Relationship of pulmonary arterial pressure to pulmonary haemorrhage in exercising horses.

Exercise-induced pulmonary haemorrhage (EIPH) is characterised by blood in the airways after strenuous exercise and results from stress failure of the pulmonary capillaries. The purpose of this experiment was to establish a threshold value of transmural pulmonary arterial pressure at which haemorrhage occurs in the exercising horse. Five geldings, age 4-14 years, were run in random order once every 2 weeks at 1 of 4 speeds (9, 11, 13, 15 m/s); one day with no run was used as a control. Heart rate, pulmonary arterial pressure and oesophageal pressure were recorded for the duration of the run. Transmural pulmonary arterial pressure was estimated by electronic subtraction of the oesophageal pressure from the intravascular pulmonary arterial pressure. Within 1 h of the run, bronchoalveolar lavage was performed and the red and white blood cells in the fluid were quantified. Red cell counts in the lavage fluid from horses running at 9, 11 and 13 m/s were not significantly different from the control value, but after runs at 15 m/s, red cell counts were significantly (P<0.05) higher. White cell counts were not different from control values at any speed. Analysis of red cell count vs. transmural pulmonary arterial pressure indicated that haemorrhage occurs at approximately 95 mmHg. Red cell lysis in the lavage fluid was also apparent at transmural pulmonary arterial pressures above 90 mmHg. We conclude that, in the exercising horse, a pulmonary arterial pressure threshold exists above which haemorrhage occurs, and that pressure is often exceeded during high speed sprint exercise.

Analysis of the right ventricular function in the exercising horse: use of the Fourier Transform.

The objective of this study was to develop and test a technique to allow dynamic cardiac function to be studied during exercise in the horse. Blood pressure waveforms in the exercising horse are difficult to interpret because of the large influence of stride and respiration. A method has been devised to study dynamic right ventricular variables during high-speed exercise in the horse. A Fast Fourier Transform was performed on the digitised pressure waveforms and the frequency components associated with stride and respiration were removed. An inverse Fourier Transform was then performed to generate a time-domain pressure signal. Several dynamic right ventricular variables were calculated using the derived signal. Various parameters associated with removing frequencies from the frequency-domain pressure signal were changed to determine their influence on the variables. Most of the variables were not sensitive to these parameters. When compared during separate exercise bouts, some variables differed among runs, while others were not significantly different. Using the signal separation technique described here, right ventricular function of an exercising horse can be critically analysed.

V(O2) recovery kinetics in the horse following moderate, heavy, and severe exercise.

At the onset of exercise, horses exhibit O2 uptake (VO2) kinetics that are qualitatively similar to those of humans. In humans, there is a marked dissymmetry between on- and off-kinetics for VO2. This investigation sought to formally characterize the off-transient (recovery) VO2 kinetics in the horse within the moderate (M), heavy (H), and severe (S) exercise domains. Six horses were run on a high-speed treadmill at M, H, and S exercise intensities (i.e., that speed which yielded approximately 50, 85, 100% peak VO2, respectively, on the maximal incremental test). The time courses for the recovery were modeled by using a three-phase model with a single-exponential (fast component) or double-exponential (fast and slow component) phase 2. The single-exponential phase 2 model provided an excellent fit to the off-transient data, with the exception of one horse in the H domain which was best modeled by a double exponential. The time delay elicited no domain dependency (M, 18.0 +/- 1.0; H, 17.6 +/- 1.1; S, 17.8 +/- 2.0 s; P > 0.05), as was the case for the fast-component time constants (M, 16.3 +/- 2.0 s; H, 13.5 +/- 1.0 s; S, 14.6 +/- 0.3 s; P > 0.05). In the H and S (but not M) domains, the VO2 following resolution of the fast component was elevated above the preexercise baseline (H, 3.0 +/- 1.0 l/min; S, 5.7 +/- 1.1 l/min). This additional postexercise VO2 was correlated to the end-exercise increase in lactate (r = 0.94, P < 0.001) but not the end-exercise pulmonary arterial blood temperature (r = 0.45, P > 0.05). These data indicate that the time delay and subsequent kinetic response of the primary (fast-component) phase of exercise VO2 recovery in the horse is independent of the preceding exercise-intensity domain. However, in the H and S domains, the fast component resolves to an elevated baseline.

Influence of frusemide on dynamic cardiac variables during exercise.

