Pulmonary artery wedge pressure measurement in healthy warmblood horses and in warmblood horses with mitral valve insufficiencies of various degrees during standardised treadmill exercise

In 12 healthy warmblood horses and 10 horses with mitral valve insufficiencies (MVI) of various degrees heart rate and pulmonary artery wedge pressure (PWP) was measured at rest and during standardised exercise on a high speed treadmill. There was a significant increase in PWP with each change in speed of the treadmill (p < 0.01). The PWP of horses with mild mitral valve regurgitation under working conditions was not significantly different compared to the healthy horses. The horses with moderate mitral valve regurgitation showed a significant higher pulmonary artery wedge pressure at rest and during exercise compared to the healthy horses (p < 0.01) at rest and during treadmill velocity. The tendencies were seen that mild mitral valve regurgitation results only in mild hemodynamic changes during exercise, while moderate MVI have an important influence on haemodynamics.     

Pulmonary wedge pressure and heart frequency measurements during standardized treadmill exercise for extension of left atrial function diagnosis in warmblood horses

In 12 healthy warmblood horses (six trained and six untrained) the pulmonary wedge pressure and heart frequency was measured at rest and during a standardised exercise test on a treadmill. The mean pulmonary wedge pressure at rest was 14.53 +/- 2.36 mmHg. There was no significant difference in pulmonary wedge pressure either at rest or during exercise between trained and untrained horses. During walking (1.8 m/s) the mean pulmonary wedge pressure was 19.62 +/- 4.03 mmHg, during trotting (4 und 5 m/s) it was between 22.38 +/- 3.92 mmHg and 25.28 +/- 3.7 mmHg. During canter (6 m/s) and gallop (8 m/s) the mean pulmonary wedge pressure increased to a level of 25.54 +/- 4.3 mmHg and 31.86 +/- 4.29 mmHg. There was a significant increase in pulmonary wedge pressure with each incremental step of the standardised treadmill test. Concerning mean heart frequency a highly significant increase could be observed at the beginning and at the end (treadmill speed of 7 and 8 m/s) of the standardised exercise test. At higher intensity of the exercise test (7 m/s and 8 m/s) untrained horses showed a significantly increased heart rate compared to trained horses. Neither at rest nor during the different exercise levels a significant correlation factor greater 0.5 between heart frequency and pulmonary wedge pressure could be observed. The increase of heart frequency and pulmonary wedge pressure during exercise showed no correlation. Between left atrial size and pulmonary wedge pressure a statistical weak correlation could be observed up to a treadmill velocity of 6 and 7 m/s.     

Stress echocardiography in warmblood horses: comparison of dobutamine/atropine with treadmill exercise as cardiac stressors

The purpose of this study was to determine whether the combination of dobutamine and atropine causes cardiac stress equivalent to treadmill exercise. Therefore, electrocardiography and echocardiography were performed on 10 warmblood horses before, during, and after different cardiac stress tests. Stressors consisted of a standardized treadmill exercise and combined administration of dobutamine (7.5 microg/kg/min) and atropine (5 microg/kg). Maxima heart rates were achieved during the treadmill exercise (175 +/- 10 bpm). After exercise, a rapid decrease in heart rate was observed. Subsequently, a stress echocardiography for which a heart rate >100 bpm was required could only be performed within 1 minute after exercise. The mean heart rate during echocardiography was 136 +/- 8 bpm after exercise. The combination of dobutamine and atropine also resulted in a significant increase in heart rate, up to 141 +/- 20 bpm. Maxima heart rate was significantly higher during the treadmill exercise, but the decrease in heart rate was significantly slower after dobutamine and atropine administration. Over a period of 7.9 minutes, the mean heart rate was 123 +/- 8 bpm during dobutamine and atropine administration. Consequently, the combination of both drugs offered sufficient time for detailed examinations. Overall, echocardiographic examination identified a decrease in left ventricular (LV) dimensions, an increase in LV wall thickness, and a decrease in stroke volume after the treadmill exercise and during pharmacologic stress testing compared with baseline. Changes in echocardiographic variables generally were more pronounced during dobutamine and atropine administration. Similar to stress echocardiography in humans, in horses the combination of dobutamine and atropine is useful to produce an increase in heart rate comparable with what is achieved with exercise but without the need of increasing dobutamine dosage.     

