|
|
||||||||
Departments of Veterinary Biosciences and Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, Illinois 61801
Manohar, Murli, and Thomas E. Goetz. Pulmonary vascular
pressures of exercising Thoroughbred horses with and without endoscopic
evidence of EIPH. J. Appl. Physiol.
81(4): 1589-1593, 1996.
Exercise-induced pulmonary hemorrhage
(EIPH) is a common occurrence in racehorses. The objective of this
study was to compare pulmonary vascular pressures of healthy
Thoroughbred horses with and without postexertion endoscopically
detectable fresh blood in the trachea. The nasopharynx, larynx, and
trachea (down to the carina) of horses were examined weekly with an
endoscope 55-60 min postexertion, and the diagnosis of EIPH was
confirmed by the presence of fresh blood in the trachea. Measurements
of heart rate and right atrial, pulmonary arterial, and pulmonary
arterial wedge pressures were made during quiet rest and during
treadmill exercise performed at 14.5 m/s on a 5% uphill
grade. This workload elicited maximal heart rate of the
horses. Mean pulmonary capillary pressure was estimated to be halfway
between the mean pulmonary arterial pressure and the mean pulmonary
arterial wedge pressure. These data from 7 healthy sound
exercise-trained horses that were positive on 12 consecutive occasions
(at 1-wk intervals) for the postexercise presence of fresh blood in the
trachea were compared with those in 8 healthy horses that were
consistently negative for the evidence of fresh blood in the trachea on
postexercise endoscopic examination over 12-16 wk. The heart rate
and the right heart and/or pulmonary vascular pressures in the two
groups of horses were similar at rest. Exercise was
attended by a large significant (P < 0.05) increase in these pressures and heart rate in both groups.
However, statistically significant differences between endoscopically
EIPH-positive and endoscopically EIPH-negative horses for heart rate
and right atrial and pulmonary vascular pressures were not found during
exercise. Thus these data revealed that the magnitude of
exercise-induced right atrial as well as pulmonary arterial, capillary,
and venous hypertension in endoscopically EIPH-positive horses that are
otherwise healthy is quite similar to that in endoscopically
EIPH-negative horses during comparable exertion.
exercise-induced pulmonary hemorrhage; pulmonary circulation; pulmonary hemodynamics
EXERCISE-INDUCED PULMONARY HEMORRHAGE (EIPH)
isfrequently observed in racehorses. On the basis of
postexercise endoscopic detection of fresh blood in the trachea, it has
been reported that the incidence of EIPH in racing Thoroughbred (9) and
Standardbred (2) horses probably exceeds 75%. It is
commonly held in "racing circles" that EIPH contributes to
exercise intolerance, i.e., loss of stamina and/or performance, even
though definite proof is lacking (2, 9). Although it has
been demonstrated that hemosiderin-laden macrophages could be recovered
in the tracheobronchial washings from all Thoroughbreds in training
(11), the fact remains that unless overt epistaxis occurs, the
diagnosis of EIPH in racehorses is made on endoscopic examination of
the airway performed ~60 min postexercise (9). Furthermore, the
decision in competitive racing as to whether a racehorse is prescribed
prerace furosemide administration for prevention and/or
management of EIPH is also based on the endoscopic
observation of fresh blood in the trachea after a race (Dr. R. Jensen, Illinois Racing Board, personal
communication).
Recent work has demonstrated that exercising horses develop marked
pulmonary arterial, capillary, and venous hypertension (3-6), and
it is believed that the high transmural (intravascular minus
perivascular alveolar) pulmonary capillary pressure exerted on the
blood-gas barrier, which has to be quite thin (0.3-0.6 µm) to
provide for diffusion of respiratory gases, probably contributes to
stress failure of pulmonary capillaries (10), resulting in EIPH.
Despite this recognition, to our knowledge there have been no reports
comparing pulmonary vascular pressures of horses that exhibit EIPH with
those that do not. Thus the primary objective in this study was to
compare the rest and exercise values of pulmonary vascular pressures of
Thoroughbred horses in which fresh blood is detected on postexercise
endoscopic examination of the trachea with those in which fresh blood
is not detected on the postexercise endoscopic examination of the
airway. In our experiments, horses performed high-intensity short-term
exercise at maximal heart rate.
Horses.
