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Biomedical subjects

W M Bayly

Publications and source records attributed to W M Bayly.

At least 19 recordsLinked to original sources

Effects of different volumes of autologous blood instilled into the airways of horses on pulmonary function during treadmill exercise.

Exercise-induced pulmonary haemorrhage has been associated with reduced performance in racing horses. However, it is unclear what volume of blood loss into the lungs impairs performance. The purpose of the present study was to determine the minimal volume of autologous Horses blood instilled into the airways that significantly affects performance and pulmonary function in exercising horses. Six Thoroughbred horses performed 2 exercise bouts on each of 4 treatment test days. Each exercise bout consisted of a 2 min warm-up at 4 m/s followed by running at a speed equivalent to 115% VO2max, until fatigued. For the first run of each testing day there was no treatment (baseline run). Prior to the second run either there was no treatment (control) or 100, 50 or 25 ml of autologous blood was instilled into the airways on the right hand side. During each test, arterial and mixed venous blood was sampled, and VO2, VCO2 and breathing mechanics measured. The results of this study indicate that unilateral instillation of 100 ml of blood or less into the airways of horses does not significantly affect pulmonary function, breathing mechanics or performance during supramaximal exercise. The results of this study may be helpful in determining the significance of exercise-induced pulmonary haemorrhage on racing performance.

Animals↗

Evaluation of binding of fibrinogen and annexin V to equine platelets in response to supramaximal treadmill exercise.

There is evidence that equine platelet reactivity is altered by strenuous exercise. Changes in platelet reactivity could impact haemostasis following exercise-induced injury and may play a role in the pathophysiology of exercise-induced pulmonary haemorrhage. Interpretation of results of previous studies is hindered by potential in vitro-induced changes in platelet activity through the choice of anticoagulant and the use of platelet inhibitors. The present study was undertaken to re-evaluate the effect of exercise on equine platelets using methodologies that minimise in vitro-induced changes in platelet activation. The percentage of platelet-neutrophil aggregates increased significantly (P = 0.01) from mean +/- s.e. 3.5 +/- 0.6% at rest to 7.2 +/- 13% during exercise. There were no significant changes in binding of anti-fibrinogen antibody or annexin V to platelets in response to exercise. An inability to detect increased binding of fibrinogen or annexin V may be a result of poor test sensitivity or low statistical power. Alternatively, activated platelets may be quickly removed from the circulation and miss detection. The significance of increased numbers of platelet-neutrophil aggregates in association with exercise is currently unknown and warrants further investigation.

Animals↗

Effects of inhaled ipratropium bromide on breathing mechanics and gas exchange in exercising horses with chronic obstructive pulmonary disease.

Six Warmblood horses suffering an acute exacerbation of COPD were tested to investigate whether inhalation of ipratropium bromide (IB) dry powder (2,400 microg) 30 min preexercise would improve their exercise capacity. A cross-over protocol with an inert powder placebo (P) was used. Mechanics of breathing and arterial blood gases were determined before treatment, after treatment but pre-exercise, and during an incremental exercise test. Oxygen consumption (VO2) was also measured before and during exercise, and the time to fatigue recorded. Inhalation of IB reduced total pulmonary resistance (RL) and maximum intrapleural pressure changes (deltaPpl(max)) and increased dynamic compliance before exercise. The onset of exercise was associated with a marked decrease in RL in P-treated horses but not those receiving IB, so that RL during exercise was not affected by treatment. Although deltaPpl(max) was lower at 8,9 and 10 m/s with IB, there were no treatment-related changes in VO2, blood gases, time to fatigue or any other measurement of breathing mechanics. Therefore, although inhalation of IB prior to exercise may have improved deltaPpl(max), it had no apparent impact on the horses' capacity for exercise.

Administration, Inhalation↗

Cardiopulmonary function in horses during anesthetic recovery in a hydropool.

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 (P(endXes)), maximal change in transpulmonary pressure (deltaP(tp)max), total pulmonary resistance (RL), dynamic compliance (Cdyn), and work of breathing (W). RESULTS: Immersion in water during recovery from general anesthesia resulted in values of ABP, PAP P(endXes), deltaP(tp)max, R(L), and W 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.