Effect of a respiratory gas collection mask on some measurements of cardiovascular and respiratory function in horses exercising on a treadmill

The effects of a respiratory gas collection mask on arterial blood gases, acid base values, oxygen content, respiratory frequency and heart rate, were investigated in standardbred horses during treadmill exercise at speeds up to 10 m sec-1 and a treadmill slope of 10 per cent. The mask had no significant effect on heart rates during exercise, but respiratory frequency was lower when the mask was used. The increase in respiratory frequency as treadmill velocity increased was also significantly slower with the mask operative. Arterial carbon dioxide tensions were significantly higher during exercise with the mask than without, and arterial oxygen tension was significantly lower at the highest exercise intensity. Arterial oxygen content was significantly lower at all work speeds when the mask was used. There were minimal effects of the mask on arterial acid base values. It was concluded that a respiratory gas collection mask caused alveolar hypoventilation in exercising horses, but did not markedly influence heart rate or arterial acid base values during exercise.     

Echocardiographic analysis of segmental left ventricular wall motion at rest and after exercise in horses with and without heart disease

An echocardiography was performed on 23 healthy warmblood horses and on 12 warmblood horses with cardiac diseases at rest and after treadmill or lungeing exercise. The B-mode technique was used, and the left ventricular wall motion was analyzed visually. The left ventricle was divided into 6 equally sized myocardial segments, 3 of them in the region of the interventricular septum, and the other 3 in the region of the left ventricular rear wall (“6-segment model”). The kinetic of each segment was determined using a kinetic score system. A normokinetic wall motion was defined with a kinetic index of 1. To the authors' knowledge, the current study is the first to present a visual qualitative method for assessment of the healthy equine heart with regard to the myocardial left ventricular wall motion at rest and after exercise under standardized conditions. First, reference values for the left ventricular myocardial kinetics were established in healthy horses. Subsequently, horses with cardiac diseases of differing severity were examined, and the diagnostic value of the method was evaluated. In contrast with human cardiology, the healthy equine heart is characterized by several deviating wall motion patterns. The majority of the healthy horses (52%) showed a normokinetic wall motion of all 6 segments at rest and a normokinetic concentrically increased hypertrophy after exercise. In 9 healthy horses, however, the middle septal segment (at the papillary muscle level) was characterized by a hypokinesia (kinetics index = 2) at rest. In 5 of these horses, the hypokinesia was not observed after exercise. The kinetic wall motion score was 1.1 ± 0.2 at rest in the healthy horses. In the horses with cardiac disorders, the score was 1.5 ± 0.4 at rest. In all healthy horses, the middle septal segment (at the papillary muscle level) was characterized by a hypokinesia (kinetics index = 2; n = 5) or akinesia (kinetics index = 3; n = 3) at rest.After standardized treadmill exercise, the wall motion score of the healthy horses was 1.12 ± 0.16 and the score of the horses with cardiac disorders was 1.52 ± 0.4. In contrast to human cardiology, the mid-septal segment showed a hypokinesia (kinetics index: 2) and an akinesia (kinetics index: 3) in two healthy horses after exercise. In all horses with low-grade and moderate cardiac disorder, an atypical wall motion pattern was observed after exercise. In all horses with high-grade cardiac disorder, an atypical motion pattern was documented in 5 out of 6 segments. An exercise test was not performed on the latter group.     

Influence of valvular insufficiency and recurrent airway obstruction on haemodynamics and therapy in warmblood horses with atrial fibrillation

The aim of this study was to investigate the potential haemodynamic effects of valvular insufficiency and recurrent airway obstruction (RAO) in horses with atrial fibrillation (AF). Therefore in ten healthy horses (group 1) and 40 horses with AF a clinical examination, a lung examination, echocardiography and right heart catheterization for measurement of intracardic and pulmonary pressures were performed. According to the clinical findings the horses with AF were subdivided into 4 groups (group 2: AF; group 3: AF/valvular insufficiency; group 4: AF/RAO; group 5: AF/valvular insufficiency/RAO). Most of the horses of group 3 and 5 suffered from two valvular insufficiencies (mitral and tricuspid valve insufficiency: n=11, mitral and aortic valve insufficiency: n=2). The remaining horses showed a single mitral (n=6), tricuspid (n=2) or aortic valve insufficiency (n=1) or more than two valvular insufficiencies (n=4). In group 2 right ventricular mean pressure (RVPm) was higher than in group 1 and 4 (P<0.025); diastolic right ventricular pressure was higher than in group 1; PWP was higher than in group 1 and group 4; PDP was lower compared to group1. Compared to group1 in group 3 left atrial diameter (LA) was greater; the PAPs was higher and the PDP lower (P<0.05). In group 4 RVPm and PWP was lower compared to group 2. In group 5 LA, fractional shortening and diastolic left ventricular diameter were greater, PWP and PAPs were higher and PDP lower compared to group1. Twenty six of the 40 horses with AF (65%) were treated. Successful cardioversion to sinus rhythm occurred in 15 horses (58%). Therapy was successful in 50% of the treated horses of group 2 and 3, in 67% of the treated horses of group 4 and in 63% of the treated horses in group 5. In conclusion the presence of valvular insufficiency or RAO influences the haemodynamics of horses with AF.     

