses than does a low-fat, high-starch diet without measurably altering muscle lactate and glycogen concentrations. Dietary bicarbonate supplementation at the concentration administered in this study did not prevent increased serum CK activity on a high-starch diet.     

Acid-base and electrolyte balance in dairy heifers fed forage and concentrate rations: effects of sodium bicarbonate

Eight Holstein heifers were fed diets of alfalfa hay, corn silage, or finely ground corn grain with or without NaHCO3 in a rotating experimental design. Acid-base status and renal excretion of electrolytes were evaluated during short-term (1 and 5 day) and long-term (24 day) feeding trials. Heifers fed alfalfa hay had a greater metabolic buffering capacity than did heifers fed corn silage. Heifers fed grain had lower blood pH and bicarbonate values than did those fed the forage diets. The most pronounced effects of grain-feeding were aciduria and phosphaturia. Aciduria did not occur when NaHCO3 was added to the grain at 2% of the ration on a dry matter basis. Grain-fed heifers had significantly (P less than 0.05) lower blood and urine pH and bicarbonate values, and excreted significantly more calcium, phosphorus, and magnesium in the urine than did those fed grain plus NaHCO3. Sodium bicarbonate, as a 2% dietary supplement, counteracted many effects of high-grain diets.     

Effects of training on biochemical values in standardbred horses.

Effects of training at a regular, fixed, standard exercise load on venous lactic acid, mixed venous and arterial blood gases and pH, and serum muscle enzymes were determined on previously unconditioned, healthy, adult, Standardbred horses. Arterial and mixed venous blood gases, pH, and serum muscle enzymes did not change in a consistent manner during training. Venous lactic acid concentrations did increase significantly with training and may be of value for the biochemical evaluation of fitness in horses.