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Exercise-Induced Pulmonary Hemorrhage: Current Concepts
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Introduction
Exercise-induced pulmonary hemorrhage (EIPH) is a major health concern and cause of poor performance in the equine athlete [1]. Significant progress has been made in recent years in our understanding of the pathogenesis of EIPH. Exercise-induced pulmonary hemorrhage occurs primarily in Quarter Horses, Standardbreds, and Thoroughbreds worldwide during sprint racing; however, it is observed in many other high performance non-racing equine athletes, such as barrel, cutting, reining, roping, polo, cross-country event, 3 day event, show jumping, hunter-jumper, steeplechase, and even draft horses.
The problem was first documented at least 4 centuries ago (Fig. 1a and Fig. 1b) [2,3]. EIPH is of great concern to the racing industry because of the financial implications resulting from decreased performance, lost training days, necessity for pre-race medication, and banning of horses from racing [3]. It is an important cause of exercise intolerance and results from strenuous exercise and/or pathophysiological changes in the equine lung and possibly airways [4-7].
Figure 1a.The famous racehorse Eclipse (1764 - 1789).
Figure 1b. Eclipse's pedigree [2]. Eclipse descended from Bartlett’s Childers (his great-grandsire, renamed from Bleeding Childers) and never lost a race. In fact, his reputation was such that on October 18th, 1770 in the King’s Plate at Newmarket no owner dared enter their horse against him and he walked the course. Eclipse subsequently sired 334 winners.
EIPH is characterized by pulmonary hypertension, edema in the gas exchange region of the lung, rupture of the pulmonary capillaries, intra-alveolar hemorrhage (Fig. 2) [5,8] and the presence of blood in the airways.
Figure 2. Stress failure of the pulmonary capillaries. Left: Red blood cell emerging from a rupture of the blood-gas barrier into the alveolar space of a rabbit lung [8]. Right: Exercise-induced pulmonary hemorrhage in the alveolar space of a pony lung [5]. R, red blood cell; P, proteinaceous material. Bar, 5 microns.
Diagnosis
Epistaxis - Exercise-induced pulmonary hemorrhage was diagnosed originally by visible epistaxis (Fig. 3). At that time, it was believed to be a serious problem but not widespread because epistaxis occurred only in 0.25 to 13% of all sprinting horses [9-12]. Indeed, a very recent study of a quarter of a million race starts reported the incidence of epistaxis to be 0.15% [13]. Takahashi and colleagues [13] found epistaxis to be more common:
- Following steeplechase rather than flat races,
- in older rather than young (2 year olds) horses, and
- in females rather than sexually active males. In addition epistaxis was more common in shorter races of a higher intensity.
Figure 3. Epistaxis in a racehorse (From: Fedde MR).
Endoscopy - As knowledge concerning the pathology and etiology of EIPH advanced, so did the sensitivity of diagnosis. In 1974, Cook [9] used a rigid endoscope to identify the lungs as the source of hemorrhage. When endoscopy is used as a diagnostic tool, the detection of EIPH after racing increased to 26 - 77% in Standardbreds [14,15], to 62% in Quarter Horses [16], and to 44 - 75% in Thoroughbreds [11,17-20]. The incidence was even higher (82 - 95%) with repeated endoscopic examination of each individual horse [15,18,19].
Tracheal Lavage - Tracheal lavage has also been used to detect EIPH by determining the presence of hemosiderophages in the aspirated fluid. However, with this technique, estimating the time course of the hemorrhage is difficult and a poor correlation is evident between the tracheal wash cytology and histopathology of the lungs [21-23]. Furthermore, the cell population in the tracheal fluid differs substantially from fluid obtained from the lower respiratory tract [22,23].
Bronchoalveolar Lavage - To detect the presence of blood in alveoli and small airways, bronchoalveolar lavage (BAL) may be the technique of choice [24,25]. BAL can be performed with either an endoscope or with a BAL tube. This technique provides an accurate reflection of the cytological population in the terminal airways and alveolar spaces. A good correlation has been found between BAL cytology and histopathology in horses with EIPH [24,26,27]. The BAL method provides a more sensitive and accurate assessment of the presence and extent of EIPH than endoscopy or tracheal lavage [26,28] and has the possible advantage of identifying more horses that bleed with greater sensitivity [29,30]. BAL studies suggest that hemorrhage occurs in essentially all horses in racing or training [30,31]. BAL studies correlate well with pulmonary histopathology, clinical disease and endoscopic evidence of EIPH [30].
