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Although controversial, due to its reported effectiveness in attenuating bleeding associated with exercise-induced pulmonary hemorrhage (EIPH), furosemide is currently a permitted race day medication in most North American racing jurisdictions. The objective of this study was to assess the efficacy of furosemide in reducing the presence and severity of EIPH when administered 24 hr prior to strenuous treadmill exercise. Eight exercised Thoroughbred horses received saline or 250 mg of furosemide either 4 or 24 hr prior to high-speed treadmill exercise in a balanced 3-way cross-over design. Blood samples were collected for determination of furosemide, lactate, hemoglobin, blood gas, and electrolyte concentrations. Heart rate and pulmonary arterial pressure were measured throughout the run and endoscopic examination and bronchoalveolar lavage (BAL) performed. Horses were assigned an EIPH score and the number of red blood cells in BAL fluid determined. Although not significantly different, endoscopic EIPH scores were lower in the 4-hr versus the 24-hr and saline groups. RBC counts were not significantly different between the treatment groups. Pulmonary arterial pressures were significantly increased at higher speeds; however, there were no significant differences between dose groups when controlling for speed. A small sample size and unknown bleeding history warrant a larger-scale study.

Background Exercise‐induced pulmonary hemorrhage (EIPH) is diagnosed and its severity assessed by post‐exercise tracheobronchoscopy, and enumeration of bronchoalveolar lavage fluid red blood cells (BALFRBC). Minimal information is available regarding the relationship of tracheobronchoscopy score to BALFRBC number. Objective Evaluate the relationship between BALFRBC number and tracheobronchoscopy scores and determine their diagnostic sensitivities. Animals Nine sedentary horses, 21 fit Thoroughbreds, 129 Barrel Racers. Methods Normal BALFRBC number and the effect of bronchoalveolar lavage (BAL) on it were evaluated by performing 2 BALs 24 hours apart in sedentary horses. Tracheobronchoscopy followed by BAL was performed 247 times on 150 horses after treadmill, racetrack, or barrel racing exercise. Lastly, a BALFRBC diagnostic threshold number that optimized the geometric mean of the sensitivity and precision (F1‐score) was determined using Bayesian analysis. Results No increase in BALFRBC occurred after the second BAL (mean ± SD, 304 ± 173/μL). Tracheobronchoscopy scores ranged from 0 (n = 112) to 4 (n = 4) and BALFRBC ranged from 102 to 4605268/μL. Spearman correlation between tracheobronchoscopy score and BALFRBC was weak (P

Background Public pressure exists in the United States to eliminate race-day furosemide administration despite its efficacy in decreasing the severity of equine exercise pulmonary hemorrhage (EIPH). No effective alternative prophylaxis strategies have been identified. Objective To investigate alternative protocols to race-day furosemide that might mitigate EIPH. Animals Seven fit Thoroughbreds with recent EIPH. Methods Double-blinded placebo-controlled Latin square crossover using a treadmill followed by a blinded placebo-controlled crossover study at a racetrack. First, horses exercised supramaximally to fatigue 24 hours after initiating 5 EIPH prophylaxis protocols: 0.5 and 1.0 mg/kg furosemide IV 24 hours pre-exercise with and without controlled access to water, and 24 hour controlled access to water. Effects were compared to those measured after giving a placebo 24 hours pre-exercise, and 0.5 mg/kg furosemide IV 4 hours pre-exercise. Bronchoalveolar lavage (BAL) erythrocyte count was determined 45-60 minutes postexercise after endoscopy to assign an EIPH score. Data were analyzed using linear mixed effects models. The most promising protocol from the treadmill study was further evaluated in 6 horses using endoscopy and BAL after 1100 m simulated races. Results Intravenous furosemide (0.5 mg/kg) administered 24 hours pre-exercise combined with controlled access to water decreased the severity of EIPH on the treadmill and at the racetrack. Conclusion and clinical importance Administering 0.5 mg/kg furosemide 24 hours pre-racing combined with controlling water intake may be a strategy to replace race-day furosemide administration for the management of EIPH. A larger study is indicated to further evaluate whether this protocol significantly mitigates EIPH severity.