Plasma cortisol and ACTH concentrations in the warmblood horse in response to a standardized treadmill exercise test as physiological markers for evaluation of training status

Reliable physiological markers for performance evaluation in sport horses are missing. To determine the diagnostic value of plasma ACTH and cortisol measurements in the warmblood horse, 10 initially 3-yr-old geldings of the Hannovarian breed were either exposed to a training schedule or served as controls. During experimental Phase 1, horses were group-housed, and half of the horses were trained for 20 wk on a high-speed treadmill. During Phase 2, groups were switched and one group was trained for 10 wk as during Phase 1, whereas the control group was confined to boxes. During Phase 3 horses were initially schooled for riding. Thereafter, all horses were regularly schooled for dressage and jumping, and half of the horses received an additional endurance training for 24 wk. During all phases horses were exposed at regular intervals to various standardized treadmill exercise tests. During and after the tests frequent blood samples were taken from an indwelling jugular catheter for determination of ACTH and cortisol. Treadmill exercise increased both hormones. Maximum ACTH concentrations were recorded at the end of exercise, and maximum cortisol levels were recorded 20 to 30 min later. Except for one test there were no differences in ACTH levels between trained horses and controls. There was no significant effect of training on the cortisol response (net increase) to treadmill exercise in any of the tests during Phase 1. During Phase 2 higher cortisol responses were recorded in controls than in trained horses (P < .05) after 10 wk of training (controls confined to boxes). During Phase 3 plasma cortisol responses were also higher in controls than in trained horses (P < .05 after 6, 18, and 24, P < or = .07 after 12 wk of training) when the inclination of the treadmill was 5%, but not at 3%. There was no overlap in net cortisol responses at 30 min between trained and untrained horses. An ACTH application after 24 wk of training resulted in higher cortisol responses in controls than in trained horses (P < or = .05), without any overlap between the groups at 30 min after ACTH. Plasma cortisol responses to either treadmill exercise or ACTH injection may be a reliable physiological marker for performance evaluation. Prerequisites are sufficient differences in training status and sufficient intensity of exercise test conditions.     

Cardiovascular effects of submaximal aerobic training on a treadmill in Standardbred horses, using a standardized exercise test

Seven healthy, unexercised, previously trained, adult Standardbred horses were allotted to 2 groups and trained 78 days on a treadmill set at a 7 degree 30' angle. The groups were trained on different schedules, and the effects of training on heart rate, cardiac output, stroke volume, arteriovenous oxygen difference, systemic blood pressure, and venous lactic acid were determined. Measurements were made at rest, during exercise on the treadmill at rates of 55 m/min, 75 m/min, 100 m/min, and 154 m/min, and at 5 minutes after exercise (standardized exercise test). Heart rate and cardiac output decreased during the training period. Significantly slower heart rates were observed at 55 m/min by day 8, at 100 m/min and 154 m/min by day 36, at 1 minute after exercise by day 57, and at 5 minutes after exercise by day 78 (P less than 0.05). Stroke volume increased with exercise, but not significantly. The arteriovenous oxygen difference increased significantly (P less than 0.05) with each increase in work load. There was no significant increase with training, although an upward trend was recorded. Mean systemic blood pressure did not differ from resting with treadmill rates of 55 m/min, 75 m/min, or 100 m/min. It was greater at 154 m/min, although this was not significant. During exercise, the total peripheral resistance decreased to as little as 30% of its resting value. After exercise, diastolic and mean arterial blood pressures and peripheral resistance increased. Marked increases in blood volume and blood viscosity during exercise were closely related to the decrease in peripheral resistance. There was no significant effect of training on blood pressure. Venous lactic acid concentrations at rest were greater than those of the horses on the treadmill at rates of 55 m/min, 75 m/min, and 100 m/min and at 5 minutes after exercise on days 1, 8, and 15. Subsequently, they were not different from resting values. Differences in the effects of the different training programs could not be detected.     