Nuclear Scintigraphy - Scintigraphy has generally been disappointing as far as demonstrating areas of tissue damaged as a result of previous EIPH or for demonstration of the region of current hemorrhage following exercise [32]. Ventilation/perfusion scans show variable reduction of ventilation and a loss of perfusion in the dorsocaudal fields with a collateral blood supply from the bronchial circulation [33]. The feasibility of scintigraphy to detect and quantify EIPH has been recently investigated by Votion et al., [34]. They concluded that small amounts of hemorrhage may potentially be detected with scintigraphy (see Scintigraphy by D.M. Votion). The limiting factor for detecting small amounts of bleeding may be the level of lung background radioactivity.
Radiography - Radiography is of limited use in the evaluation of EIPH and interpretation is difficult. In horses with EIPH, there is a vaguely discernible increase in interstitial density in the dorsocaudal lobe of the lung [35-37]. Radiography is only likely to provide evidence of the progression of EIPH in an individual horse in the case of severe, repeated episodes of hemorrhage and is of limited use in the horse that has an "average" degree of hemorrhage for its age [32].
Echocardiography - Echocardiography has been investigated as a means of diagnosis of EIPH. Horses with a history of EIPH have been reported to have a higher incidence of spontaneous contrast at rest [38-40].
Causes and Mechanisms
Numerous causes and pathophysiologic mechanisms have been proposed for EIPH, including small airway disease, upper airway obstruction [10], exercise-induced hyperviscosity [41-43], mechanical stresses of respiration and locomotion [44-45], redistribution of blood flow in the lung [46], alveolar pressure fluctuations, and pulmonary hypertension. Several factors may actually cause the pulmonary system to become heavily stressed to the point where capillaries fail.
Infusion of 10 and 15 micron microspheres of different colors into the jugular vein and left atrium revealed that only those injected into the jugular vein appeared in the airways [47]. This observation identifies the pulmonary rather than the bronchial circulation as the source of EIPH. Current evidence suggests that stress failure of the pulmonary capillaries results from pulmonary vascular hypertension (which can exceed 120 mmHg mean arterial pressure [47] combined with very negative intrapleural and alveolar pressures that summate at the blood-gas barrier to create a high capillary transmural pressure leading to hemorrhage (Fig. 4) [48-51]. Within a given horse, the severity of EIPH increases as a function of mean pulmonary arterial pressure [52] and may be exacerbated by inclined as opposed to flat running [13,53]. The cause of hypertension may also be related to the enormous cardiac outputs in excess of 300 liters per minute [54] that are demanded by the racehorse and which may be associated with maximal recruitment and distension of the pulmonary capillaries [53,54].
Figure 4. Schematic showing the structure of the blood-gas barrier. The transmural pressure, thought crucial for causing rupture of the pulmonary capillary and extravasation of blood into the alveolar space, is the summation of capillary luminal and alveolar pressures.
Other factors which may limit ventricular function and contribute to elevated left atrial pressure and pulmonary vascular pressures are:
- The cross-sectional area of the atrioventricular valves may be too small to allow high flow without a large increase in driving pressure,
- the high ventricular pressure associated with exercise may result in regurgitation through the AV valves during ventricular systole; and
- the rate of relaxation of the left ventricle may be too slow to allow rapid filling at normal filling pressure when cardiac output and heart rate are high [56].
EIPH may result in decreased performance associated with edema in the gas exchange region of the lung (interstitial edema) and blood in the airways (alveolar edema and hemorrhage). This culminates in irritation and inflammation of the airways, exacerbation of small airway disease, and perpetuation of the cycle. With repeated strenuous exercise, either in training or actual competition, the hemorrhage results in fibrosis/scarring, a weakened blood gas barrier and sustained inflammation. The blood within the alveoli may adversely affect lung health and exercise capacity by interfering with gas exchange. EIPH often worsens with repeated exercise and increased age.
