Bronchial circulation during prolonged exercise in ponies.

Tracheal, bronchial, and renal flow were studied in 8 healthy ponies at rest and during exercise performed on a treadmill at a speed setting of 20.8 km/h and 7% grade (incline) for 30 minutes. Blood flow was determined with 15-microns-diameter radionuclide-labeled microspheres that were injected into the left ventricle when the ponies were at rest, and at 5, 15, and 26 minutes of exertion. Heart rate and mean aortic pressure increased from resting values (40 +/- 2 beats/min and 124 +/- 3 mm of Hg, respectively) to 152 +/- 8 beats/min and 133 +/- 4 mm of Hg at 5 minutes of exercise, to 169 +/- 6 beats/min and 143 +/- 5 mm of Hg at 15 minutes of exercise, and to 186 +/- 8 beats/min, and 150 +/- 5 mm of Hg at 26 minutes of exercise. Tracheal blood flow at rest and during exercise remained significantly (P less than 0.05) less than bronchial blood flow. Tracheal blood flow increased only slightly with exercise. Vasodilation caused bronchial blood flow to increase throughout exercise. Pulmonary arterial blood temperature of ponies also increased significantly (P less than 0.05) with exercise and a significant (P less than 0.005) correlation was found between bronchial blood flow and pulmonary arterial blood temperature during exertion. At 5 minutes of exercise, renal blood flow was unchanged from the resting value; however, renal vasoconstriction was observed at 15 and 26 minutes of exercise. We concluded that bronchial circulation of ponies increased with exercise in close association with a rise in pulmonary arterial blood temperature.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Effect of splenectomy on exercise-induced pulmonary and systemic hypertension in ponies

Large increases in systemic and pulmonary arterial pressures of exercising healthy ponies have been observed. Because exercise causes a considerable increase in PCV of ponies, we examined the effect of splenectomy on exercise-induced changes in systemic and pulmonary pressures. These pressures (taken with catheter-tip micromanometers) and indicator dilution cardiac output were determined on 9 healthy ponies that had undergone splenectomy 4 to 9 weeks before the study. Data obtained at rest and during submaximal (10.5 to 11.0 mph) and maximal (14 to 15 mph) exercise from these ponies were compared with similar data from clinically normal ponies. Following splenectomy, PCV increased by only 4 vol% during maximal exercise, but cardiac output of splenectomized ponies reached values similar to those of clinically normal ponies. Despite this similarity in cardiac output, the systemic and pulmonary arterial pressures of exercising splenectomized ponies increased to significantly lower levels than those in clinically normal ponies (P less than 0.01); total pulmonary vascular resistance and total peripheral resistance decreased to values significantly less than those in clinically normal ponies (P less than 0.01). Thus, it appears that increases in blood viscosity induced by increases in PCV may contribute substantially to the pulmonary and systemic hypertension of exercise in clinically normal ponies.     

Regional brain blood flow during prolonged submaximal exercise in ponies.

Experiments were carried out on 8 healthy ponies to examine the effects of prolonged submaximal exercise on regional distribution of brain blood flow. Brain blood flow was ascertained by use of 15-microns-diameter radionuclide-labeled microspheres injected into the left ventricle. The reference blood was withdrawn from the thoracic aorta at a constant rate of 21.0 ml/min. Hemodynamic data were obtained with the ponies at rest (control), and at 5, 15, and 26 minutes of exercise performed at a speed setting of 13 mph on a treadmill with a fixed incline of 7%. Exercise lasted for 30 minutes and was carried out at an ambient temperature of 20 C. Heart rate, mean arterial pressure, and core temperature increased significantly with exercise. With the ponies at rest, a marked heterogeneity of perfusion was observed within the brain; the cerebral, as well as cerebellar gray matter, had greater blood flow than in the respective white matter, and a gradually decreasing gradient of blood flow existed from thalamus-hypothalamus to medulla. This pattern of perfusion heterogeneity was preserved during exercise. Regional brain blood flow at 5 and 15 minutes of exercise remained similar to resting values. However, at 26 minutes of exercise, vasoconstriction resulted in a significant reduction in blood flow to all cerebral and brain-stem regions. In the cerebellum, the gray matter blood flow and vascular resistance remained near control values even at 26 minutes of exercise. Vasoconstriction in various regions of the cerebrum and brainstem at 26 minutes of exertion may have occurred in response to exercise-induced hypocapnia, arterial hypertension, and/or sympathetic neural activation.     