Effects of muscle glycogen depletion on some metabolic and physiological responses to submaximal treadmill exercise.

The aim of this study was to investigate the effects of reduced muscle glycogen concentration on some physiological and metabolic responses during moderate intensity treadmill exercise in horses. Six Thoroughbred geldings were randomly allocated to 2 treatments (protocols A and B) or control in a 3 x 3 replicated Latin square design. In protocol A, horses performed low intensity exercise while horses in protocol B performed short bursts of high intensity exercise. Protocol A was designed to induce glycogen depletion mainly of slow twitch muscle fibers while protocol B aimed to deplete mainly fast twitch muscle fibers. Horses in the control group did not undergo exercise prior to the exercise test. Five hours after glycogen depletion, horses performed treadmill exercise at 60% VO2max at a treadmill slope of 10% until fatigue (20-30 min). The induced glycogen depletion prior to exercise had no significant effect on plasma glucose, insulin, or lactate concentrations during the exercise test, and there was no effect on glycogen utilization rate, although respiratory exchange ratios were lower in the glycogen-depleted groups. The VO2, heart rate and central blood temperature did not vary significantly between the protocols A and B and control throughout the exercise test. It was concluded that 20-30% depletion of glycogen concentration in the middle gluteal muscle resulted in a shift towards fat metabolism, but does not significantly affect heart rate, oxygen uptake, or concentrations of plasma glucose and lactate during moderate intensity exercise.     

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.     

Haemodynamic response to exercise in Standardbred trotters with red cell hypervolaemia

In order to evaluate the haemodynamic response to exercise in Standardbred trotters with red cell hypervolaemia (RCHV), 12 trotters with RCHV were compared with 9 normovolaemic (NV) trotters. Haemodynamic data were recorded during exercise at 4 different speeds on a treadmill. Oxygen uptake was determined with an open bias flow system. Pulmonary artery pressure (PAP), systemic artery pressure (SAP), heart rate, packed cell volume (PCV) and plasma lactate and haemoglobin ([Hb]) concentrations were measured. Arteriovenous O2 content difference, cardiac output, stroke volume, pulmonary vascular resistance (PVR) and total systemic resistance (TSR) were calculated. Oxygen uptake, arteriovenous O2 content difference, heart rate, cardiac output, stroke volume, TSR and lactate did not differ between groups. The RCHV horses had significantly higher both mean diastolic and systolic PAP compared to NV horses and this difference increased with higher workload. Further, a higher SAP, PVR, PCV and [Hb] were found in RCHV horses during the course of exercise. Eleven of the RCHV horses, but none of the NV, showed exercise-induced pulmonary haemorrhage on endoscopic examination. The increase in red cell volume, resulting in a high PCV and high total blood volume, is suggested to be an important contributor to both the increased blood pressures in pulmonary and systemic circulation during exercise and to the development of exercise-induced pulmonary haemorrhage in RCHV horses.     

Pulmonary artery and aortic pressure changes during high intensity treadmill exercise in the horse: effect of frusemide and phentolamine.

Intravenous frusemide (1.0 mg/kg bwt) or phentolamine (0.33 mg/kg bwt) was given to 7 horses 1 h before exercise and their effects on pulmonary artery and aortic pressure changes during strenuous exercise were examined. Short-term near-maximal treadmill exercise (10 m/sec, 3 degrees incline) produced increases in heart rate, mean pulmonary artery pressure (PAP), mean aortic pressure (AP), and packed cell volume (PCV). Frusemide did not affect heart rate, PAP or PCV during exercise. Frusemide significantly decreased mean AP by 10 to 15 mmHg during exercise. Phentolamine produced an increase in heart rate relative to control only early in exercise but not during later, more strenuous, exercise. Phentolamine had no statistically significant effect on AP, PAP, or PCV, but a significant reduction was observed between 180 and 230 sec of exercise when PAP and AP were standardised against heart rate. Frusemide did not prevent horses from haemorrhaging during exercise in this study. Treatment with phentolamine did not sufficiently reduce the PAP and AP to test our hypothesis that a reduction in PAP and AP would eliminate EIPH.     