Prevention and Treatment of EIPH
The development of an ideal treatment for EIPH has been difficult due to controversy regarding the mechanisms causing EIPH and failure of early investigations to quantify EIPH, prior to the use of BAL. There is a demand for effective prophylaxis and/or treatment to control the bleeding. Many pharmacotherapeutic and management interventions have been tried, but few have proven efficacy in treating EIPH [57-59]. The different interventions and treatments include dehydration, furosemide and other diuretics, anti-hypertensive agents or pulmonary vasodilators to dilate the pulmonary vasculature, bronchodilators, pentoxifylline and other drugs to decrease blood viscosity, surgical correction of laryngeal hemiplegia to decrease upper airway resistance, nasal dilator strips to reduce the resistance and maintain full patency of the nasal passages, anti-inflammatory drugs to reduce lower airway inflammation, drugs to inhibit platelet aggregation, hesperidin-citrus bioflavonoids to alter capillary fragility, aminocaproic acid and tranexamic acid to inhibit fibrinolysis, herbal remedies, and estrogens. This paper will focus on interventions and treatments for which new information has recently been made available.
Furosemide - Horses with EIPH frequently are treated with furosemide [60-65] which attenuates the exercise-induced increases in right atrial, pulmonary arterial, pulmonary wedge, and pulmonary capillary pressures [66-71] as well as the concentration of red cells in the BAL fluid [71,72]. Kindig and colleagues [72] recently demonstrated that furosemide (1 mg/kg, IV, 4 hours prior) administered according to track regulations, reduces EIPH by 90% in Thoroughbred horses run to ~95% of their maximum aerobic capacity (Fig. 5). This decrease was associated with a significant reduction in mean pulmonary arterial pressure. The reduction in pulmonary vascular pressures is compatible with a reduction in the stress failure of the pulmonary capillaries, reduced transcapillary filtration, reduced accumulation of lung water during exercise, and reduced EIPH. Geor et al., [73] recently observed an 80% reduction in EIPH in Thoroughbred horses running at 120% of maximum oxygen consumption for 2 min on an inclined treadmill 4 hours after furosemide administration (0.5 mg/kg, IV).
Figure 5. Furosemide significantly reduced the severity of EIPH (bronchoalveolar lavage) and pulmonary artery pressure in 5 Thoroughbred horses run to near maximal speeds (14 m/s) on the treadmill [72].
The hemodynamic effect of furosemide is mediated, in large part, by a reduction in plasma and blood volume [74,75]. The mechanisms responsible for the effects of furosemide and reduced vascular pressures during exercise may also be associated with a redistribution of pulmonary blood flow. In vitro studies have shown that equine pulmonary arteries in the dorsal portion of the lung dilate more in response to methacholine than do vessels located in the ventral portion of the lung [76]. The effect of furosemide on the spatial distribution of pulmonary blood flow has been determined with fluorescent-labeled microspheres in resting and exercising Thoroughbred horses [77]. The primary finding of this study was that pulmonary blood flow redistribution occurred from rest to exercise, both with and without furosemide. However, there was less blood flow to the dorsal portion of the lung during exercise post-furosemide compared with pre-furosemide.
Furosemide is permitted in most of North and South America; it is also approved for use in the Philippines and Saudi Arabia [58]. Recent studies, however, suggest that furosemide is associated with enhanced athletic performance in Thoroughbred horses [78,79]. The association between enhanced athletic performance and furosemide treatment may be attributable to a reduction in body weight, but other mechanisms may play a role, such as the reduction in pulmonary vascular pressures and bronchodilation. Bayly et al., [80] suggested that a positive effect on race performance is at least partly attributable to an increase in mass-specific maximal oxygen consumption rather than improvements in breathing mechanics or gas exchange.
Nasal Dilators - During quiet breathing, as well as during exercise, 40 - 50% of the total pulmonary resistance may be located within the nasal passages [81]. During inspiration, the extrathoracic airways account for more than 90% of the total resistance.
An external nasal dilator strip has been increasingly adopted by human athletes to reduce nasal resistance and to promote easier nasal breathing during exercise [82,83]. Horses are obligate nasal breathers; thus nasal resistance is likely of much greater importance than in humans. During exercise, partial collapse of the unsupported nasal passages may occur during inspiration.
The FLAIRtm nasal strip was introduced recently for horses to prevent or reduce collapse of the nasal passages and to decrease upper airway resistance [84], particularly nasal resistance and to reduce intrapleural and alveolar pressure swings that may contribute to high pulmonary capillary transmural pressures and EIPH. Seven horses running at 12+1 m/s (~27 mph) were evaluated on the treadmill under control conditions and wearing an external nasal dilator in individual, random-ordered trials two weeks apart [85,86]. Compared with controls, the nasal dilator significantly reduced oxygen uptake (Fig. 6) and carbon dioxide production while running at high speed. BAL revealed a 33% reduction on average in EIPH when the external nasal dilator was worn (Fig. 7) [86]. Specifically, 5 out of 7 horses elicited a reduction in EIPH during the nasal strip trial and those horses that bled the most on the control run, decreased EIPH the most when wearing the nasal strip (Fig. 8). These data demonstrate that the nasal dilator can lower whole body oxygen consumption and reduce EIPH.
Figure 6. Nasal strip application reduced pulmonary oxygen uptake (VO2) in six horses running at an average of 12 m/s (final stage) [86].
Figure 7. Nasal strip application reduced the mean severity of exercise-induced pulmonary hemorrhage ~33% in 7 horses running at 12 m/s but did not affect pulmonary artery pressure [86].
Figure 8. Nasal strip application decreased the severity of exercise-induced pulmonary hemorrhage (EIPH) in 5 of 7 horses running at 12 m/s [86]. Notice that the greatest attenuation of EIPH was seen in those two horses with the most severe EIPH under control conditions.
These results have subsequently been reproduced by our laboratory [72,87] and also by Geor et al., [73], both studies demonstrating a 40 - 50% reduction in EIPH. One of these investigations [87] demonstrated an increased exercise tolerance in horses wearing the nasal strip and field studies have suggested that these laboratory findings translate into tangible benefits for the racehorse on the track. Specifically, 400 horses were evaluated at the Calder Race Course in Florida in the 1999 - 2000 Thoroughbred season (Scollay, M., and Hernandez, J. unpublished findings, 2000). Those horses wearing the nasal strip had a 3.4% higher win percentage than those not wearing a strip and application of the strip decreased significantly (15%, P<0.05) the between-race interval from 29 to 23 days. Moreover, Valdez and colleagues [88] who studied 30 Thoroughbred racehorses with a history of severe EIPH at the Golden Gate Fields Racetrack in California found that the nasal strip resulted in a 65% reduction in the number of red blood cells in bronchoalveolar lavage fluid measured 12 - 18 h following the race. In contrast to the above, there is one study reporting that wearing the nasal strip does not reduce bleeding in Thoroughbred horses [89]. Unfortunately, the authors of that study [89] chose to use endoscopy that only confirms the presence of blood in the large airways. From Fig. 7 and Fig. 8, it is apparent that whereas the nasal strip reduces EIPH it certainly does not abolish it. Thus, quantitative bronchoalveolar lavage rather than qualitative endoscopy is required to demonstrate the beneficial effect of the nasal strip on constraining the severity of EIPH. It is possible that the reduction in pulmonary oxygen uptake and EIPH demonstrated with the nasal strip are secondary to a decreased inspiratory resistance [84,90], lowered inspiratory muscle work, and less negative intrapulmonary pressure swings. The effects of the nasal strip on end-inspiratory and end-expiratory lung volumes during high intensity exercise remain to be determined.
The FLAIRtm nasal strip has been broadly approved for use in flat- and harness-racing within North America. The FLAIRtm strip has also been approved for use by all key non-racing regulatory bodies, including: Federation Equestrian International, American Horse Shows Association, National Reining Association, United States Equestrian Team, United States Polo Association, National Barrel Horse Association, and the American Quarter Horse Association. In the international market, the FLAIRtm strip has been approved for racing in the following countries: Mexico, Brazil, Trinidad, Barbados, Jamaica, The Netherlands, United Arab Emirates, Qatar, India, Australia (Harness), New Zealand, Korea, and Singapore.
Nitric Oxide - Nitric oxide (NO) is a vascular smooth muscle relaxing factor that is produced by the action of NO synthase on L-arginine predominantly within vascular endothelial cells. Inhaled nitric oxide reduces the pulmonary artery pressure in horses during strenuous exercise [91,92]. Nitroglycerin is denitrated in the body to nitric oxide, a potent vasodilator and smooth muscle relaxant. However, nitroglycerin, either intravenous or oral, does not appear to protect the pulmonary vascular bed from exercise-induced hypertension [93,94]. In our laboratory we have determined that, whilst NO inhalation does reduce pulmonary artery pressure, rather than reducing EIPH NO inhalation actually increases the severity of EIPH [[95]].