Experiments were carried out on 15 Thoroughbred horses (7 fillies and 8 geldings) aged 2.5-5 yr and weighing between 375 and 523 kg. The
horses were divided into two groups (see EIPH-positive and EIPH-negative groups), designated as
endoscopically EIPH-positive (n = 7)
and endoscopically EIPH-negative (n = 8) horses. The horses were housed in an air-conditioned
building and were accustomed to being handled by people. They were fed
a diet of alfalfa hay and oats, and free access to water was provided.
The horses were healthy, sound, and received routine treatments meeting
veterinary medical standards for the equine species. Our protocols and
procedures were approved by the Institutional Laboratory Animal Care
and Use Committees.
Significant differences in heart rate, mean right atrial pressure, or
pulmonary vascular pressures were not found between the two groups of
horses either at rest or during exercise (Figs. 1, 2, 3, 4, 5, 6).
In both groups, exercise resulted in significant tachycardia and in
right atrial as well as pulmonary arterial, capillary, and venous
hypertension. During exercise at 14.5 m/s on a 5% uphill incline, mean
right atrial, mean pulmonary arterial, mean pulmonary arterial wedge,
and mean pulmonary capillary blood pressures of endoscopically
EIPH-positive horses approached 61 ± 4, 96.5 ± 4.0, 70.1 ± 3.3, and 83.3 ± 3.6 mmHg, respectively. Exercise also caused a
significant increment in the pulmonary arterial pulse pressure (Fig.
3), and the pulmonary perfusion pressure gradient increased
significantly from 5 ± 1 mmHg at rest to 27 ± 1 mmHg.
Significantly
different from 14.5 m/s for same group of horses, P < 0.05.
Significantly different
from 14.5 m/s for same group of horses, P < 0.05.
ive) horses, increments
in work intensity were accompanied by similar progressive rises in
systolic and diastolic pulmonary arterial pressure values. Gap between
corresponding systolic and diastolic pressure values represents
pulmonary arterial pulse pressure. Significant difference in pulmonary
arterial pulse pressure of EIPH-positive and EIPH-negative horses was
not detected at rest or during exertion.
* P < 0.05.
P < 0.05.
Significantly different from 14.5 m/s
for same group of horses, P < 0.05.
Significantly different
from 14.5 m/s for same group of horses, P < 0.05.
Significantly different
from 14.5 m/s for same group of horses, P < 0.05.
Postexercise endoscopic examination of the airway revealed fresh blood in the trachea of each of the seven horses belonging to the EIPH-positive group. However, blood was not detected in the airways on the postexercise endoscopic examination in any of the horses belonging to the EIPH-negative group.
Our data have demonstrated that right atrial, pulmonary arterial, pulmonary capillary, and pulmonary venous pressures of Thoroughbred horses that exhibit fresh blood in the trachea during postexercise endoscopic examination are not different from those that do not exhibit fresh blood in the trachea postexercise; this was true at rest as well as during strenuous exertion. These data also confirmed earlier observations (3-6) that galloping horses develop significant pulmonary arterial, capillary, and venous hypertension.
It has been suggested that the incidence of EIPH may increase with age, but conclusive evidence is lacking (9). In the present study, an age-related trend for the occurrence of EIPH was not observed. Interestingly, the youngest horse (2.5 yr old) in this study belonged to the EIPH-positive group. It should be noted that all of our horses had previously raced competitively in Illinois and/or other US racing jurisdictions.
