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.     

Day-to day variability of cardiac pressure values in horses measured with right heart catheterization on 3 consecutive days

In the present study, a right heart catheterisation was carried out on three consecutive days in 17 healthy horses to evaluate the day-to-day variability of cardiac pressure values. Cardiac pressure values were measured in the right atrium, the right ventricle, the pulmonary artery, and the pulmonary capillaries (pulmonary artery wedge pressure). Additionally it was examined wether the cardiac pressure variability was influenced by the heart rate and if there are differences between trained and untrained horses. Beside the coefficient of variances, statistical analysis with assessment of variance components were carried out. Therefore the variation between repeated measurements at one day and within one horse, and the variation between repeated measurements over three days and within the horses (day to day intraindividual variation) as well as the variation between the horses (interindividual variation) were taken into account. The absolute interindividual variance of the pressure values and the heart rate was between 0.4 and 19.6 at all day and for all horses. Between trained and untrained horses the variation of the pressure values and the heart rate was lower than in the trained horses. A significant difference between trained and untrained horses was seen in right atrial mean pressure (p < 0.001) and right atrial diastolic pressure (p < 0.005). The coefficient of variances of the mean heart rate was 11.8%. The coefficient of variances of the different pressure values ranged between 13.1 (mean pulmonary artery pressure) and 46.4% (right ventricular pressure). By splitting the variances, 54.4-78.9% of the variation was caused by the effect of days, 6.2-30.7% of the variation was caused by the effect of horses and 12.5-23% of the variation was caused by the repeated measurements at the different days. In sumary the results shows that nearly all of the pressure values had a low effect of days on the variation, thus cardiac pressure measurements at one day seem to be sufficient.     

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 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.     

Reference values for echocardiographic parameters of trained and untrained Icelandic horses

The aim of this study was to establish echocardiographic reference values for healthy Icelandic horses. For this purpose cardiologic examinations were performed on 44 healthy trained and untrained Icelandic horses without known cardiologic or pulmonary disease. The atrial diameter of the trained horses were significantly greater than in the untrained horses and the left ventricular free wall diameter was also higher in the trained than in the untrained horses. These findings confirm that the changes of the heart caused by training which have previously been described by other authors in warmbloods, thoroughbreds, dogs and humans are present in Icelandic horses as well. However, in contrast to the findings in race horses, no enlargement of the left ventricle was found in trained Icelandic horses, which may indicate that training conditions of Icelandic horses are not comparable to those of race- or jumping-horses in high level training. The reference values established in this study will serve as basis for the current interpretation of the results of echocardiographic examinations in Icelandic horses. This should enable cardiologists to perform a more detailed and precise examination similar to cardiological examinations in warmbloods and race horses.     

Pulmonary artery wedge pressure during treadmill exercise in warmblood horses with atrial fibrillation

The heart rate and the pulmonary artery wedge pressure (PWP) was measured in 10 healthy warmblood horses and in six warmblood horses with atrial fibrillation (AF) at rest and during standardised treadmill exercise. During treadmill exercise, the increase in heart rate was significantly higher in the horses with AF than in the healthy horses. Horses with AF showed a significantly higher increase in PWP at treadmill velocities of 5m/s and faster, than did the healthy horses. The differences in PWP between both groups increased with treadmill strain. The present study demonstrates that there is an influence on the haemodynamics in horses with AF during treadmill exercise, which could explain exercise intolerance in some horses with lone AF.     