Influence of furosemide on hemodynamic responses during exercise in horses.

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 RAP 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.     

Clenbuterol plasma concentrations after repeated oral administration and its effects on cardio-respiratory and blood lactate responses to exercise in healthy Standardbred horses

To evaluate the effects of clenbuterol on cardio-respiratory parameters and blood lactate relation to exercise tolerance, experimental horses performed standardized exercise tests on a high-speed treadmill before and after administration of the drug. Clenbuterol was administered in feed to six healthy Standardbreds at a dose rate of 0.8 micrograms/kg b.wt twice daily for 5.5 days. Each horse was tested twice, without and with a respiratory mask, during two consecutive days. One week elapsed between the baseline tests without drug and the tests with clenbuterol treatment (each horse served as its own control). The results show an unchanged heart rate response to exercise 2 h after the last clenbuterol administration. The blood lactate response and the arterial oxygen tension during exercise did not differ before and after drug treatment. The oxygen uptake as well as pulmonary ventilation relative to the work load performed was essentially unaffected. The arterial pH during exercise was significantly increased (P less than 0.05) following clenbuterol treatment. Plasma levels of clenbuterol were maximal 2 h post-administration with values between 0.45 and 0.75 ng/ml. The plasma half-life of elimination was 10.4 h (+/- 2.25 SD). In conclusion, clenbuterol did not cause any major effects on the cardio-respiratory and blood lactate parameters studied in healthy horses performing submaximal exercise tolerance tests.     

Effect of atropine-dobutamine stress test on left ventricular echocardiographic parameters in untrained warmblood horses

The aim of this study was to investigate the effect of combined atropine low-dose dobutamine stress test on left ventricular parameters in adult warmblood horses, to establish a potential protocol for pharmacological stress echocardiography. Seven healthy untrained warmblood horses aged 9 to 22 years were used. Heart rate (HR) and left ventricular B- and M-mode dimensions were recorded at baseline and during stress testing with 35 microg/kg atropine IV followed by incremental dobutamine infusion of 2 to 6 microg/kg/min. HR increased significantly (P < .05) during the pharmacological challenge, and a maximal HR of 156.6 +/- 12.5 bpm was reached at maximal dobutamine infusion rate. Systolic and diastolic interventricular septum thickness, systolic and diastolic left ventricular free wall thickness, and fractional shortening increased significantly and reached a maximum at the highest infusion rate (mean +/- SD: 4.51 +/- 0.27 versus 5.65 +/- 0.31 cm, 2.89 +/- 0.19 versus 3.78 +/- 0.10 cm, 3.72 +/- 0.34 versus 4.77 +/- 0.18 cm, 2.44 +/- 0.28 versus 3.11 +/- 0.34 cm, 34.98 +/- 3.82 versus 50.56 +/- 3.42%, respectively). Systolic and diastolic left ventricular internal diameter decreased significantly during dobutamine infusion. Left ventricular external and internal area were significantly lower at a dobutamine infusion rate of 2 microg/kg/min but no further decrease was observed during the subsequent steps. Systolic and diastolic myocardial area was significantly lower after the administration of dobutamine but not significantly different during dobutamine infusion, when compared to baseline values. This pharmacological stress test induced significant changes in left ventricular echocardiographic parameters in adult warmblood horses. Additional research should evaluate the value of this stress test in horses suffering from cardiac disease.     

Effect of commercially available nasal strips on airway resistance in exercising horses

OBJECTIVE: To determine the effect of a commercially available nasal strip on airway mechanics in exercising horses. ANIMALS: 6 horses (5 Standardbreds and 1 Thoroughbred). PROCEDURE: Horses exercised on a treadmill at speeds corresponding to 100 and 120% of maximal heart rate with and without application of a commercially available nasal strip. Concurrently, tracheal pressures, airflow, and heart rate were measured. Peak inspiratory and expiratory tracheal pressures, airflow, respiratory frequency, and tidal volume were recorded. Inspiratory and expiratory airway resistances were calculated by dividing peak pressures by peak flows. Endoscopic examination of the narrowest point of the nasal cavity (ie, nasal valve) was performed in 1 resting horse before, during, and after application of a nasal strip. RESULTS: During exercise on a treadmill, peak tracheal inspiratory pressure and inspiratory airway resistance were significantly less when nasal strips were applied to horses exercising at speeds corresponding to 100 and 120% of maximal heart rate. Application of the nasal strip pulled the dorsal conchal fold laterally, expanding the dorsal meatus. CONCLUSIONS AND CLINICAL RELEVANCE: The commercially available nasal strip tented the skin over the nasal valve and dilated that section of the nasal passage, resulting in decreased airway resistance during inspiration. The nasal strip probably decreases the amount of work required for respiratory muscles in horses during intense exercise and may reduce the energy required for breathing in these horses.     

Pulmonary vascular pressures of strenuously exercising Thoroughbreds during intravenous infusion of nitroglycerin

OBJECTIVE: To determine whether intravenous infusion of nitroglycerin would modify pulmonary arterial, capillary, or venous hypertension in strenuously exercising Thoroughbreds. ANIMALS: 5 healthy Thoroughbred horses. PROCEDURE: Right atrial, right ventricular, and pulmonary vascular pressures were measured. Each horse was used in a control treatment (not medicated) and a nitroglycerin infusion (20 microg/kg of body weight/min) at rest and during exercise on a treadmill. Sequence of treatments was randomized for each horse, and treatments were separated by a 7-day interval. Galloping at 14.2 m/s on a 5% uphill grade elicited maximal heart rate (mean +/- SEM, 212 +/- 2 beats/min) and could not be sustained for > 90 seconds. Nitroglycerin dosage was selected, because maximal pulmonary and systemic hemodynamic effects of i.v. nitroglycerin were elicited at 5 microg/kg/min and increasing the dosage to 20 microg/kg/min did not cause adverse effects. RESULTS: In the control treatment, exercise performed at maximal heart rate resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures. Nitroglycerin infusion in standing horses significantly decreased right atrial and pulmonary vascular pressures, whereas heart rate increased. Exercise in nitroglycerin-infused horses also resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures, and these values were not significantly different from data for the control treatment. All horses experienced exercise-induced pulmonary hemorrhage for both treatments. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of nitroglycerin does not modify exercise-induced pulmonary hypertension and is unlikely to affect the incidence or severity of exercise-induced pulmonary hemorrhage in Thoroughbreds.     

Influence of subclinical pulmonary findings on cardiac parameters in Icelandic horses

In the present study we examined, if in Icelandic horses an increase in heart and/ or breathing rate is physiological and breed dependend or a sign of a pulmonary or cardiac disease. Therefore we examined 37 Icelandic horses with the prereport of being healthy. During clinical lung examination four horses showed symptoms of a pulmonary disease like increased breathing rate and enforced breathing at rest. These horses were excluded from the study. The other 33 horses were clinically normal. 17 of these horses were unridden (untrained) and 16 horses were regularly worked (trained). After clinical examination in all horses analysis of arterial blood gas, endoscopy with tracheo- bronchial secret analysis and radiographic examination of the lung were carried out. Additionally electro- and echocardiographic examinations and standardised exercise tests with determination of heart and breathing rate as well as plasma lactate values were performed in all horses. During electro- and echocardiographic examination no pathological findings were observed. In total 22 of the 33 horses showed abnormal lung findings. Seven horses had mild signs of RAO and 15 horses had mild signs of interstitial bronchitis. Three horses had additional pulmonary haemorrhage. Eleven out of the 33 horses showed no abnormal lung findings. The breathing rate at rest differed not significantly between horses with (21 +/- 1/min) or without (23 +/- 2/min) pulmonary findings. The heart rate also did not differ significantly between horses with (39 +/- 1/min) or without (42 +/- 1/min) pulmonary findings. In contrast to this the trained Icelandic horses with abnormal pulmonary findings had significantly higher heart rates (p = 0.01) and significantly lower breathing rates (p = 0.009) compared to those without abnormal pulmonary findings. During echocardiography Icelandic horses with abnormal pulmonary findings had significantly larger left atrial diameter (without abnormal pulmonary findings: 82 +/- 7 mm, with abnormal pulmonary findings: 90 +/- 8 mm, p = 0.02). Compared to the untrained Icelandic horses (5.4 +/- 2 mmol/l) the trained horses showed significantly lower plasma lactate values (3.1 +/- 2 mmol/l, p = 0.001) immediately after exercise. After exercise the icelandic horses with abnormal pulmonary findings had significantly higher breathing rates (p < 0.05) and longer recovery periods (30 minutes) than horses without abnormal respiratory findings (15 minutes). Recovery of heart rate after exercise showed no differences between groups.     

Pulmonary artery wedge pressure and heart rate measurement during pharmacological stress induction for left cardial function diagnosis in horses with and without heart disease

In 18 horses, the pulmonary artery wedge pressure and the heart rate were measured during pharmacological stress load. 12 horses were healthy (4 trained, 8 untrained) and 6 horses had a heart disease (3 trained, 3 untrained). Pharmacological stress induction was carried out with the sympathomimetic drug dobutamine at a dosage rate of 7.5 microg/kg/min over 10 minutes of infusion. At the fourth minute, the parasympatholytic drug atropine was administered (5 microg/kg bw), and the heart rate and the pulmonary artery wedge pressure were continuously measured over 26 minutes. During sole dobutamine infusion, a significant decrease in heart rate and a significant increase in pulmonary artery wedge pressure were observed. After the application of atropine in the fourth minute, a significant increase in heart rate (from 35.7 +/- 6 up to 106 +/- 38/ min) and in pulmonary artery wedge pressure (from 15.7 +/- 3 up to 24 +/- 8.6 mmHg) were visible in the group of healthy horses. The horses with heart diseases had a significantly higher increase in both parameters (heart rate and pulmonary artery wedge pressure) with a significantly positive correlation (r = 0.7). The heart rate increased in the horses with heart diseases from 35.2 +/- 2,8 beats/min up to 132 +/- 45.7 beats/min and the pulmonary artery wedge pressure increased from 17.3 +/- 3,2 mmHg up to 32.7 +/- 13 mmHg. The cardiac status (healthy or heart disease) as well as the training level of the horses (untrained or trained) had a significant influence on the heart rate and the pulmonary artery wedge pressure. The untrained horses (healthy and heart disease) showed significantly higher values over a longer period of time than did the trained horses with the same cardiac status. Additionally the influence of pharmacological stress induction on echocardiographic parameters was investigated. The left atrial size (p = 0.015) and left ventricular diameter were significanly different in the systole (p = 0.008) and in the diastole (p = 0.001) between healthy horses and horses with heart diseases. All horses showed a positive correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.8), as well as between the left ventricular systolic (r = 0.6) and the diastolic diameter (r = 0.6). The correlation between the pulmonary artery wedge pressure and the left atrial size was nearly the same in the healthy horses (r = 0.74) and in the horses with heart diseases (r = 0.76). Regarding the training level, all untrained horses had a significantly higher correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.87) in comparison to the trained horses (r = 0.74). Particularly in the untrained horses with heart diseases, this correlation was remarcable (r = 0.99).     

Atrial natriuretic peptide and cardiac troponin I concentrations in healthy Warmblood horses and in Warmblood horses with mitral regurgitation at rest and after exercise

ObjectiveAtrial natriuretic peptide (ANP) and cardiac troponin I (cTnI) serve as biomarkers for increased cardiac pressure/volume loading and for myocardial stress or damage. The objective was to describe the time course of plasma ANP concentrations (Cp_ANP) and plasma cTnI concentrations (Cp_cTnI) in horses with mitral regurgitation (MR) compared to healthy horses at rest and after exercise, and to describe the relationship of Cp_ANP with cardiac dimensions and intracardiac pressures.Animals15 healthy Warmblood horses and 7 Warmblood horses with MR.MethodsCardiac dimensions at rest were measured using echocardiography. All horses underwent standardized treadmill exercise. Biomarker concentrations and intracardiac pressures were measured at rest and after exercise. Hypotheses were tested using statistical methods. The level of significance was P < 0.05.ResultsHorses with MR showed increased left atrial (LA) and left ventricular (LV) dimensions but similar exercise capacity compared to healthy horses. Pulmonary capillary wedge pressures (PCWP) and Cp_ANP increased with exercise. Horses with MR had higher PCWP and higher Cp_ANP at rest and after exercise compared to healthy horses, with the maximum difference in Cp_ANP reached 10 min after exercise. Cp_ANP was significantly related to PCWP and – although inconsistently and only in healthy horses – to echocardiographic indices of LA and LV size and function. Cp_cTnI was low throughout the study in both groups.ConclusionsCp_ANP is increased in horses with MR and is related to LA pressures and to left heart dimensions. MR is not necessarily associated with exercise intolerance and exercise-induced myocardial stress or damage.