Background Exercise‐induced pulmonary hemorrhage (EIPH) refers to bleeding from the lungs in association with strenuous exercise. It has been documented in race horses but little information exists on EIPH in barrel racing horses. Hypothesis/Objectives Our goals were to evaluate the presence of EIPH in barrel racing horses and estimate its prevalence in the Pacific Northwest. Animals 149 barrel racing horses enrolled at events in WA (11), ID (3), and MT (33). Methods Observational cross‐sectional study. Data collected included signalment, history of illness, respiratory disease, race division, and pre‐race medications. Endoscopy was performed and tracheobronchoscopic (TBE) EIPH score was assigned based on quantity of blood in the trachea (0 = no blood to 4 = abundance of blood within the trachea). After TBE, bronchoalveolar lavage (BAL) was performed. Erythrocyte (red blood cell, RBC) counts were obtained from bronchoalveolar lavage fluid (BALF). Statistical analysis included linear and logistic regression, Fisher's exact t test, and calculation of correlation coefficient. Significance was set at P 1,000 cells, EIPH prevalence was 66%. Race time did not significantly affect the presence of EIPH. A significant (P

Background Poor performance is often suspected to be associated with EIPH in barrel racing horses; however, there are no published reports of EIPH for this discipline. The prevalence of EIPH in barrel racing horses is also unknown. Objectives This study was performed to determine the prevalence of EIPH and signs of airway inflammation in barrel racing horses under normal racing conditions in Alberta. Animals About 170 barrel racing horses. Methods Observational cross‐sectional study. Tracheobronchoscopic examinations were performed at least 30 minutes postrace. Video recordings were scored off‐site independently by two observers for EIPH and tracheal mucus accumulation (TMA). Horses with an EIPH score ≥2 were not assessed for TMA. Interobserver agreement was calculated by weighted κ statistics. Run times, environmental variables, and clinical information were also recorded for analysis. Results 77/170 (45.3%) of horses examined showed evidence of EIPH (grade ≥ 1). Interobserver agreement was 0.94. 140/141 (99.3%) of horses assessed for TMA showed evidence of tracheal mucus accumulation (grade ≥ 1) with 104/141 (73.8%) having a TMA score ≥ 2. Interobserver agreement was 0.73. A weak positive association was found between EIPH scores and average run speed, the presence of cough at rest reported by the riders, increased recovery time, exercise intolerance, and outdoor pattern. Conclusions and clinical importance The high prevalence of EIPH observed in the sampled population indicates that barrel racing induces substantial stress on the lungs. The presence of EIPH did not impact negatively on performance. Factors such as environmental dust and frequent traveling might have contributed to the high prevalence of TMA observed.

Background Exercise-induced pulmonary hemorrhage (EIPH) is a common disorder of equine athletes. The role of polymorphisms in genes encoding hemostasis-regulatory proteins in horses with abnormal hemorrhage is unknown. Objectives The goal of this study was to evaluate the genes encoding 2 ectonucleotidases, CD39/NTPDase-1 and CD39L1/NTPDase-2, and one ecto-5′ nucleotidase, CD73, in horses with abnormal hemorrhage or pathologic changes consistent with EIPH. Methods Twenty-three horses with histories of abnormal hemorrhage, 8 horses with gastrointestinal signs, and 45 healthy horses were evaluated using polymerase chain reaction-based techniques. Formalin-fixed tissues from 21 horses with pathologic changes consistent with EIPH were also evaluated. Results Three single nucleotide polymorphisms (SNPs) were identified in the gene encoding CD39 and one SNP was identified in the gene encoding CD39L1. No SNPs were identified in the gene encoding CD73. CD39 SNPs were identified in 19 of 20 (95%) horses with unexplained hemorrhage and 20 of 21 (95%) horses with pathologic features consistent with EIPH. CD39L1 SNPs were identified in 6 of 20 (30%) horses with unexplained hemorrhage and 8 of 21 (38%) horses with pathologic features consistent with EIPH. CD39 and CD39L1 SNPs were identified in 5 of 8 (62.5%) and one of 8 (12.5%) horses, respectively, presenting with colic or weight loss. CD39 and CD39L1 SNPs were identified in 28 of 45 (62%) and 13 of 45 (28.8%) healthy horses, respectively. Conclusions CD39 and CD39L1 are critically important in maintaining normal hemostasis and limiting inflammation. Further studies are needed to evaluate their role in the pathogenesis of equine EIPH.