Exercising horses have extremely high right and left atrial pressures. Limitation in ventricular function (i.e. relaxation) may play a role in these high pressures. We studied relaxation characteristics of the right ventricular myocardium and the impact of frusemide (2.0 mg/kg bwt i.v.) on these characteristics in horses exercising at 8, 10, 12 and 14 m/s. Exercise tests were performed 4 h after administration of frusemide. Right ventricular (RV) pressure was analysed using Fast Fourier Transform techniques to remove non cardiac components of the pressure signal. Mean right atrial (RA) pressure increased with exercise and was significantly attenuated at all speeds by frusemide. RV maximum and minimum rates of pressure change with respect to time (RV + dP/dtmax, RV-dP/dtmax) increased with exercise and RV relaxation time constant (RV tau) and time of RV relaxation from 65-20% of the difference between maximum and minimum ventricular pressure (delta 65-20) decreased with exercise. Frusemide produced no significant differences in +dP/dtmax, -dP/dtmax, RV tau or delta 65-20 except at 12 m/s where RV tau was longer after frusemide (23.4 ms for frusemide vs. 19.7 ms for control). Significant reductions in stroke volume were seen at 8, 10 and 14 m/s after frusemide. These results suggest that the reduction of atrial pressure by frusemide is not due to changes in ventricular relaxation rate.

Quantification of exercise-induced pulmonary haemorrhage with bronchoalveolar lavage.

Exercise-induced pulmonary haemorrhage (EIPH) causes serious economic losses in the horse racing industry. Endoscopic examination indicates that 40-90% of horses exhibit EIPH following sprint exercise, but the limitations of the endoscope prevent diagnosis in many horses. Bronchoalveolar lavage (BAL) was utilised to detect red blood cells (RBCs) in the terminal airways in 6 horses. Two lavages were performed at weekly intervals prior to exercise, one within 90 min after exercise, and 5 at weekly intervals after exercise. The horses were exercised strenuously at 12.5-14.6 m/s on a treadmill (3 degree incline). Heart rates ranged from 192-207 beats/min, and mean pulmonary arterial pressures (mPAP) ranged from 80-102 mmHg. Neither epistaxis nor endoscopic evidence of EIPH was seen in any of the 6 horses following exercise. However, the number of RBCs in the lavage fluid increased significantly over control values immediately after exercise in all horses but returned to control values by one week after exercise. Haemosiderophages in the BAL fluid did not increase until one week after exercise and remained elevated for 3 weeks after exercise. Twenty per cent of the total population of alveolar macrophages contained haemosiderin. A positive relationship occurred between the number of RBCs in the lavage fluid and mPAP; the amount of haemorrhage increased as the mPAP exceeded 80 to 90 mmHg. The results with BAL used as the diagnostic tool, suggest that all strenuously exercised horses may exhibit EIPH; the amount of haemorrhage appears to be associated with the magnitude of the high pulmonary arterial pressure.

Paraneoplastic pruritus and alopecia in a horse with diffuse lymphoma.

An 8-year-old castrated male Paint Horse was referred because of generalized pruritus, alopecia, and intermittent fever. Results of gross evaluation of the skin and microscopic evaluation of skin scrapings were inconclusive. Histologic examination of skin biopsy specimens revealed vasculitis. The horse had persistent hypercalcemia; therefore, lymphosarcoma was considered a possibility. Ultrasonography revealed hypoechoic nodules within the parenchyma of the spleen and liver. Results of microscopic evaluation of an aspirate from a splenic nodule were suggestive of lymphosarcoma. The condition of the horse deteriorated, and it was subsequently euthanatized. Postmortem examination revealed diffuse lymphoma. In human beings, generalized pruritus may be an indication of serious internal disease, including malignancy. Paraneoplastic pruritus is most common in patients with Hodgkin's lymphoma but can also develop in patients with non-Hodgkin's lymphoma, leukemia, or a solid neoplasm. Lymphoma should be considered in the differential diagnoses when examining horses with generalized pruritus for which another cause cannot be identified.

VO2 kinetics in the horse during moderate and heavy exercise.

The horse is a superb athlete, achieving a maximal O2 uptake (approximately 160 ml . min-1 . kg-1) approaching twice that of the fittest humans. Although equine O2 uptake (VO2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peak VO2 (VO2 peak), and kinetic features of their VO2 response to "square-wave" work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 +/- 0.7 m/s (i.e., between Tlac and VO2 peak) sustained for 6 min. VO2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate. VO2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (tau1 = 10.0 +/- 0.9 s) that followed a time delay (TD1 = 18.9 +/- 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 +/- 1.2 s); however, the phase 2 time constant was significantly slower (tau1 = 20.7 +/- 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase in VO2 became evident 135.7 +/- 28.5 s after the exercise transition. This "slow component" accounted for approximately 12% (5.8 +/- 2.7 l/min) of the net increase in exercise VO2. We conclude that, at exercise intensities below and above Tlac, qualitative features of VO2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2 utilization within equine muscle fibers.