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- Author or Editor: Warwick M. Bayly x
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Objective—To determine the relationship between plasma β-endorphin (EN) concentrations and exercise intensity and duration in horses.
Animals—8 mares with a mean age of 6 years (range, 3 to 13 years) and mean body weight of 450 kg.
Procedure—Horses were exercised for 20 minutes at 60% of maximal oxygen consumption (O2max) and to fatigue at 95% O2max. Plasma EN concentrations were determined before exercise, after a 10- minute warmup period, after 5, 10, 15, and 20 minutes at 60% O2max or at the point of fatigue (95% O2max), and at regular intervals after exercise. Glucose concentrations were determined at the same times EN concentrations were measured. Plasma lactate concentration was measured 5 minutes after exercise.
Results—Maximum EN values were recorded 0 to 45 minutes after horses completed each test. Significant time and intensity effects on EN concentrations were detected. Concentrations were significantly higher following exercise at 95% O2max, compared with those after 20 minutes of exercise at 60% O2max (605.2 ± 140.6 vs 312.3 ± 53.1 pg/ml). Plasma EN concentration was not related to lactate concentration and was significantly but weakly correlated with glucose concentration for exercise at both intensities (r = 0.21 and 0.30 for 60 and 95% O2max, respectively).
Conclusions and Clinical Relevance—A critical exercise threshold exists for EN concentration in horses, which is 60% O2max or less and is related to exercise intensity and duration. Even under conditions of controlled exercise there may be considerable differences in EN concentrations between horses. This makes the value of comparing horses on the basis of their EN concentration questionable. (Am J Vet Res 2000;61:969–973)
Objective—To investigate the effects of formaldehyde fixation on equine platelets using flow cytometric methods to evaluate markers of platelet activation.
Sample Population—Blood samples from 6 Thoroughbreds.
Procedure—The degree of fluorescence associated with binding of fluorescein isothiocyanate (FITC)-conjugated anti-human fibrinogen antibody and FITCannexin V in unactivated and adenosine diphosphate (ADP)-, platelet activating factor (PAF)-, and A23187- activated platelet samples in unfixed and 0.5, 1.0, and 2.0% formaldehyde-fixed samples was assessed by use of flow cytometry.
Results—In samples incubated with FITC-anti-human fibrinogen antibody prior to fixation, addition of 2.0% formaldehyde resulted in a 30% increase in total fluorescence in ADP- and PAF-activated samples and a 60% increase in A23187-activated samples. Fixation for 24 hours prior to addition of antibody resulted in reduced fluorescence of samples containing antihuman fibrinogen antibody for all 3 concentrations of formaldehyde in PAF-activated samples. The addition of all 3 concentrations of formaldehyde after incubation with FITC-annexin V resulted in significant increases in fluorescence in unactivated and activated platelet samples. As length of fixation time increased, there was a gradual increase in fluorescence that was significant at 24 hours.
Conclusion and Clinical Relevance—Because fixation with 2.0% formaldehyde results in significant changes in fluorescence in activated platelet samples containing anti-fibrinogen antibody, lower concentrations of formaldehyde should be used to fix equine platelet samples. Formaldehyde-fixed platelet samples should be analyzed within 12 hours of fixation to avoid artifactual increases in fluorescence. Fixation of samples containing FITC-annexin V should be avoided because of significant increases in fluorescence that may interfere with interpretation of results. (Am J Vet Res 2002;63:840–844)
Objective—To investigate the potential use of fluorescent- labeled annexin V, anti-human fibrinogen antibody, and anti-human thrombospondin antibody for detection of the activation of equine platelets by use of flow cytometry.
Sample Population—Platelets obtained from 6 Thoroughbreds.
Procedure—Flow cytometry was used to assess platelet activation as indicated by detection of binding of fluorescent-labeled annexin V, anti-human fibrinogen antibody, and anti-thrombospondin antibody to unactivated and ADP-, collagen-, platelet activating factor (PAF)-, and A23187-activated equine platelets. Human platelets were used as control samples. Determination of 14C-serotonin uptake and release was used to assess the extent of platelet secretion.
Results—Anti-human thrombospondin antibody failed to bind to equine platelets. Annexin V bound to platelets activated with PAF or A23187 when platelets had undergone secretion. Anti-human fibrinogen antibody bound to ADP-, PAF-, and A23817- activated platelets, but binding was not dependent on platelet secretion. The extent of binding of anti-fibrinogen antibody was less in equine platelets, compared with that for human platelets, despite maximal stimulation.
Conclusions and Clinical Relevance—Activation of equine platelets can be detected by use of fluorescent- labeled annexin V and anti-human fibrinogen antibody but not by use of anti-human thrombospondin antibody. These flow cytometric techniques have the potential for detection of in vivo platelet activation in horses at risk of developing thrombotic disorders. (Am J Vet Res 2002;63:513–519)
Objectives—To establish maximum oxygen consumption (O2max) in ponies of different body weights, characterize the effects of training of short duration on O2max, and compare these effects to those of similarly trained Thoroughbreds.