In an epidemiological study of risk factors for exercise-induced pulmonary haemorrhage (EIPH) in young Thoroughbreds in the UK, in which 148 horses contributed 1614 horse-months of data, there were 64 (4%) episodes of endoscopically visible tracheal bleeding and 824 (51%) episodes of increased quantities of haemosiderophages in tracheal washes. There were increases in prevalence and risk of EIPH by both definitions with age fromor = 2-or = 4 years, season of sampling from winter (Nov-Jan) to autumn (Aug-Oct) and several different measures of airway inflammation, including tracheal mucus, neutrophil proportion, inflammation score and fungal material in tracheal washes. There was considerable variability in the prevalence of EIPH between trainers. EIPH in the preceding month significantly increased the risk of the condition the following month. There was no evidence that EIPH was associated with infection of the airways with even large numbers of Streptococcus zooepidemicus or Pasteurella-like spp., which are significantly associated with airway inflammation in younger racehorses. Multiple logistic regression modelling that took account of random variability between horses and the effects of each trainer and an episode the preceding month, confirmed that after controlling for the other risk factors, EIPH was still significantly associated with increasing age, different seasons, airway inflammation and evidence of airway fungal material.

Summary 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 fluld 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

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.

Sixty Standardbred horses, aged 3 to 10 years, were examined endoscopically for exercise-induced pulmonary haemorrhage (EIPH) 1 h after racing, on at least 3 occasions. Racing time, finishing position and post exercise venous lactate concentrations were also recorded. Horses positive for tracheal blood on endoscopy were classified as having either grade 1 EIPH (one or a few spots of blood in the trachea), or grade 2 (stream of blood). Air temperature, relative humidity and air pollutant levels were recorded on each examination day. Of the 60 horses, 52 (87%) were EIPH-positive on at least one evaluation out of 3 and 40 of the 52 (77%) showed grade 2 EIPH on at least one occasion. Of the 52 EIPH-positive horses, 52% bled 3 times out of 3, 21% 2 out of 3 and 27% once. When only the first examination was considered, 37 of the 60 horses (62%) were EIPH-positive. There was no significant relation detected between either presence or frequency of EIPH and age, sex, or gait. Horses that showed grade 2 EIPH bled significantly (P = < 0.001) more frequently (mean: 83% of examinations) than horses having shown no more than grade 1 EIPH (47% of examinations). No significant differences could be detected between EIPH-positive and EIPH-negative races in the average racing times, finishing positions and blood lactate concentrations of the 29 horses which showed intermittent EIPH. The proportion of horses showing EIPH on each day where at least 5 horses were examined was correlated with air temperature, relative humidity, and the levels of several air pollutants on those days.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise induced pulmonary haemorrhage (EIPH) is a serious problem in the Thoroughbred industry. The condition apparently occurs essentially in all Thoroughbreds in training but the mechanism has proved elusive. There is now strong evidence that the condition is caused by mechanical failure of the walls of the pulmonary capillaries when the pressure inside them rises to very high levels. It is well known that pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently we have shown that the wall stresses are very large when the capillary transmural pressure is raised, and in anesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mmHg and above. The incidence of stress failure is greatly increased at high lung volumes; and many of the ultrastructural changes are rapidly reversible when the capillary pressure is reduced. The principal forces acting on the capillary have been analysed. The strength of the thin part of the capillary wall can be attributed to the Type IV collagen in the extracellular matrix. The pulmonary vascular pressures of galloping Thoroughbreds reach very high levels. Mean pulmonary artery and left atrial pressures of up to 120 and 70 mmHg respectively have been directly measured with indwelling catheters. The reason for the high pulmonary vascular pressures is that these animals have been selectively bred over hundreds of years to run at great speeds over short distances and their maximal oxygen consumptions are very high. As a consequence, cardiac outputs are substantial, and the left ventricle needs very high filling pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Significant differences were detected by bronchoalveolar lavage (BAL) between horses racing successfully and those showing exercise intolerance. Neutrophil percentage, haemosiderophage percentage and total bacterial numbers were significantly elevated in horses with exercise intolerance. BAL provided a more accurate indication of the incidence and extent of exercise induced pulmonary haemorrhage (EIPH) than visual inspection.