Recently, mean pulmonary arterial pressure of a 3-yr-old Throughbred filly that experienced EIPH (based on postexercise endoscopic examination of the airway) was reported to be 138 mmHg during exertion at 13.5 m/s, when the heart rate approached 210 beats/min (10). This exercise value of mean pulmonary arterial pressure from the EIPH-positive filly (10) exceeded values (89-105 mmHg) reported from EIPH-negative horses exercised at similar or higher workloads in previous studies (3-6). In horse racing circles, this has been interpreted as meaning that the pulmonary vascular pressures of Thoroughbreds that exhibit fresh blood in the trachea on postexercise endoscopy of the airway may be higher than those in horses that do not exhibit fresh blood in the trachea postexercise. Support for this is often provided by citing data from a preliminary report (1) where three Thoroughbred horses (undescribed EIPH status) exercised at 10 m/s [a much lower workload than in the present and previous (3-6) studies] had mean pulmonary arterial and mean left atrial pressures of 115 and 70 mmHg, respectively. It is worth noting that neither of these reports (1, 10) compared the pulmonary vascular pressures of EIPH-positive and EIPH-negative horses. Because our experiments sought to clarify this issue, we studied horses that were consistently negative (n = 8) or positive (n = 7) for EIPH during postexercise airway endoscopic examinations (a minimum of 12 consecutive times at weekly intervals) over 12-16 wk of performing high-intensity treadmill exercise (cf. EIPH-positive and EIPH-negative groups in MATERIALS AND METHODS). Also, the same hemodynamic procedures were employed to obtain data from both groups of horses. Our data (Figs. 3, 4, 5, 6), thus obtained, do not support the view that pulmonary vascular pressures of endoscopically EIPH-positive horses that are otherwise healthy exceed those in the endoscopically EIPH-negative horses either at rest or during high-intensity exercise performed at the same workloads. We remain cognizant, however, that none of our horses exhibited epistaxis, and, therefore, our data may not relate to the latter situation.
While stress failure of pulmonary capillaries (10) may occur at high transmural (intravascular minus perivascular/alveolar) pulmonary capillary pressures, the question arises as to why some horses consistently exhibit fresh blood in the trachea postexercise, whereas others may not, despite similarity of intravascular pulmonary capillary pressures during strenuous exertion (Fig. 6). Several possibilities may be considered. First, it needs to be emphasized that in the context of stress failure of pulmonary capillaries, the key variable (6, 10) is the transmural (intravascular minus perivascular) pulmonary capillary pressure. Given the similarity of pulmonary capillary blood pressure values during exertion in the endoscopically EIPH-positive and EIPH-negative horses (Fig. 6), it may be suggested that there may be differences in the perivascular alveolar pressure of EIPH-positive and EIPH-negative horses during exertion. To our knowledge, measurements of alveolar pressure in galloping EIPH-positive and EIPH-negative Thoroughbreds have not been made to date. Second, it is possible that there may be differences between EIPH-positive and EIPH-negative horses in terms of the strength of the blood-gas barrier. The strength of the blood-gas barrier is primarily in its connective and elastic tissue components (10). Studies comparing this aspect of the blood-gas barrier in EIPH-negative vs. EIPH-positive horses have also not been reported, to our knowledge. Third, the endoscopic diagnosis of EIPH in this study was based on the postexercise macroscopic detection of fresh blood in the trachea. Although it has been demonstrated that all Thoroughbreds in training had hemosiderin-laden macrophages in the tracheobronchial washings several days postexercise (11), the fact remains that, at present, postexercise endoscopic examination of the airway is accepted as the most practical method of detecting EIPH in competitive horse racing (2, 9) and that only those racehorses that exhibit fresh blood in the trachea become eligible for prerace furosemide administration for prevention/management of EIPH. Chronologically, because racehorses are exercised frequently, tracheobronchial washings cannot determine with certainty which particular episode of high-intensity exercise caused EIPH. Finally, it remains to be definitively determined whether EIPH originates from the pulmonary circulation; the bronchial circulation may be the culprit instead (7, 9).
It is difficult to explain why our values of various pulmonary vascular pressures from both groups of horses (Figs. 2, 3, 4, 5, 6), which exercised at a much higher workload (14.5 m/s on a 5% uphill grade), were less than the values reported from a filly exercised at 13.5 m/s in the study by West et al. (10) and in the three horses exercised at 10 m/s in a preliminary report (1). One likely possibility is that the differences in these studies may be related to the different reference sites for pressure signals. In the present and previous (3-6) studies, pressure signals were referenced at the level of the point of the shoulder. Whereas Jones et al. (1) did not note the referencing of their pressure signals, West et al. (10) referenced the mean pulmonary arterial pressure at the level of the right atrium (it was, however, not described how the latter was established). In large animals, the hydrostatic pressure effect (due to gravitational force acting on a column of fluid) can be substantial and may account for these disparities.
In conclusion, our data have demonstrated that right heart and/or pulmonary vascular pressures of horses that exhibit fresh blood in the trachea on postexercise endoscopic examination are similar to those of endoscopically EIPH-negative horses both at rest and during high-intensity short-term exercise.