Anesthesia Recovery Period↗

Effects of sodium citrate, low molecular weight heparin, and prostaglandin E1 on aggregation, fibrinogen binding, and enumeration of equine platelets.

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. 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 x 10(3) cells/microl) was significantly less than the number in samples containing sodium citrate (187.3+/-30.3 x 10(3) cells/microl). 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. CONCLUSIONS 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.

Adenosine Diphosphate↗

Effects of inhalation of albuterol sulphate, ipratroprium bromide and frusemide on breathing mechanics and gas exchange in healthy exercising horses.

The possibility that pre-exercise inhalation of a bronchodilator by healthy horses could improve their mechanics of breathing and enhance performance was investigated. Ipratropium bromide (0.35 microg/kg bwt; n = 7) was administered by nebulisation 30 min before exercise and frusemide (1 mg/kg bwt; n = 6) was given in the same manner 2 h before exercise. Albuterol sulphate (360 and 720 microg; n = 7) were administered with a metered dose inhaler 2 h before exercise. Each drug was investigated independently of the others using cross-over protocols. Horses completed incremental exercise tests and oxygen consumption, carbon dioxide production, arterial blood gases, heart rate and measures of breathing mechanics including total pulmonary resistance (RL) and nasopharyngeal resistance (RU) were determined for each exercise intensity. The resistance of the lower airways was calculated subsequently from the difference between RL and RU. None of the drugs tested had an effect on any of the variables measured, possibly because maximal bronchodilation is stimulated in healthy horses by the normal sympathoadrenergic response to exercise. Therefore, the pre-exercise inhalation of a bronchodilator by a healthy horse is unlikely to improve performance capacity.

Albuterol↗

Effects of exercise intensity and duration on plasma beta-endorphin concentrations in horses.

OBJECTIVE: To determine the relationship between plasma beta-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 (VO2max) and to fatigue at 95% V02max. Plasma EN concentrations were determined before exercise, after a 10-minute warmup period, after 5, 10, 15, and 20 minutes at 60% VO2max or at the point of fatigue (95% VO2max), 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% VO2max, compared with those after 20 minutes of exercise at 60% VO2max (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% VO2max, respectively). CONCLUSIONS AND CLINICAL RELEVANCE: A critical exercise threshold exists for EN concentration in horses, which is 60% VO2max 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.

Animals↗

Effects of training on maximum oxygen consumption of ponies.

OBJECTIVES: To establish maximum oxygen consumption VO2max) in ponies of different body weights, characterize the effects of training of short duration on VO2max, 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 VO2max. At the beginning and end of the training program, each horse performed a standard incremental exercise test in which VO2max was determined. Cardiac output (Q), 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 VO2max for each group was 82.6 = 2.9, 97.4 +/- 13.2, and 130.6 +/- 10.4 ml/kg/min, respectively. Following training, mean VO2max increased to 92.3 +/- 6.0, 107.8 +/- 12.8, and 142.9 +/- 10.7 ml/kg/min. Improvement in VO2max was significant in all 3 groups. For the 2 groups of ponies, this improvement was mediated by an increase in Q; 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 VO2max than Thoroughbreds, and larger ponies have a greater VO2max than smaller ponies. Although mass-specific VO2max changed similarly in all groups, response to training may have differed between Thoroughbreds and ponies, because there were different effects on body weight.

Animals↗

Effects of inhaled dry powder ipratropium bromide on recovery from exercise of horses with COPD.