Cardiopulmonary effects of continuous intravenous infusion of guaifenesin, ketamine, and xylazine in ponies

Eight ponies were anesthetized with a solution containing 50 mg of guaifenesin, 1 mg of ketamine, and 0.5 mg of xylazine X ml-1 of 5% dextrose in water. Anesthesia was induced by IV injection (1.1 ml X kg-1), followed by continuous IV infusion at 2.75 ml X kg-1 X hr-1. Heart rate, rate-pressure product, mean pulmonary artery pressure, and standard bicarbonate were not significantly changed throughout the study. Systolic, diastolic, and mean arterial pressures and left ventricular stroke work index were significantly decreased at 5 and 15 minutes after a bolus of the anesthetic solution was injected. Systolic blood pressure returned to within the base-line range at 30 minutes, but diastolic and mean arterial pressures were significantly decreased throughout the study. Cardiac index and arterial pH were decreased at 5 minutes only. Systemic vascular resistance was significantly decreased 60 minutes after bolus injection was given. Hypoventilation, as indicated by increased PaCO2, occurred 5 minutes after bolus injection was given.     

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.     

Influence of cyclooxygenase inhibitors on furosemide-induced hemodynamic effects during exercise in horses.

Furosemide, which commonly is used as a prophylactic treatment for exercise-induced pulmonary hemorrhage in horses, may mediate hemodynamic changes during exercise by altering prostaglandin metabolism. To determine if furosemide's hemodynamic effects during exercise in horses could be reversed, cyclooxygenase inhibitors were administered with furosemide. Four treatments were administered 4 hours prior to treadmill exercise at 9 and 13 m/s. They included a control treatment (10 ml of 0.9% NaCl solution, IV), furosemide (1 mg/kg of body weight, IV) administered alone, and furosemide in combination with phenylbutazone (4 mg/kg, IV, q 12 h for 2 days) or with flunixin meglumine (1.1 mg/kg, IV, on the day of experiment). Five horses were randomly assigned to complete all treatments. Physiologic variables at rest prior to exercise were not influenced by treatments. Furosemide, administered alone, reduced mean right atrial pressure and mean pulmonary artery pressure during exercise. The combinations of furosemide and flunixin meglumine or furosemide and phenylbutazone, at both levels of exercise intensity, returned mean right atrial pressure and mean pulmonary artery pressure to the value of the control treatment. During rest and exercise, plasma lactate concentration, PCV, heart rate, mean carotid artery pressure, oxygen consumption, carbon dioxide elimination, and cardiac output were not altered by any of the treatments. At 5 minutes after exercise, the administration of furosemide, alone or with phenylbutazone, reduced mean right atrial pressure. Other measured variables were not significantly influenced by treatments during recovery from exercise. These results suggested that cyclooxygenase inhibition partially reverses the decrease in mean right atrial pressure or pulmonary artery pressure induced by furosemide during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of 7.2% hypertonic saline solution in halothane anaesthetized ponies

The haemodynamic effects of intravenously (iv) administered hypertonic saline solution (7.2%, 4 ml/kg of body weight [bwt]) were investigated in normovolaemic ponies during halothane anaesthesia (dorsal recumbent position, intermittent pressure ventilation). Heart rate, arterial blood and pulmonary artery pressures, cardiac output, and arterial blood gases were measured throughout the experiment while related haemodynamic parameters (cardiac index, systemic and pulmonary vascular resistance, stroke volume, ventricular work) were calculated.
A transient decrease in arterial blood pressure occurred during the administration of the hypertonic solution. Significant increases in cardiac output and index, stroke work, and systolic arterial pressure were observed 5 min after the administration of the hypertonic infusion. A gradual normalization of the increased parameters occurred afterwards. Heart rate and arterial blood gases remained constant throughout the study. No clinical side-effects, except for an increase in urinary production in the recovery period, were seen during and after anaesthesia.     

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.     

Distribution of blood flow during moderate and strenuous exercise in ponies (Equus caballus)

Blood flow to the brain, heart, kidneys, diaphragm, and skeletal muscles was studied at rest and during graded treadmill exercise, using radionuclide-labeled microspheres (15 microns diameter), in 11 healthy adult ponies. Hemodynamic changes brought about by exercise included marked increases in cardiac output, mean aortic pressure, left ventricular end-diastolic pressure, and right ventricular systolic and end-diastolic pressures. Blood flow to the brain stem and cerebral hemispheres was unchanged during both moderate exercise (heart rate = 154 +/- 3 beats/min) and severe exercise (heart rate = 225 +/- 7 beats/min). Despite marked hypocapnia during severe exercise, cerebellar blood flow increased by 32% above control value (94 +/- 7 ml/min/100 g). Myocardial blood flow increased transmurally with both levels of exercise. The endo:epi (inner:outer) perfusion ratio for the left ventricle and the interventricular septum decreased during exercise. It was, however, not different from unity. During severe exercise, renal blood flow decreased to 19% of its control value. Blood flow to the diaphragm exceeded that to the skeletal muscles during both intensities of exercise. Blood flow to the exercising muscles of the brachium and thigh increased by 31- to 38-fold during moderate exercise and by 70- to 76-fold during severe exercise. It is concluded that the cardiovascular response to strenuous exercise in the pony included an increase in blood flow to the cerebellum, myocardium, diaphragm, and exercising skeletal muscles, while blood flow was diverted away from the kidneys. It would appear that the pony's cardiovascular response to severe exercise is similar to that of persons.     