Summary Platelet function was evaluated in horses with exercise-induced pulmonary hemorrhage (bleeder) and in control horses (nonbleeder). Platelet aggregation, secretion, and adhesion to rabbit aortic suben-dothelium were similar for bleeders and nonbleeders. Platelets readily aggregated in response to ADP, thrombin, collagen, and arachidonic acid, but platelet secretion occurred only with high concentrations of thrombin. Platelets readily adhered to rabbit aortic subendothelium and tended to form large thrombi rather than platelet monolayers or aggregates. These data suggest that horses may be predisposed to thrombus formation and subsequent microvascular obstruction.

Summary This paper reviews a series of clinical, post mortem and imaging studies on exercise-induced pulmonary haemorrhage (EIPH) performed on 26 Thoroughbred racehorses. Post mortem techniques included routine gross, subgross and histological examination; coloured latex perfusions of pulmonary and bronchial circulations; and microradiography and computerised tomography scans of lungs with contrast injected vasculature. The major lesions were multiple, separate and coalescing foci of moderately proliferative small airway disease accompanied by intense neovascularisation of the bronchial circulation. As a result of bronchial artery angiogenesis, the systemic circulation dominated the vascular supply of the air exchange structures in affected areas, producing an apparent left to right shunt. Extensive areas of sequestered haemosiderophages indicated previous haemorrhage from vessels apparently supplied by the bronchial arteries. Diffuse and focal parenchymal destruction and connective tissue reactions in affected areas were considered to be secondary to localised haemorrhage and macrophage-induced damage. The aetiology of EIPH was not determined, but the multifocal, small airway-centred lesions indicated that low grade bronchiolitis, possibly of viral origin, was a factor. Gravitational effects also appear to contribute to dorsal distribution of the lesions. The mild focal and subclinical lesions confined to secondary lobules are thought to evolve into the serious lung pathology observed in EIPH cases through the effects of localised hypoxia induced by maximal exercise and partial airway obstruction. Once initiated, a vicious cycle of increasing inflammatory damage and further local bleeding is set in motion.

Summary A group of racehorses in training was examined on several occasions with a fibreoptic endoscope and monitored for viral infection. Only equine herpes virus-2 (EHV-2) infection was detected. Pharyngeal lymphoid hyperplasia (PLH) was present in all horses and decreased in severity with age. There was no association between PLH severity and antibody titres to EHV-1, or with the isolation of EHV-2. Finishing position in races was not affected by PLH severity. Exercise induced pulmonary haemorrhage (EIPH) was evident on 23 out of 49 (47 per cent) examinations after maximal speed training exercise. Eighteen out of 19 (95 per cent) horses examined on at least two occasions had EIPH but its occurrence was not predictable. Observable mucoid or mucopurulent exudate was present in the trachea in 60 out of 118 (50 per cent) examinations and the amount seen was increased following exercise.

Abnormal pulmonary radiopacities were identified in 13 racing horses in which a diagnosis of exercise-induced pulmonary hemorrhage (EIPH) had been confirmed. The lesions were in the caudal lung lobe in all horses; seven were on the right and three on the left, and the laterality for three could not be determined. In ten horses the opacities, which were large and peripherally located, obliterated the thoracophrenic angle. They merged with the silhouette of the diaphragm and had a circular or ovoid surface directed toward the hilum. The intensity of opacification of the consolidated areas varied, and they often were not sharply marginated. Dorsal displacement of the pulmonary arteries was noted in the region of the radiopacity in seven horses. Varying volumes of pleural effusion were observed in nine horses. Serial radiographic examinations were performed in seven horses. The pulmonary radiopacities cleared within ten days in two horses. In the remaining five horses, gradual resolution, characterized by a reduction in lesion size with improved margination, occurred during several months. The central region of the radiopaque lesion commonly had a patchy appearance, suggesting cavitation. Normal pulmonary vascular and interstitial markings were evident following complete resolution of these lesions. The cause of these abnormal pulmonary opacities has not been determined. Pathologic-radiologic correlations will be required to improve understanding of the pathophysiology of EIPH in the racing horse.