L-arginine analogs, such as L-NAME, competitively inhibit NO formation from L-arginine and have been used to determine the role of NO in blood flow regulation. Mills et al., [96] demonstrated that L-NAME increases pulmonary artery pressure during submaximal exercise. On the other hand, Manohar and Goetz [97] reported that L-NAME infusion did not significantly alter exercising pulmonary vascular pressures in Thoroughbred horses across a range of exercise intensities. To further investigate the role of NO in cardiopulmonary function during exercise, we studied 5 horses on a treadmill at speeds that were equivalent to 50%, 80%, and 100% of peak pulmonary oxygen uptake [54]. Each horse underwent one control and one L-NAME trial in randomized order. L-NAME reduced exercise tolerance (i.e., peak speed), as well as cardiac output, oxygen delivery, oxygen uptake and both pulmonary and systemic vascular conductances at peak running speeds (Fig. 9). Administration of L-NAME significantly increased EIPH in all 5 horses despite a reduced maximal pulmonary arterial pressure in 4 of the 5 horses (Fig. 10) [98] and decreased cardiac output in all 5 horses. These data demonstrate that the NO synthase inhibitor, L-NAME, impairs hemodynamics during exercise in the horse, suggesting an important role for NO in mediating endothelial function during exercise.
Figure 9. Nitric oxide (NO) synthase inhibition with L-NAME significantly reduced peak running speed (not shown) and also cardiac output, whole body oxygen delivery, systemic and pulmonary vascular conductances and pulmonary oxygen uptake (VO2 ) whilst increasing percentage oxygen extraction in 5 racehorses [54].
Figure 10. Nitric oxide (NO) synthase inhibition with L-NAME significantly increased the severity of exercise-induced pulmonary hemorrhage in 5 racehorses run to their peak speed. Pulmonary artery pressure was significantly reduced [99].
The hypothesis that NO breathing could modify pulmonary hemodynamics at maximal exercise was confirmed directly by running Thoroughbred horses to fatigue at 15 m/s (~33 m.p.h.) whilst breathing 80 ppm NO [95,100]. As demonstrated previously in the horse [91,92], NO reduced mean pulmonary arterial pressure (Fig. 11). However, the severity of EIPH was increased significantly. This finding suggests that NO-induced pulmonary vasodilation and consequent reduction of pulmonary arterial pressures is not beneficial to preserving the integrity of the blood-gas barrier.
Figure 11. Nitric oxide breathing (80 ppm) significantly increased the severity of exercise-induced pulmonary hemorrhage in 5 racehorses run to volitional fatigue at 15 m/s. Pulmonary artery pressure was significantly reduced [95,100].
Equine Concentrated Serum - EIPH may potentially be exacerbated by inflammatory airway disease [30,101-102] that causes long term parenchymal tissue damage and scarring. Seramune® is a concentrated equine serum (CES) collected from multiple draft horse donors, that contains high levels of equine IgG and other immunoglobulins. Initial field studies provided support for the efficacy and safety of this product, indicating a potentially therapeutic benefit to treat chronic bleeders. Subsequently, to provide rigorous scientific testing the product was given at a dosage of 20 cc intratracheal and 10 cc intravenously for 5 days in a row, with a booster dose weekly and 24 - 48 hours before a standardized bout of heavy treadmill exercise. The CES treatment resulted in a 53% reduction in red blood cells (EIPH) and a 32% decrease in white blood cells in bronchoalveolar lavage fluid [103].
Herbal Formulations - A number of herbal formulations are used to treat horses with EIPH; however, until recently no published scientific research had been conducted to determine the effectiveness of these herbal remedies. The stated goals of herbal formulations are to clear heat and edema from the lung, cool and nourish the blood, and to move stagnated blood out of the airways [104,105].