The authors gratefully acknowledge the excellent technical assistance of Beth Saupe, Donald Lantz, Eileen Sullivan, Richard Griffin, and Jay E. Kobel in carrying out these experiments.
Address for reprint requests: M. Manohar, Dept. of Veterinary Biosciences, College of Veterinary Medicine, Univ. of Illinois, 212 Large Animal Clinic, 1102 W. Hazelwood Dr., Urbana, IL 61801.
Received 21 February 1996; accepted in final form 23 May 1996.
| 1. | Jones, J. H., B. L. Smith, E. K. Birks, J. R. Pascoe, and T. R. Hughes. Left atrial and pulmonary arterial pressures in exercising horses (Abstract). FASEB J. 6: A2020, 1992. |
| 2. | LaPointe, J. M., A. Vrins, and E. McCarvill. A survey of exercise-induced pulmonary haemorrhage in Quebec Standardbred racehorses. Equine Vet. J. 26: 482-485, 1994. |
| 3. | Manohar, M. Pulmonary artery wedge pressure increases with high-intensity exercise in horses. Am. J. Vet. Res. 54: 142-146, 1993. |
| 4. | Manohar, M. Pulmonary vascular pressures of strenuously exercising Thoroughbreds after administration of flunixin meglumine and furosemide. Am. J. Vet. Res. 55: 1308-1312, 1994. |
| 5. | Manohar, M. Unsteadiness of pulmonary vascular pressures in rapid acceleration supramaximal exercise. Equine Vet. J. Suppl. 18: 90-94, 1995. |
| 6. | Manohar, M., E. Hutchens, and E. Coney. Pulmonary haemodynamics in the exercising horse and their relationship to exercise-induced pulmonary haemorrhage. Br. Vet. J. 149: 419-428, 1993. |
| 7. | O'Callaghan, M. W., J. R. Pascoe, W. S. Tyler, and D. K. Mason. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post-mortem, and imaging study. VIII. Conclusions and implications. Equine Vet. J. 19: 428-434, 1987. |
| 8. | Steel, R. G. D., and J. H. Torrie. Principles and Procedures in Statistics. New York: McGraw-Hill, 1960. |
| 9. | Sweeney, C. R. Exercise-induced, pulmonary hemorrhage. Vet. Clin. North Am. Equine Pract. 7: 93-104, 1991. |
| 10. | West, J. B., O. Mathieu-Costello, J. H. Jones, E. K. Birks, R. B. Logemann, J. R. Pascoe, and W. S. Tyler. Stress failure of pulmonary capillaries in racehorses with exercise-induced pulmonary hemorrhage. J. Appl. Physiol. 75: 1097-1109, 1993. |
| 11. | Whitwell, J. E., and T. R. C. Greet. Collection and evaluation of tracheobronchial washes in the horse. Equine Vet. J. 16: 499-508, 1984. |
This article has been cited by other articles:
![]() |
M. Manohar and T. E. Goetz Intrapulmonary arteriovenous shunts of >15 {micro}m in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses J Appl Physiol, July 1, 2005; 99(1): 224 - 229. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds J Appl Physiol, April 1, 2004; 96(4): 1349 - 1356. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise J Appl Physiol, June 1, 2003; 94(6): 2135 - 2144. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, A. S. Hassan, T. Depuy, and S. Humphrey Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds J Appl Physiol, July 1, 2002; 93(1): 99 - 106. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses J Appl Physiol, September 1, 2001; 91(3): 1105 - 1112. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, and A. S. Hassan Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses J Appl Physiol, June 1, 2001; 90(6): 2371 - 2377. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. E. Goetz, M. Manohar, A. S. Hassan, and G. J. Baker Nasal strips do not affect pulmonary gas exchange, anaerobic metabolism, or EIPH in exercising Thoroughbreds J Appl Physiol, June 1, 2001; 90(6): 2378 - 2385. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar and T. E. Goetz L-NAME does not affect exercise-induced pulmonary hypertension in Thoroughbred horses J Appl Physiol, June 1, 1998; 84(6): 1902 - 1908. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Manohar, T. E. Goetz, S. Humphrey, and T. Depuy H1-receptor antagonist, tripelennamine, does not affect arterial hypoxemia in exercising Thoroughbreds J Appl Physiol, April 1, 2002; 92(4): 1515 - 1523. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |