Objective--To study whether end products of 2 pathways of anaerobic energy metabolism, lactate and purines, that accumulate in the blood after intense exercise indicate any relation to exercise performance. Design--Venous blood samples were taken within 1 and 15 minutes after a trotting race of 2,100 m. Animals--16 Clinically healthy Standardbred trotters. Procedure--Blood and plasma lactate concentrations were measured by enzymatic analyzer, and purines, uric acid and allantoin, were determined by high-performance liquid chromatography. The concentrations of metabolites were then correlated to racing time and individual performance indexes that are annually calculated from the percentage of winnings, placings, and starts rejected, average earnings per start, and the racing record. Results--Blood lactate concentration immediately and calculated cell lactate concentration immediately and 15 minutes after the race correlated positively (P < 0.05 to P < 0.01) with the individual performance indexes. Plasma lactate concentration was not correlated to the individual performance indexes. Uric acid concentration, immediately and 15 minutes after the race, was negatively correlated (P < 0.05) to the individual performance indexes, and a positive relation (P < 0.05) was found between the highest concentration of uric acid and the racing time. Concentration of allantoin immediately or 15 minutes after the race did not have any significant correlation to the individual performance indexes. Conclusions--Accumulation of lactate in the blood, which was greater in the superior performing horses, may prove to be an useful predictor of anaerobic capacity. The results also indicate that the loss of purine nucleotides was less in the superior performing horses, although further studies are needed to confirm this.

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, IV, 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, FL), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, FU). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (V(O2)) and carbon dioxide production (V(CO2)) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < .001) greater weight loss than did saline administration; mean +/- SEM weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (SEM = 2.0) for C, FL, and FU trials, respectively. The speed at which peak V(O2) was achieved was 9.31, 9.56, and 9.50 (SEM = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (SEM = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (SEM = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (SEM = 1.9) ml/min/kg, respectively. There was a significant (P = 0.070) group X speed interaction for V(CO2); during trial FU, horses had significantly (P < 0.05) lower rate of CO2 production at speed of 9 m/s and at the speed that caused peak V(O2), than during trial C. The respiratory exchange ratio during the FU trial was significantly (P < 0.05) less than that during the C trial at the speed that caused peak V(O2). Plasma lactate concentration at speed of 9 m/s for C, FL, and FU trials was 15.4, 16.5, and 13.3 (SEM = 0.8) mmol/L, respectively; values for the FL and C trials were not significantly different, whereas the mean value for the FU trial was significantly (P < 0.05) less than that for the C trial. Thus, administration of furosemide to horses altered the energetic response to exertion. Replacement of the furosemide-induced weight loss resulted in V(CO2), plasma lactate, and respiratory exchange values indistinguishable from those during the control trial.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Strongylus vulgaris, massive infections of nonimmune and immune ponies, pathogenesis characterized, blood chemical and peritoneal fluid values as possible diagnostic aids

Objective--To measure arterial and venous blood gas, coagulation, and fibrinolysis variables in blood from isolated segments of control and ischemic large colons for the purpose of identifying variables for rapid, indirect assessment of colonic mucosal injury. Design--Variables were determined at specific intervals during the 4-hour study (3 hours of ischemia and 1 hour of reperfusion). Animals--Seven clinically normal horses between 2 and 15 years old. Procedure--Horses underwent laparotomy and occlusion of the lumen and vasculature of the mid-portion of the pelvic flexure of the large colon. During ischemia of 1 randomly-chosen colonic segment, variables were measured to determine colonic mucosal damage and were compared with histologic scores of colonic biopsy specimens. Results--Significant (P < 0.05) differences from control values were observed over time for venous pH, Pco2, PO2, oxygen saturation, oxygen content, arteriovenous oxygen difference, and lactate and glucose concentrations. Mean histologic scores of biopsy specimens obtained from ischemic colons were significantly (P < 0.05) greater (indicating greater damage) than those from control colons, and increased significantly (P < 0.05) with duration of ischemia. Conclusions--Venous lactate, oxygen saturation, and PO2 values were the most significant predictors of the severity of histologic damage within the ischemic colons (R2 = 0.661). Clinical Relevance-Venous blood gas and lactate values in the large colon are good predictors of the amount of intestinal damage incurred during 3 hours of ischemia, and may be clinically useful for the rapid determination of colonic viability.

Health and ruminal variables were intensively measured during adaptation to grain-based diets in 6 beef cattle with fistulated rumens. The cows had been maintained on prairie grass hay-supplemented diets, and were converted to a grain-based finishing ration by feeding each successive diet (diets 1-4, respectively) for a period of 7 days. Each cow was evaluated and samples were obtained 3 times each day for the first 5 days that each diet was fed. Health variables monitored were rectal temperature, pulse, respiratory and rumen motility rates, fecal consistency, demeanor, blood pH, and blood glucose and L(+) lactate concentrations. Ruminal variables monitored were pH and glucose, DL-lactate, and volatile fatty acid concentrations of rumen contents. Data were analyzed by use of a multivariate ANOVA. We determined that most of the health variables were within reference rang limits throughout the adaptation period; however, analysis of pulse and respiratory rates indicated that diets 2 and 4 were stressful. Although blood pH continually decreased during feeding of the 4 diets (7.38 to 7.30), blood L(+) lactate and glucose concentrations had large increases only within diet 4. The pH of ruminal contents decreased progressively from 6.8 to 5.3. Rumen glucose concentration was low (< 1 micromole/ml), except with diet 4 in which values were 8 times higher than for other diets. By the end of the study, the ruminal contents of all animals were acidic (pH < 5.5), and, on the basis of higher than background amounts of ruminal glucose and DL-lactate, it was determined that rumen microbial equilibrium had not yet been achieved. Analysis of results of this study suggested that ruminal imbalance could be evaluated by monitoring pulse and respiratory rates, blood pH, and blood glucose concentrations. Assessment of the rumen alone could be accomplished by monitoring the variables of rumen pH, rumen glucose, and DL-lactate concentrations. Respiratory rate, blood and rumen content pH, and blood L(+) lactate concentrations were significantly (P < 0.001) affected by time after feeding.

A monoclonal antibody (MAB) against equine tumor necrosis factor-alpha (Eq TNF) was used to investigate the role of TNF in cytokine, eicosanoid, and metabolic responses of Miniature Horses given endotoxin. Plasma concentrations of interleukin 6 (IL-6), lactate, thromboxane A2 metabolite, and prostacyclin metabolite (6-keto-PGF(1 alpha)) were measured in 10 Miniature Horses given 0.25 micrograms of lipopolysaccharide (LPS; Escherichia coli O55:B5)/kg of body weight. Five horses were given Eq TNF MAB and 5 were given isotype-matched MAB as control. All horses were given 1.86 mg of antibody/kg by IV infusion, 5 minutes before LPS was given IV. Blood samples were taken 20 minutes before and at multiple intervals for 24 hours after LPS was given. Interleukin 6 bioactivity in plasma was measured, using IL-6-dependent cell line (B9). Eicosanoid activities were assessed by enzyme immunoassay, and plasma lactate concentration was determined enzymatically. Data were analyzed by ANOVA and Tukey's honest significant difference test for significant (P < 0.05) effect of treatment. Horses given Eq TNF MAB had significantly (P < 0.050) lower peak mean +/- SEM IL-6 (59 +/- 29 U/ml), lactate (16 +/- 2.00 mg/dl), and 6-keto-PGF(1 alpha) (254 +/- 79 pg/ml) values then did horses given control MAB (880 +/- 375 U/ml for IL-6; 26 +/- 0.04 mg/dl for lactate; and 985 +/- 290 pg/ml for 6-keto-PGF(1 alpha)). There was no effect of anti-TNF treatment on LPS-induced thromboxane A2 metabolite production. Tumor necrosis factor mediated IL-6, lactate, and prostacyclin responses, without affecting thromboxane production in horses given LPS.

Blood ionized calcium (Ca2+) and pH; plasma lactate concentrations; and total protein, total calcium (CaT), albumin, and phosphorus concentrations in serum were determined in 40 healthy horses before (T1), at the finish line (T2), and 10 minutes after the finish (T3) of the cross-country phase of a 3-dayevent competition. Mean (+/- SEM) Ca2+ concentrations decreased from 6.22 +/- 0.04 mg/dl at T1 to 5.04 +/- 0.07 mg/dl at T2 (P less than or equal to 0.05). This decrease was accompanied by a nonsignificant increase in CaT between T1 and T2. The mean (+/- SEM) percent ionization of calcium decreased significantly (P less than or equal to 0.05), from 50.9 +/- 2.75% at T1 to 40.3 +/- 3.58% at T2. Significant increases in mean albumin, total protein, phosphorus, and lactate concentrations and a significant decrease in mean pH were observed at T2 (P less than or equal to 0.05). At T3, mean Ca2+ and percent ionization had increased, but remained significantly less than resting values. Mean CaT was significantly decreased at T3, compared with values at T1 and T2. Correlation of mean Ca2+ concentration with all other measured variables at each time was evaluated; correlation coefficients between mean Ca2+ and all other variables were low (r2 less than or equal to 0.38), indicating low biological significance.

Collection of a satisfactory blood sample requires special procedures to prevent changes in glucose and lactate content after the sample has been obtained. Changes in measured plasma glucose and blood lactate concentrations attributable to anticoagulants and storage procedures, respectively, were examined in blood samples obtained from horses at rest and after exercise. To evaluate the effect of anticoagulants on measured plasma glucose concentration, blood was preserved with either sodium fluoride/potassium oxalate or lithium heparin. Measured plasma glucose concentration in blood obtained at rest and after exercise was 6 and 10% lower (P = 0.0038), respectively, when blood was preserved with fluoride/oxalate, compared with heparin. The erythrocyte volume in the blood sample was 15% smaller (P = 0.0001) in samples preserved with fluoride/oxalate, indicating a movement of water out of erythrocytes in the blood sample mixed with that anticoagulant. To evaluate the effect of storage procedure on measured blood lactate concentration, part of the blood sample was immediately deproteinized for blood lactate analysis, and the remaining blood was maintained for 30 and 60 minutes at either 0 or 22 C before deproteinization. When blood samples were maintained at 0 C prior to deproteinization, there was no difference in blood lactate concentration, regardless of the incubation time, compared with that in samples immediately deproteinized. Blood lactate concentration was greater (P < 0.01) in samples maintained at 22 C, compared with that in samples immediately deproteinized, and with that in equivalent samples maintained at 0 C. Blood preserved with fluoride/oxalate had lower measured plasma glucose concentration, compared with blood preserved with heparin, which was probably attributable to shrinkage of erythrocytes and dilution of the plasma with intracellular water. Minimal changes in blood lactate concentration were observed in samples maintained at 0 C up to 60 minutes.