Pressures in the right side of the heart and esophagus (pleura) in ponies during exercise before and after furosemide administration

Pressures in the right side of the heart and esophagus (pleural) have not been determined in the exercising equine subjects. In the present study, 8 healthy ponies were examined to determine the changes in these variables caused by 2 degrees of exercise done on a treadmill (heart rate:183 +/- 5 beats/min [trot] and 220 +/- 6 beats/min [canter]). Measurements were also made during both degrees of exertion 10 minutes and 120 minutes after furosemide (1.0 mg/kg) administration. It was observed that both gaits resulted in significant increases in pulmonary artery, right ventricular, and right atrial pressures. The pulmonary artery systolic, mean, and diastolic pressures during strenuous exertion were 306%, 252%, and 242% of the respective resting values. At canter, when respiratory frequency (138 +/- 4 breaths/min) is synchronized with stride frequency, the delta esophageal pressure approached 30.4 +/- 2.86 cm of water. During exercise 10 minutes after furosemide administration, the increment in right atrial pressure was markedly attenuated. During strenuous exertion 120 minutes after furosemide administration, the right atrial and pulmonary arterial pressures increased, but to a significantly lower level than did the prefurosemide values. However, the mean pulmonary artery pressure was still 240% of the resting value. It is concluded that marked pulmonary hypertension is a consistent feature of moderate, as well as strenuous, exertion in the pony. Although furosemide administration attenuated the pulmonary hypertension somewhat, the significance remains unclear.     

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.     

Do Thoroughbred and Standardbred horses have similar increases in pulmonary vascular pressures during exertion?

To test the hypothesis that the pulmonary vascular pressures of Thoroughbred and Standardbred horses behave similarly during exertion. Measurements were made on 5 Thoroughbred and 5 Standardbred horses on a treadmill at rest and during 3-minute exercise intervals at speeds predicted to produce 75%, 90%, and 100% maximal heart rate. Left forelimb acceleration, heart rate, esophageal pressure, and pulmonary artery pressure were measured continuously. Pulmonary capillary and wedge pressures were measured during intermittent occlusion of the pulmonary artery. Breathing rate and gait frequency were the fundamental frequencies of the esophageal pressure and limb acceleration signals respectively. The ratio of speed:gait frequency gave stride length. The effects of exertion and breed were evaluated using two-way analysis of variance. Exertion produced significant increases in pulmonary artery (P = 0.001), capillary (P= 0.002), and wedge (P= 0.005) pressures. No significant effect of breed was detected on pulmonary artery pressure, but at exertion pulmonary capillary and wedge pressures were 15% (P= 0.03) and 23% (P= 0.04) greater in Thoroughbreds, respectively. Treadmill speed was ~12% greater (P= 0.04), stride length was ~25% greater (P= 0.0003), gait frequency was ~10% less (P= 0.006), breathing rate was ~10% less (P= 0.001), and heart rate was ~6% less (P= 0.06) for Thoroughbreds. There was no effect of breed on inspiratory or expiratory esophageal pressure although mean esophageal pressure was ~2 mmHg greater (P= 0.03) in exercising Standardbreds. In conclusion, pulmonary capillary and wedge pressures are greater in Thoroughbreds than in Standardbreds at similar fractions of maximal heart rate. This is compatible with the higher incidence of exercise-induced pulmonary hemorrhage observed in Thoroughbreds.     

Pulmonary vascular pressures of thoroughbred horses exercised 1, 2, 3 and 4 h after furosemide administration

Furosemide premedication of horses 4 h prior to exercise significantly attenuates exercise-induced pulmonary capillary hypertension which may help diminish the severity of exercise-induced pulmonary haemorrhage. As pulmonary hemodynamic effects of furosemide may be mediated via a reduction in plasma volume (which is most pronounced 15-30 min postfurosemide administration, with plasma volume recovering thereafter), we hypothesized that administration of furosemide at intervals shorter than 4 h before exertion may be more effective in attenuating the exercise-induced rise in pulmonary capillary blood pressure. Thus, our objective was to determine whether furosemide-induced attenuation of exercise-induced pulmonary arterial, capillary and venous hypertension would be enhanced when the drug is administered at intervals shorter than 4 h before exercise. Using established techniques, right atrial, and pulmonary arterial, capillary and wedge (venous) pressures were ascertained in seven healthy, sound, exercise-trained Thoroughbred horses in a randomized split-plot experimental design. Measurements were made at rest and during exercise performed at maximal heart rate (217 +/- 3 beats/min) in the control (no medications) experiments and following furosemide administration (250 mg intravenously (i.v.)) at 1, 2, 3 and 4 h before exercise. Sequence of treatments was randomized and 7 days were allowed between experiments on each horse. Although furosemide administration in the four treatment groups caused only insignificant changes in the pulmonary arterial, capillary and wedge pressures of standing horses, furosemide-induced reduction in mean right atrial pressure achieved statistical significance in the 2 h postfurosemide experiments. In the control studies, exercise was attended by statistically significant increments in mean right atrial, as well as pulmonary arterial, capillary and wedge pressures. Although exercise in each of the four furosemide experiments was also attended by significant increments in right atrial as well as pulmonary vascular pressures, in the 1, 2 and 3 h postfurosemide experiments, mean right atrial pressure increased to a significantly lower value than in the control study. Exercise-induced changes in pulmonary vascular pressures in the 1 h postfurosemide experiments were not different from the pressures in the control study. There was a significant attenuation of exercise-induced pulmonary capillary and venous hypertension in the 2, 3 and 4 h postfurosemide experiments, but significant differences among these treatments were not found. Thus, these data did not support the contention that administration of furosemide at intervals shorter than 4 h before exercise is more effective in attenuating exercise-induced pulmonary capillary or venous hypertension in Thoroughbred horses.     

Pulmonary vascular pressures of strenuously exercising Thoroughbreds after administration of varying doses of frusemide

The frusemide dose-response for attenuation of exercise-induced pulmonary capillary hypertension was studied in 7 healthy, exercise-conditioned Thoroughbred horses using previously described haemodynamic procedures. Four different doses of frusemide were tested: 250 mg regardless of bodyweight (amounting to 0.56 +/- 0.03 mg/kg bwt), 1.0 mg/kg bwt, 1.5 mg/kg bwt and 2.0 mg/kg bwt. Frusemide was administered i.v., 4 h before exercise. Haemodynamic data were obtained at rest and during treadmill exercise performed at 14.2 m/s on a 3.5% uphill grade; this workload elicited maximal heart rate of horses. Airway endoscopy was performed post exercise to detect exercise-induced pulmonary haemorrhage (EIPH). In standing horses, frusemide administration resulted in a significant (P<0.05) decrease in mean pulmonary arterial, pulmonary capillary and pulmonary artery wedge pressures, but significant differences among the various frusemide doses were not observed. In the control experiments, exercise caused significant increments in the right atrial as well as pulmonary arterial, wedge, and capillary pressures, and all horses experienced EIPH. Following frusemide administration, the exercise-induced rise in right atrial and pulmonary vascular pressures was significantly attenuated, but significant differences between the frusemide doses of 250 mg, 1.0 mg/kg, and 1.5 mg/kg were not discerned and all horses remained positive for EIPH. Although a further significant (P<0.05) attenuation of the exercise-induced rise in pulmonary capillary blood pressure occurred when frusemide dose increased from 250 mg to 2.0 mg/kg bwt, all horses still experienced EIPH. It is concluded that a linear response to increasing frusemide dosage in terms of attenuation of the pulmonary capillary hypertension does not exist in strenuously exercising Thoroughbred horses.     

Clenbuterol administration does not enhance the efficacy of furosemide in attenuating the exercise-induced pulmonary capillary hypertension in Thoroughbred horses

The stimulation of pulmonary beta2-adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol-a beta2-adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise-induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre-exercise)-control, and furosemide (250 mg i.v., 4 h pre-exercise)+clenbuterol (0.8 microg/kg i.v., 11 min pre-exercise) experiments. The sequence of these treatments was randomized for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, pulmonary vascular pressures were determined at rest, sub-maximal exercise, and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate. In the control study, incremental exercise resulted in progressive significant (P<0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P<0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide-control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P<0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P<0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P<0.05), but these data were not different from the furosemide-control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood-gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.     

Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses

The present study was carried out to ascertain whether beta2-adrenergic receptor stimulation with clenbuterol would attenuate the pulmonary arterial, capillary and venous hypertension in horses performing high-intensity exercise and, in turn, modify the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Experiments were carried out on 6 healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications) and the clenbuterol (0.8 pg/kg bwt, i.v.) treatments. The sequence of these treatments was randomised for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, right heart/pulmonary vascular pressures were determined at rest, sub-maximal exercise and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate and induced EIPH in all horses. In the control experiments, incremental exercise resulted in progressive significant increments in right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures and all horses experienced EIPH. Clenbuterol administration to standing horses caused tachycardia, but significant changes in mean right atrial or pulmonary vascular pressures were not observed. During exercise performed after clenbuterol administration, heart rate as well as right atrial and pulmonary arterial, capillary and wedge pressures also increased progressively with increasing work intensity. However, these values were not found to be statistically significantly different from corresponding data in the control study and the incidence of EIPH remained unaffected. Since clenbuterol administration also does not affect the transpulmonary pressure during exercise, it is unlikely that the transmural force exerted onto the blood-gas barrier of exercising horses is altered following i.v. clenbuterol administration at the recommended dosage.     

Aldosterone plasma concentration in horses with heart valve insufficiencies

In humans and small animals, heart disease can lead to an increase in aldosterone, and the aldosterone level correlates with the severity of the heart disease. In horses similar interactions may be possible and may lead to an increase in aldosterone in horses with heart valve insufficiencies. In a prospective clinical trial eight healthy horses (control group) and 40 horses with heart valve disease were examined. In all horses, a clinical (auscultation), electro- and echocardiographic examination was performed and aldosterone plasma concentration was determined. The median aldosterone plasma concentration in the control group was 23.95 pg/ml. Twenty-one out of 40 horses with heart valve insufficiencies and without dimensional changes by echocardiography (group 1) showed a median aldosterone plasma concentration of 45.5 pg/ml. Five out of the 40 horses had a left atrial (LA) dilation and an average LA size with 147.6+/-11 mm (group 2) and a median aldosterone plasma concentration of 95.9 pg/ml. Five other horses had a left ventricular (LV) dilation with an average LV size of 141.6+/-6.8 mm (group 3) and a median aldosterone plasma concentration of about 115.3 pg/ml. In this group a positive correlation between aldosterone plasma concentration and LV existed (r=0.9, P=0.03). Nine horses with both LA (152.8+/-11.4 mm) and LV dilatation (145+/-9 mm, group 4) had a median aldosterone plasma concentration of 161.2 pg/ml. Significant differences of the aldosterone concentrations were observed between the control group and the horses with LA and LV dilation (group 4, P=0.0005), as well as between group 1 (horses with heart valve insufficiency but without dilation) and group 4 (P=0.0006). The study confirms that, as reported for other species, aldosterone rises as the severity of valvular disease increases. However, in this study, as there is only significant difference from normal in the most affected group, it will require further study before the plasma aldosterone level can be relied on as an indicator of the severity of heart disease in an individual horse.     

Effects of Training on Phagocytic and Oxidative Metabolism of Peripheral Neutrophils in Horses Exercised in the Aerobic–Anaerobic Transition Area

Using simple techniques, the neutrophil function, in its phagocytosis and oxidative metabolism stages, was evaluated in horses. This was done before and after moderate exercise at the aerobic-anaerobic threshold (standardized heart rate 150 beats/min and lactate level of 3.07 +/- 0.21 mmol/L). The objective was to determine whether regular training and moderate exercise improved the neutrophil function. A group of 19 horses was used; 11 of these were untrained and the remainder trained for national jumping events. The exercise test consisted of a 5 min trot followed by a 3 min gallop on a long lunge. Blood samples were taken for analysis before, immediately after and 15 min after exercise. The results showed that (a) there is a difference in the internalization of particles (PI, PP and PE) by neutrophils from trained and untrained horses at a single time point during active recovery, and PP is higher in trained horses immediately after exercise; and (b) oxidative metabolism is significantly lower in untrained animals before and 1 min after exercise. The moderate exercise at the aerobic-anaerobic threshold did not have any influence on the peripheral blood neutrophil function of the phagocytosis and oxidative metabolism of particles.     

Effects of two different dosages of dobutamine on pulmonary artery wedge pressure, systemic arterial blood pressure and heart rate in anaesthetized horses

The purpose of the present study was to investigate the effects of two different dobutamine concentrations on pulmonary artery wedge pressure (PAWP) and on mean systemic arterial blood pressure (MAP) in horses anaesthetized with isoflurane, after induction of general anaesthesia with xylazine, ketamine and diazepam. Eight healthy warm-blood horses were included in the study. Each horse was subjected to general anaesthesia twice with two different dosages of dobutamine, 3 and 5 microg/kg bw/min, being infused over 15 min, starting 50 min after induction of general anaesthesia (T(0)). The heart rate, the PAWP and the MAP were recorded after 10 min (T(1)) and then every 5 min until 15 min after cessation of intravenous dobutamine administration (T(3)-T(5)). The PAWP was measured by a right heart catheter, which was positioned in the pulmonary capillaries. Mean systemic arterial blood pressure was monitored at the facial artery for the duration of general anaesthesia. All parameters increased at both dosage rates of dobutamine and decreased significantly when dobutamine administration ceased. The increase in heart rate was significantly higher after administration of 3 microg/kg bw/min dobutamine compared with the dosage of 5 microg/kg bw/min dobutamine. The increase in MAP was also higher at this dosage, but not significantly different to the dosage of 5 microg/kg bw/min dobutamine. During both dosages the MAP was above a value considered to be compatible with good peripheral circulation. The greater increase in PAWP was observed during administration of 5 g/kg bw/min dobutamine, but PAWP was not significantly different with the dosage of 3 microg/kg bw/min dobutamine. In conclusion, the administration of dobutamine led to an increase in MAP and PAWP above a value considered to be compatible with a good peripheral circulation. The results of the present study indicate that dobutamine improves circulation, in addition to its well-known effect on the periphery.     

Determination of oral dosage and pharmacokinetic analysis of flecainide in horses.

To determine oral dosage and to evaluate the pharmacokinetics in horses of orally administered flecainide, an antiarrhythmic drug, the correlations between its plasma concentration and PR, QRS and QT intervals in equine electrocardiograms (ECG) were investigated. Six healthy horses were administered a randomly ordered dose of 4 or 6 mg/kg of flecainide acetate. The ECG was monitored (heart rate (HR), PR, QRS, and QT intervals) and blood was taken at timed intervals to measure the plasma flecainide concentrations pre- and post-administration. The maximum plasma concentration reached 1014+/-285 (SD) ng/m/ in 45+/-13 min and 1301+/-400 ng/ m/l in 60+/-37 min for doses of 4 and 6 mg/kg flecainide, respectively. From the pharmacokinetic analysis, clearance rates were 14.6+/-6.4 and 11.7+/-5.2 ml/kg/min and terminal elimination half-lives were 228+/-53 and 304+/-87 min. The QRS and QT intervals increased significantly for both doses following administration, though HR and PR intervals did not change. Plasma flecainide concentrations were significantly correlated with QRS (r=0.935, P<0.001) and QT intervals (r=0.753, P<0.001). In conclusion, plasma concentrations of flecainide for treating equine atrial fibrillation were obtained by oral administration of 4 and 6 mg/kg, and the drug was rapidly eliminated from plasma in horses.     