The present study evaluated ventilatory, cardiovascular and metabolic parameters during recovery from strenuous exercise in horses suffering from a crisis of chronic obstructive pulmonary disease (COPD) and to determine whether ipratropium dry powder inhalation (DPI) before exercise has an effect on these parameters. When 6 saddle horses, affected with COPD, developed airway obstruction, they inhaled placebo and ipratropium (2400 microg/horse), the order being randomly chosen. Pulmonary function tests were then recorded 15 min after inhalation. Following these tests, the horses underwent a strenuous treadmill exercise, followed by a recovery period that consisted of a 10 min walk. Measurements were made at the first and tenth min of recovery. Respiratory flow, O2 and CO2 fractions in the respired gas, pleural pressure changes and heart rate were recorded. Arterial and mixed venous blood samples were analysed for gas tensions, haemoglobin and plasma lactate concentrations. Oxygen consumption (VO2), CO2 production, tidal volume, alveolar oxygen tension (PAO2), alveolar ventilation, the alveolar-pulmonary capillary oxygen difference ((A-a)dO2) and total pulmonary resistance (RL) were measured. The PAO2 was the only parameter significantly improved during recovery following ipratropium DPI. This improvement was not accompanied by evidence of improvement of other ventilatory or cardiorespiratory parameters. The results showed that in horses suffering from a crisis of COPD, recovery is characterised by an exercise-induced bronchodilation. Secondly, ipratropium DPI at a dose of 2400 microg/horse is an effective bronchodilator in these horses at rest but it has little effect on the airway calibre during the recovery period. It is suggested that the short term recovery period is still influenced by exercise-induced adjustments that may exceed the bronchodilatory effect of inhaled ipratropium that are observed before exercise.

Administration, Inhalation↗

Effect of breathing frequency and airflow on pulmonary function in high-intensity equine exercise.

It has been postulated that the hypoxaemia and hypercapnoea that characterize strenuous equine exercise are partly due to flow limitations imposed by high breathing frequencies (fb), and that gas exchange would be improved if fb could be lowered. To evaluate this possibility, 6 Thoroughbred horses underwent 4 incremental treadmill exercise tests at inclines of 0, 5, 10 and 25%, respectively. In the test, horses were given a warm-up for 2 min, then ran sequentially for 1 min each at 60, 100 and 115% VO2max. Oxygen consumption (VO2), blood gas tensions (PaO2, PaCO2), fb, tidal volume (VT), minute ventilation (Ve), transpulmonary pressure (Ptp), peak inspiratory and expiratory airflows (VI, VE) and work of breathing (Wrm) were determined during the last 15 s of exercise at each intensity. The only effect of fb on PaO2 was seen at 60% VO2max. Also, maximal transpulmonary pressure difference (delta Ptpmax), and peak VI, and VE on a 25% slope were lower than those recorded at the other 3 inclines at 60% VO2max. At 100 and 115% VO2max, the effect of fb was less clear. While fb still differed, the only effects of fb at 100% VO2max were on delta Ptpmax. At 115% VO2max, fb on a 25% incline was lower than that for 0 and 5% slopes. The only other difference noted at this intensity was in VT on 10% slope. However, there was no difference between VTS recorded at inclines of 0, 5 or 25% at 115% VO2max. There was no effect of fb or exercise intensity on Ve at 100 or 115% VO2max. There was no change in PaO2, fb, VT, delta Ptpmax or VI and VE as exercise intensity increased from 60-115% VO2max on slopes of 0, 5 or 10%. However, for exercise on the 25% incline (i.e. with lower fb), each of these parameters increased (or decreased for PaO2) from 60-100%, but not from 100-115% VO2max. Failure of peak airflow and VT to increase when intensity increased was associated with the development of hypoxaemia and hypercapnoea, regardless of slope or fb. It is concluded that while a low fb may have some beneficial effect on gas exchange during submaximal exercise at approximately 60% VO2max, this effect disappears as exercise intensity increases. There appear to be limits to the peak airflows that can be generated by horses during strenuous exercise, and these limits may be reached regardless of fb. Flow limitation per se may play a greater role in the development of exercise-induced hypoxaemia and hypercapnoea in horses than dose fb.

Animals↗

Differences in the ventilatory responses of horses and ponies to exercise of varying intensities.

Horses exercising at > or = approximately 90% VO2max develop arterial hypoxaemia with concurrent hypercapnoea, whereas ponies exercising at comparative levels become hypocapnoeic and maintain arterial oxygen tensions close to resting values. We sought to investigate the possibility that these differences relate to the ventilatory responses of these animals to exercise. Six Thoroughbred horses weighing mean +/- s.e. 501 +/- 27 kg and 5 ponies weighing mean +/- s.e. 164 +/- 18 kg exercised for 2 min on a 10% slope at speeds calculated to require 60% VO2max and for at least 1 min at speeds calculated to require 115% VO2max. Oxygen consumption (VO2), arterial oxygen (PaO2) and carbon dioxide (PaCO2) tensions, acid-base balance, tidal volume (VT), minute ventilation (VE), peak inspiratory (VImax) and expiratory (VEmax) flow, and maximal changes in transpulmonary pressures (delta PtPmax) were measured immediately before exercise and in the last 15 s of exercise at each intensity. The results confirmed that, unlike horses, ponies do not become hypoxaemic or hypercapnoeic during exercise. Despite having a higher delta PtPmax, higher VImax and VEmax and VE/kg0.75 at the same relative intensities, horses were less capable of mounting an appropriate ventilatory response to exercise. This was reflected by lower mass specific and metabolic weight-based ventilations at similar absolute workloads, and their higher PaCO2 and arterial HCO3-[, and lower ventilatory equivalent for oxygen (VE/VO2). This suggests that horses become hypoxaemic and hypercapnoeic at work loads > or = approximately 90% VO2max because their metabolic demand surpasses the capacity of their ventilatory system to meet this demand. Because ponies are less capable athletes, they can match their ventilatory response to their metabolic requirements.

Acid-Base Equilibrium↗

Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue.

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.

Acid-Base Equilibrium↗

The effect of supramaximal exercise on equine platelet function.

When blood is collected into sodium citrate in the proportion of 9 parts blood:1 part sodium citrate, the concentration of plasma sodium citrate in the sample will depend on the packed cell volume (PCV) of the blood sample. This difference in plasma sodium citrate concentration secondary to alterations in PCV significantly affects human platelet aggregation responses. Since horses attain a high PCV in response to high-intensity exercise we investigated the effect of differences in sample plasma sodium citrate concentration on equine platelet aggregability. In addition, low molecular weight heparin (LMWH) was evaluated as an alternative anticoagulant for assessment of platelet aggregability during strenuous exercise in horses. Blood samples were collected pre-exercise and at fatigue after supramaximal treadmill exercise into either 3.8% sodium citrate (9 parts blood:1 part sodium citrate) or 20 u LMWH/ml of blood. Platelet aggregation responses to 1.25 mumol/l adenosine diphosphate (ADP) were measured via optical aggregometry. For samples collected into sodium citrate, aggregability was significantly less than pre-exercise values in samples collected at fatigue and in pre-exercise samples in which sodium citrate concentrations were adjusted to equal those in fatigue samples. However, samples collected into LMWH showed significantly increased platelet aggregability in samples collected at fatigue when compared to pre-exercise samples. In conclusion, higher plasma sodium citrate concentration had a marked inhibitory effect on equine platelet aggregation responses. Low molecular weight heparin was a good alternative anticoagulant for assessment of equine platelet function and results indicate that equine platelet aggregability was enhanced in response to supramaximal exercise.

Adenosine Diphosphate↗

Relationship between VO2max, heart score and echocardiographic measurements obtained at rest and immediately following maximal exercise in thoroughbred horses.

We evaluated the relationships of heart score (HS) and echocardiographic measures to maximal oxygen consumption (VO2max), maximal cardiac output (Qmax), and maximal stroke volume (SVmax). Six fit, mature Thoroughbred horses weighing (mean +/- s.e.) 487 +/- 11 kg were run 4 times on an inclined (10%) treadmill. Each run consisted of a 3 min warm-up at 4 m/s followed by completion of an incremental exercise test in which each horse ran until VO2max was reached. Arterial and mixed venous blood was collected to determine arteriovenous oxygen content difference C(a-v)O2[ in the last 15 s of exercise. An ATL HDI 3000 ultrasound system and a 3.5 MHz phased array transducer were used to make echocardiographic measurements before and within 2 min of run completion. Guided M-mode echocardiographic measurements of left ventricular diameter (LVD), interventricular septal thickness (IVS) and left ventricular free wall thickness (LVFW) during diastole (D) and systole (S) were made from the right parasternal short axis view at the level of the chordae, and VO2 and C(a-v)O2 were measured as the appropriate M-mode view was recorded. Maximum heart rate (HRmax) was determined using a cardiotachometer, and HS was calculated on nonexercise days using the established technique. Maximum cardiac output and SVmax were calculated from the Fick equation and HRmax. Backward stepwise regression analysis was used to relate pre- and post exercise echocardiographic measurements and HS to VO2, Q, and SV at the time of measurement, and to VO2max, Qmax, and SVmax. Pre- and post exercise LVDD appeared to be the most important variable in these equations. Mean pre-exercise HR at the time of measurement was 54.7 +/- 1.9 beats/min, while the mean post exercise rate was 111.7 +/- 2.6 beats/min. The mean +/- s.e. VO2max was 150.4 +/- 13.2 ml/(kg.min). Heart score was not correlated with VO2max, Qmax, or SVmax. There was no significant difference between pre- and post exercise measurements of LVD, IVSS, and LVFWS.

Animals↗

Effect of frusemide and hypertonic saline on electrolytes during post exercise anaesthesia.

This study evaluated the effects of pre-exercise frusemide administration and hypertonic saline (H) infusion during anaesthesia on arterial pH, blood gases and electrolytes in 6 Thoroughbred horses anaesthetised immediately post exercise. Horses received either frusemide (F) (0.5 mg/kg, i.v.) or a saline placebo (P) injection 4 h prior to treadmill exercise. Exercise consisted of a 3 min warm-up at 40% VO2max followed by exercise to fatigue. Detomidine (40 micrograms/kg, i.v.) was given within 5 min of stopping and followed 5 min later by zolazepam-tiletamine (1.25 mg/kg, i.v.) to induce anaesthesia. During maintenance of anaesthesia using isoflurane in O2, either isotonic saline solution (I) or 7.5% H (4 ml/kg, i.v.) was administered. Arterial blood was sampled at the following times: prior to (Pre-F/P) and 4 h after (Pre-ex) F or P administration, 1 min after fatigue (Fatigue), 5 min after induction of anaesthesia (Post-ind), and just prior to and 15, 30 and 60 min after beginning isoflurane (ISFL) anaesthesia. Arterial pH and blood gas tensions, pulmonary arterial blood temperature, plasma [lactate], total protein and plasma [Na+], [K+], and [Cl-] were measured. Data were analyzed using 2-way ANOVA for repeated measures (P < 0.05). There were significant differences over time for all variables except total protein. Plasma [Na+] increased at Fatigue compared to Pre-F/P or Pre-ex in all treatment groups. Plasma [Na+] and [Cl-] increased during ISFL anaesthesia compared to Pre-F/P and Pre-ex in horses given H. During ISFL anaesthesia, plasma [Cl-] decreased compared to Pre-F/P in Group F+I horses. We conclude that acid-base, blood gas, and electrolyte changes associated with F are unlikely to influence management of horses anaesthetised immediately following supramaximal exercise to fatigue. Hypertonic saline infusion may help restore plasma [Cl-] faster in hypochloraemic horses requiring anaesthesia immediately after strenuous exercise.

Acid-Base Equilibrium↗

Equine plasma beta-endorphin concentrations are affected by exercise intensity and time of day.

Eight mature mares were exercised for 20 min at 60% VO2max and to fatigue at 95% VO2max. Plasma beta-endorphin (EN) concentrations were determined before exercise, after a 10 min warm-up, and at the end of each exercise test. Mean +/- s.e. beta-endorphin concentrations were significantly (P < 0.05) higher following work at 95% VO2max when compared to that at 60% VO2max (420.0 +/- 102.7 vs. 269.9 +/- 30.69 pg/ml). Pre-exercise samples were collected between 1000 and 1500 h. In order to evaluate whether any cyclic changes in EN secretion effects may have influenced results, a subsequent study was completed using 12 horses to assess diurnal fluctuations in EN concentrations, by measuring EN concentration every 2 h for a 24 h period. There was no statistical difference in mean values at any time between 0800 and 2000 h. Whether individual differences in EN concentrations reflected varying degrees of stress associated with the exercise could not be determined. Any possible link between EN concentration and exercise stress in exercising horses awaits clarification.

Animals↗

Anesthesia of horses with a combination of detomidine, zolazepam, tiletamine, and isoflurane immediately after strenuous treadmill exercise.

OBJECTIVES: To evaluate effects of strenuous exercise in adult horses immediately before anesthesia and to determine whether prior exercise affects anesthesia induction, recovery, or both. ANIMALS: 6 healthy Thoroughbreds in good condition and trained to run on a treadmill, each horse serving as its own control. PROCEDURE: Horses ran on a treadmill until fatigued, then were sedated immediately with detomidine hydrochloride and anesthetized with a zolazepam hydrochloride-tiletamine combination. Anesthesia was maintained with isoflurane in oxygen for another 90 minutes. Blood samples were taken before, during, and after exercise and during anesthesia. RESULTS: During exercise, changes in heart rate, core body temperature, plasma lactate concentration, arterial pH, and PaCO2 were significant. Plasma ionized calcium concentration was lower after exercise, compared with baseline values, and remained lower at 30 minutes of isoflurane anesthesia. Compared with baseline values, plasma chloride concentration decreased significantly during anesthesia after exercise. Cardiac output during anesthesia was significantly lower than that during preexercise, but significant differences between experimental and control periods were not observed. Arterial blood pressure during anesthesia was significantly lower than that during preexercise and initially was maintained better during isoflurane anesthesia after exercise. Cardiac output and blood pressure values were clinically acceptable throughout anesthesia. CONCLUSION: Administration of detomidine hydrochloride followed by zolazepam hydrochloride-tiletamine appeared to be safe and effective for sedation and anesthesia of horses that had just completed strenuous exercise. CLINICAL RELEVANCE: Anesthetic given in accordance with this protocol can be used to anesthetize horses that are injured during athletic competition to assess injuries, facilitate first aid, and possibly allow salvage of injured horses.

Anesthesia, General↗

Effect of intravenous administration of furosemide on mass-specific maximal oxygen consumption and breathing mechanics in exercising horses.

OBJECTIVES: To determine whether i.v. administration of furosemide (250 mg) to horses before maximal exercise affected maximal oxygen consumption (VO2max), breathing mechanics, or gas exchange during exercise. ANIMALS: 7 healthy, well-conditioned Thoroughbred horses. PROCEDURES: 5 horses initially performed an incremental treadmill exercise test to determine VO2max 4 hours after i.v. administration of furosemide (250 mg i.v.) or placebo (saline [0.9% NaCl] solution). Time to fatigue and distance run were recorded. All 7 horses were then used to determine the effects of furosemide on gas exchange and breathing mechanics at 40, 60, 80, and 100% of VO2max. Horses were weighed immediately before exercise. RESULTS: Furosemide treatment significantly increased mass-specific VO2max (5.3%), but absolute VO2max was not significantly altered. In the 2 parts of the study, body weights were 2.9 and 2.5% higher when horses were given placebo than when they were given furosemide. Time and distance run at speeds > or = 11.0 m/s were significantly greater following furosemide administration. Furosemide treatment had no effect on breathing mechanics or gas exchange. CONCLUSIONS AND CLINICAL RELEVANCE: Previous studies have suggested that prerace administration of furosemide may have a positive effect on performance. Results of this study indicate that this may be attributable, in part, to an increase in mass-specific VO2max but not to improvements in breathing mechanics or gas exchange. Most of the increase in mass-specific VO2max appeared to be attributable to weight loss associated with diuresis induced by furosemide.

Animals↗