Animals—5 small ponies, 4 mid-sized ponies, and 6 Thoroughbreds.
Procedure—All horses were trained for 4 weeks. Horses were trained every other day for 10 minutes on a 10% incline at a combination of speeds equated with 40, 60, 80, and 100% of O2max. At the beginning and end of the training program, each horse performed a standard incremental exercise test in which O2max was determined. Cardiac output (), stroke volume (SV), and arteriovenous oxygen content difference (C [a-v] O2) were measured in the 2 groups of ponies but not in the Thoroughbreds.
Results—Prior to training, mean O2max for each group was 82.6 ± 2.9, 97.4 ± 13.2, and 130.6 ± 10.4 ml/kg/min, respectively. Following training, mean O2max increased to 92.3 ± 6.0, 107.8 ± 12.8, and 142.9 ± 10.7 ml/kg/min. Improvement in O2max was significant in all 3 groups. For the 2 groups of ponies, this improvement was mediated by an increase in ; this variable was not measured in the Thoroughbreds. Body weight decreased significantly in the Thoroughbreds but not in the ponies.
Conclusions and Clinical Relevance—Ponies have a lower O2max than Thoroughbreds, and larger ponies have a greater O2max than smaller ponies. Although mass-specific O2max changed similarly in all groups, response to training may have differed between Thoroughbreds and ponies, because there were different effects on body weight. (Am J Vet Res 2000; 61:986–991)
Objective—To investigate the effects of sodium citrate, low molecular weight heparin (LMWH), and prostaglandin E1 (PGE1) on aggregation, fibrinogen binding, and enumeration of equine platelets. Sample Population—Blood samples obtained from 4 Thoroughbreds.
Sample Population—Blood samples obtained from 4 Thoroughbreds.
Procedure—Blood was collected into syringes in the ratio of 9 parts blood:1 part anticoagulant. Anticoagulants used were sodium citrate, LMWH, sodium citrate and LMWH, or 300 nM PGE1/ml of anticoagulant. Platelet aggregation in response to ADP, collagen, and PGE1 was assessed, using optical aggregometry. Platelet activation was evaluated, using flow cytometry, to detect binding of fluorescein- conjugated anti-human fibrinogen antibody. Plasma concentration of ionized calcium was measured, using an ion-selective electrode.
Results—Number of platelets (mean ± SEM) in samples containing LMWH (109.5 ± 11.3 × 103 cells/µl) was significantly less than the number in samples containing sodium citrate (187.3 ± 30.3 × 103 cells/µl). Increasing concentrations of sodium citrate resulted in reductions in platelet aggregation and plasma concentration of ionized calcium. Addition of PGE1 prior to addition of an agonist inhibited platelet aggregation in a concentration-dependent manner, whereas addition of PGE1 4 minutes after addition of ADP resulted in partial reversal of aggregation and fibrinogen binding.
Conclusion and Clinical Relevance—A high concentration of sodium citrate in blood samples decreases plasma concentration of ionized calcium, resulting in reduced platelet aggregation and fibrinogen binding. Platelets tend to clump in samples collected into LMWH, precluding its use as an anticoagulant. Platelet aggregation and fibrinogen binding can be reversed by PGE1, which may result in underestimation of platelet activation. (Am J Vet Res 2001; 62:547–554)
Objective—To determine the cardiovascular and respiratory effects of water immersion in horses recovering from general anesthesia.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized 3 times with halothane and recovered from anesthesia while positioned in lateral or sternal recumbency in a padded recovery stall or while immersed in a hydropool. Cardiovascular and pulmonary functions were monitored before and during anesthesia and during recovery until horses were standing. Measurements and calculated variables included carotid and pulmonary arterial blood pressures (ABP and PAP, respectively), cardiac output, heart and respiratory rates, arterial and mixed venous blood gases, minute ventilation, end expiratory transpulmonary pressure (PendXes), maximal change in transpulmonary pressure (ΔPtpmax), total pulmonary resistance (RL), dynamic compliance (Cdyn), and work of breathing ().
Results—Immersion in water during recovery from general anesthesia resulted in values of ABP, PAP, PendXes, ΔPtpmax, RL, and that were significantly greater and values of Cdyn that were significantly less, compared with values obtained during recovery in a padded stall. Mode of recovery had no significant effect on any other measured or calculated variable.
Conclusions and Clinical Relevance—Differences in pulmonary and cardiovascular function between horses during recovery from anesthesia while immersed in water and in a padded recovery stall were attributed to the increased effort needed to overcome the extrathoracic hydrostatic effects of immersion. The combined effect of increased extrathoracic pressure and PAP may contribute to an increased incidence of pulmonary edema in horses during anesthetic recovery in a hydropool. (Am J Vet Res 2001;62:1903–1910)