Omega-3 Fatty Acids - - Omega-3 fatty acids are found in high levels in many equine supplements and it has been hypothesized that they may reduce EIPH via their effects on the arachadonic acid cascade and consequent decrease of airway inflammation. As discussed above, in relation to CES, airway inflammation secondary to rupture of the blood gas barrier and blood in the airways has been considered to be an important component of EIPH. Diets rich in docasahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may also modulate the decrease in erythrocyte membrane fluidity that occurs during exercise [107]. In theory, enhanced preservation of erythrocyte membrane fluidity by DHA and EPA may improve pulmonary vascular hemodynamics and thereby ameliorate rupture of the blood-gas barrier and extravasation of erythrocytes. At Kansas State University 10 Thoroughbred horses fed a DHA and EPA enriched diet for 83 and 145 days did, in fact, evidence a reduced EIPH [59].
Conjugated Estrogens and Anti-fibrinolytics - Uncontrolled bleeding in patients suffering from systemic fibrinolysis is often treated using hemostatic agents. Whereas there is no scientific evidence that horses with EIPH have increased fibrinolysis or impaired coagulation [108,109] use of conjugated estrogens and antifibrinolytics to prevent EIPH in the racing industry is widespread. Following the work of Heidemann et al., [110], who demonstrated antifibrinolytic effects of aminocaproic acid at 30 and 100 mg/kg (IV) doses in resting horses, our laboratory evaluated the effect of combined conjugated estrogens and aminocaproic acid, in separatum, on EIPH (59). Preliminary results indicated that these treatments tended to reduce EIPH (decrease of ≈ 50% in 4 of 5 horses) after severe intensity treadmill exercise. Interestingly, there was a trend for exercise performance to decrease with aminocaproic acid and increase with conjugated estrogens.
Conclusions
Several lines of evidence support a primary role for high pulmonary arterial pressures in the etiology of EIPH. These include:
- Pulmonary arterial pressures in excess of 120 mmHg during intense exercise [47,48].
- Pulmonary capillary stress failure occurs above ~90 mmHg in both in vitro [50] and in vivo [52] studies of horses.
- Furosemide lowers pulmonary artery pressures and EIPH severity [71,72].
- Under racing conditions, the incidence of EIPH is greater in shorter, higher intensity events that are expected to generate higher pulmonary arterial pressures [13].
It has been recognized that both intravascular (positive) and extravascular (e.g., alveolar, negative) pressures summate to produce very high capillary transmural pressures. However, relatively little emphasis has been placed upon the role of extravascular pressures in determining the severity of EIPH [10,86]. It is clear from studies with the nasal strip, NO synthase inhibition (L-NAME) and NO breathing that the severity of EIPH as determined by bronchoalveolar lavage can be manipulated independently from pulmonary arterial pressure (See Fig. 7, Fig. 10 and Fig. 11). This hypothesis is also supported by the observation that maximal inclined running compared to that on the flat, elevates EIPH in the face of reduced pulmonary artery pressures [53] and horse races run on the flat have a lower incidence of epistaxis than incurred by steeplechase events [13]. This effect may be caused by elevated intrathoracic and alveolar pressure swings related to the greater tidal volumes achieved during inclined running [45].
In recent years, there has been increasing interest in exploring aerosol administration of medications to treat conditions such as recurrent airway obstruction ("heaves") [111,112]. Candidate medications include dexamethasone, ipratropium bromide and pirbuterol acetate for which parenteral, intratracheal or IV routes of delivery are far from ideal. At present, the authors are unaware of experimental or clinical evidence that any aerosolized product is effective in treating EIPH.
Figure 12 compiles data from 3 interventions that dissociate EIPH and mean pulmonary arterial pressure [53,86,98,99]. If EIPH were a unitary function of pulmonary arterial pressure, all data would be expected to fall in quadrants II and III and these two variables would correlate significantly. Clearly, this is not the case. One global interpretation of these data is that factors other than pulmonary arterial pressures per se play a major deterministic role in EIPH. Furthermore, under certain circumstances a high pulmonary arterial pressure might reflect an arteriolar vasoconstriction that effectively protects the fragile blood-gas barrier from the very high upstream pressures generated by the prodigious cardiac output necessary to power muscle oxidative function at high speeds.
Figure 12. Relationship between pulmonary artery pressure and changes in the severity of exercise-induced pulmonary haemorrhage (EIPH) altered in horses during high speed running under three conditions: nitric oxide (NO) synthase inhibition with L-NAME, nasal dilator and inclined running (10%) [99]. If EIPH severity was a unitary function of pulmonary arterial pressure, these two variables should be correlated significantly. They were not.
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Department of Veterinary Anatomy, Physiology and Kinesiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
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