Intravenous pentoxifylline does not affect the exercise-induced pulmonary arterial, capillary or venous hypertension in Thoroughbred horses

The present study was carried out to examine whether intravenously administered pentoxifylline-a phosphodiesterase inhibitor which increases red blood cell deformability and decreases blood viscosity-would attenuate the magnitude of exercise-induced pulmonary capillary hypertension in healthy, fit Thoroughbred horses and in turn, diminish the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. Hemodynamic data were collected at rest, and during exercise performed at 8 and 14 m/sec on 3.5% uphill grade in the control (no medications) and the pentoxifylline (8.5 mg/kg, i.v.) experiments. The sequence of treatments was randomized for every horse and 7 days were allowed between treatments. Galloping at 14 m/sec on 3.5% uphill grade elicited maximal heart rate. In both treatments, simultaneous measurements of phasic and mean right atrial and pulmonary arterial, capillary and wedge pressures were made using catheter-tip-manometers whose signals were carefully referenced at the point of the left shoulder. In the control study, exercise resulted in progressive significant increments in heart rate, right atrial and pulmonary arterial, capillary and venous pressures; thereby, confirming that exercising Thoroughbreds develop significant pulmonary hypertension. All horses experienced exercise-induced pulmonary hemorrhage (EIPH) in the control experiments. Pentoxifylline administration to standing horses caused anxiety, tachycardia, muscular fasciculations/tremors and mild sweating, but statistically significant changes in right atrial and pulmonary arterial, capillary and venous pressures were not detected. Exercise in the pentoxifylline treatment also resulted in progressive significant increments in heart rate and right atrial as well as pulmonary vascular pressures, but these data were not statistically significantly different from those in the control study and the incidence of EIPH remained unchanged. Thus, it was concluded that i.v. pentoxifylline is ineffective in attenuating the exercise-induced pulmonary arterial, capillary and venous hypertension in healthy, fit Thoroughbred horses.     

Effects of Intermittent Positive Pressure Ventilation on Cardiopulmonary Function in Horses Anesthetized with Total Intravenous Anesthesia Using Combination of Medetomidine,Lidocaine, Butorphanol and Propofol (MLBP-TIVA)

Effects of intermittent positive pressure ventilation (IPPV) on cardiopulmonary function were evaluated in horses anesthetized with total intravenous anesthesia using constant rate infusions of medetomidine (3.5 µg/kg/hr), lidocaine (3 mg/kg/hr), butorphanol (24 µg/kg/hr) and propofol (0.1 mg/kg/min) (MLBP-TIVA). Five horses were anesthetized twice using MLBP-TIVA with or without IPPV at 4-week interval (crossover study). In each occasion, the horses breathed 100% oxygen with spontaneous ventilation (SB-group, n=5) or with IPPV (CV-group, n=5), and changes in cardiopulmonary parameters were observed for 120 min. In the SB-group, cardiovascular parameters were maintained within acceptable ranges (heart rate: 33–35 beats/min, cardiac output: 27–30 l/min, mean arterial blood pressure [MABP]: 114–123 mmHg, mean pulmonary arterial pressure [MPAP]: 28–29 mmHg and mean right atrial pressure [MRAP]: 19–21 mmHg), but severe hypercapnea and insufficient oxygenation were observed (arterial CO₂ pressure [PaCO₂]: 84–103 mmHg and arterial O₂ pressure [PaO₂]: 155–172 mmHg). In the CV-group, normocapnea (PaCO₂: 42–50 mmHg) and good oxygenation (PaO₂: 395–419 mmHg) were achieved by the IPPV without apparent cardiovascular depression (heart rate: 29–31 beats/min, cardiac output: 17–21 l /min, MABP: 111–123 mmHg, MPAP: 27–30 mmHg and MRAP: 15–16 mmHg). MLBP-TIVA preserved cardiovascular function even in horses artificially ventilated.