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.     

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.     

Intravenous pentoxifylline does not enhance the pulmonary haemodynamic efficacy of frusemide in strenuously exercising thoroughbred horses

The present study was carried out to examine whether pentoxifylline administration to horses premedicated with frusemide would attenuate the exercise-induced pulmonary arterial, capillary and venous hypertension to a greater extent than frusemide alone, thereby affecting the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Using established techniques, we determined right heart and pulmonary vascular pressures in 6 healthy, sound Thoroughbred horses at rest and during exercise performed at maximal heart rate at a workload of 14 m/s on 3.5% uphill grade in the control (no medications), frusemide (250 mg i.v., 4 h pre-exercise)-control, and the frusemide (250 mg i.v., 4 h pre-exercise) + pentoxifylline (8.5 mg/kg bwt i.v., 15 min preexercise) treatments. Sequence of the 3 treatments was randomised for every horse and 7 days were allowed between them. In the control study, galloping at 14 m/s on 3.5% uphill grade elicited significant right atrial as well as pulmonary arterial, capillary and venous hypertension and all horses experienced EIPH as detected by the presence of fresh blood in the trachea on endoscopic examination. Frusemide administration was not attended by changes in heart rate at rest or during exercise. Although in the frusemide-control experiments, a significant reduction in mean pulmonary arterial, capillary and wedge pressures was observed both at rest and during galloping at 14 m/s on 3.5% uphill grade, all horses still experienced EIPH. Pentoxifylline administration to standing horses premedicated with frusemide caused nervousness, muscular fasciculations, sweating and tachycardia. Although these symptoms had largely abated within 15 min, there were no significant changes in the right atrial or pulmonary vascular pressures. Exercise in the frusemide + pentoxifylline experiments also caused significant right atrial as well as pulmonary arterial, capillary and venous hypertension, but these data were not found to be significantly different from the frusemide-control experiments. All horses in the frusemide + pentoxifylline experiments also experienced EIPH. In conclusion, our data indicate that pentoxifylline (8.5 mg/kg bwt i.v., 15 min pre-exercise) is ineffective in modifying the pulmonary haemodynamic effects of frusemide in exercising horses. It should be noted, however, that we did not examine whether erythrocyte plasticity was altered by the administration of pentoxifylline. Since the intravascular force exerted onto the blood-gas barrier of exercising horses premedicated with frusemide remained unaffected by pentoxifylline administration, it is concluded that concomitant pentoxifylline administration is unlikely to offer additional benefit to horses experiencing EIPH.     

Cardiovascular effects of a high dose of romifidine in propofol-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of IM administration of romifidine hydrochloride in propofol-anesthetized cats. ANIMALS: 15 adult domestic shorthair cats. PROCEDURE: Cats were randomly assigned to receive romifidine (0, 400, or 2,000 microg/kg, IM). Cats were anesthetized with propofol and mechanically ventilated with oxygen. The right jugular vein, left carotid artery, and right femoral artery and vein were surgically isolated and catheterized. Heart rate; duration of the PR, QRS, and QT intervals; mean pulmonary artery pressure; mean right atrial pressure; systolic, diastolic, and mean arterial pressures; left ventricular systolic pressure; left ventricular end-diastolic pressure; and cardiac output were monitored. Systemic vascular resistance, rate of change of left ventricular pressure, and rate pressure product were calculated. Arterial and venous blood samples were collected anaerobically for determination of pH and blood gas tensions (Po2 and Pco2). RESULTS: Administration of romifidine at 400 and 2,000 microg/kg, IM, decreased heart rate, cardiac output, rate of change of left ventricular pressure, rate pressure product, and pH. Arterial and pulmonary artery pressures, left ventricular pressure, left ventricular end-diastolic pressure, and right atrial pressure increased and then gradually returned to baseline values. Arterial blood gas values did not change, whereas venous Pco2 increased and venous Po2 decreased. Significant differences between low and high dosages were rare, suggesting that the dosages investigated produced maximal hemodynamic effects. CONCLUSIONS AND CLINICAL RELEVANCE: Romifidine produces cardiovascular effects that are similar to those of other alpha2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise.     

Cardiovascular and pulmonary effects of recumbency in two conscious ponies

Respiratory dead-space, tidal volume, respiratory rate, blood gases, cardiac output, heart rate and arterial and pulmonary arterial blood pressures were measured in two conscious, trained ponies in the standing position and in left lateral recumbency. The ponies were reluctant to remain lying down for more than about 20 mins but the reason for this did not become apparent. Tidal volume was reduced during recumbency but the respiratory rate increased, tending to maintain the minute volume at about that of the standing animal. Arterial carbon dioxide tension did not change significantly from standing values but the mean arterial oxygen tension values tended to decrease in both ponies during recumbency because of a slight increase in pulmonary venous admixture. Venous admixture in these two laterally recumbent conscious animals was considerably less than previously reported for anaesthetised subjects.     

THE USE OF GATED RADIONUCLIDE VENTRICULOGRAPHY AS A NONINVASIVE METHOD OF EVALUATING RIGHT VENTRICULAR FUNCTION IN DOGS WITH EXPERIMENTALLY INDUCED CONGESTIVE HEART FAILURE

Gated radionuclide ventriculography was evaluated as a noninvasive method of quantifying right ventricular function in dogs with experimentally induced congestive heart failure. Gated radionuclide ventriculography measurements of right ventricular function (right ventricular ejection fraction, right ventricular average emptying rate, and right ventricular average filling rate) were related to standard hemodynamic and echocardiographic measurements. Congestive heart failure was induced by rapid ventricular pacing in eight normal dogs. Hemodynamic, echocardiographic, and gated radionuclide ventriculography measurements were obtained before and after development of biventricular failure. Congestive heart failure resulted in significant changes in all hemodynamic, echocardiographic, and gated radionuclide ventriculography measurements with the exception of systemic arterial pressure. Right ventricular ejection fraction was inversely related to pulmonary artery systolic, diastolic, and mean pressure, and right ventricular average emptying rate was inversely related to the pulmonary artery systolic, diastolic, and mean pressure. Right ventricular ejection fraction was inversely related to left ventricular filling pressure, (pulmonary capillary wedge pressure). Neither the echocardiographic measurements of right ventricular size (right ventricular internal diastolic dimension) nor the right ventricular end-diastolic pressure were related to right ventricular ejection fraction and right ventricular average emptying rate. However, echocardiographic measurements of right ventricular dimension were related to right ventricular filling pressure. The gated radionuclide ventriculography indexes of right ventricular function, right ventricular ejection fraction and right ventricular average emptying rate, are affected by afterload but unaffected by preload, whereas the echocardiographic measurement of right ventricular dimension is related to preload. Gated radionuclide ventriculography provides right ventricular data which is unique from that obtained by standard echocardiographic imaging. Also, gated radionuclide ventriculography has potential value as a noninvasive means of estimating a change in pulmonary artery pressure.     

Haemodynamic effects of hyoscine-N-butylbromide in ponies

The haemodynamic effects of hyoscine- N -butylbromide (0.30 mg/kg, intravenously) were studied in eight adult ponies in a blinded two-period crossover experiment with repeated measures. Values for heart rate were 63%, 48% and 13% greater than control values at 1, 16 and 46 min, respectively, after administration of hyoscine-N-butylbromide. Cardiac output increased by 16% at 16 min after drug injection. Mean right atrial pressure was decreased by 79%, 63%, 45% and 52% at 1, 16, 46 and 61 min, respectively, after drug administration. Stroke volume was decreased by 32% at 1 min and pulmonary arterial wedge pressure was decreased by 44% at 16 min. We detected no significant difference in mean systemic arterial pressure, mean pulmonary arterial pressure, systemic vascular resistance or pulmonary vascular resistance at any time.     

Pharmacology of Furosemide in the Horse: A Review

Furosemide, a diuretic, is frequently administered to horses for the prophylaxis of exercise-induced pulmonary hemorrhage and the treatment of a number of clinical conditions, including acute renal failure and congestive heart failure. Furosemide increases the rate of urinary sodium, chloride, and hydrogen ion excretion. Plasma potassium concentration decreases after furosemide administration but urinary potassium excretion in horses is minimally affected. Renal blood flow increases after furosemide administration. Systemically, furosemide increases venous compliance and decreases right atrial pressure, pulmonary artery pressure, pulmonary artery wedge pressure, and pulmonary blood volume. The systemic hemodynamic effects of furosemide are only manifest in the presence of a functional kidney, but can occur in the absence of diuresis, emphasizing the importance of the renal-dependent extra-renal effects of furosemide. The renal and systemic hemodynamic effects of furosemide are modified by prior administration of nonsteroidal anti-inflammatory drugs. Furosemide administration attenuates exercise-induced increases in right atrial, aortic, and pulmonary artery pressures in ponies. Furosemide prevents exercise and allergen-induced bronchoconstriction in humans and decreases total pulmonary resistance in ponies with recurrent obstructive airway disease. These pharmacologic effects are frequently used to rationalize its questionable efficacy in the prevention of exercise-induced pulmonary hemorrhage. Neither the effect of furosemide on athletic performance nor its efficacy in the prevention of exercise-induced pulmonary hemorrhage has been convincingly demonstrated.     

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.     

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.