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1.
Reasons for performing the study: Exercise‐induced pulmonary haemorrhage (EIPH) occurs in nearly all strenuously exercising horses. Recent studies have attempted to identify the role of free blood within the airspaces, in the lung fibrosis that develops within the lungs of EIPH horses. Hypothesis: Repeated exposure of the equine lung to autologous blood results in lung fibrosis similar to that observed in spontaneous EIPH. Methods: Forty ml of autologous blood from the jugular vein was instilled into preselected lung regions of 6 horses one, 2, 3, 4 or 5 times at 2 week intervals, with 40 ml of saline instilled into the contralateral lung serving as a control. The time interval between instillation of the first blood and euthanasia ranged from 2–10 weeks. The lung from each instillation site was harvested, and the histopathology was scored from each region based upon the presence and abundance of blood, haemosiderin and interstitial collagen. Consequently, at the time of euthanasia, the time since instillation of the first blood ranged from 2–10 weeks. Results: Beyond retention of blood, and the accumulation of haemosiderin, there was no visible increase in perivascular and interstitial collagen within the blood‐instilled lung sites. In a small number of regions, there were foci of bronchiolitis obliterans organising pneumonia with collagen accumulation within these foci, but no collagen accumulation with the characteristic perivascular and interstitial histological distribution seen in EIPH. Conclusions: Free blood within the airways of horses does not result in a qualitative increase in the amount of interstitial collagen within 8–10 weeks, and is therefore an unlikely aetiological factor in the lung collagen accumulation that occurs in EIPH. Potential relevance: This study emphasises the efficiency of the equine lung in clearing blood from the airspaces. Further, it suggests that the aetiopathogenesis of EIPH is not driven by events within the airspace lumen, but rather emanates from within the vasculature and lung interstitium.  相似文献   

2.
Exercise-induced pulmonary hemorrhage (EIPH) is common in horses following intense exertion, occurring in up to 75% of racing Thoroughbreds and Standardbreds. In spite of this, the pathogenesis of EIPH is poorly understood. In 7 racing Thoroughbred horses with EIPH, 6 sections were collected from the left and right lung, representing the cranial, middle, and caudal region of the dorsal and ventral lung (84 sites total). Grossly, both right and left lungs had numerous dark brown to blue-black foci along the caudodorsal visceral pleura. Tissue sections were stained with hematoxylin-eosin, Masson's trichrome, and Prussian blue. Verhoeff Van Gieson and immunohistochemistry for alpha-smooth muscle actin were used to assess the pulmonary vasculature. Histologic scores (HS = 0-3) were assigned to each region/slide for the presence and severity of 5 findings: interstitial fibrosis, hemosiderin accumulation, pleural/interlobular septal thickness, arterial and venous wall thickness, and evidence of angiogenesis (maximum cumulative HS = 15). Thirty-nine of the 84 (46%) sections were histologically normal (HS = 0); 33/84 (39%) were mildly to moderately affected, with small amounts of hemosiderin and fibrosis (HS = 1-9) while 12/84 (14%), primarily from the dorsocaudal lung, had severe vascular remodeling, fibrosis, and hemosiderin accumulation (HS = 10-15). In the latter, veno-occlusive remodeling of the intralobular veins colocalized with hemosiderosis, fibrosis, hypertrophy of vessels within the pleura, and interlobular septa and bronchial neovascularization. We propose that regional veno-occlusive remodeling, especially within the caudodorsal lung fields, contributes to the pathogenesis of EIPH, with the venous remodeling leading to regional vascular congestion and hemorrhage, hemosiderin accumulation, fibrosis, and bronchial angiogenesis.  相似文献   

3.
Detailed post mortem examination of the lungs of horses with exercise-induced pulmonary haemorrhage (EIPH) has demonstrated significant small airway disease and intense bronchial arterial proliferation in the dorsocaudal lungfields. The purpose of this study was to investigate ventilation and perfusion distribution in the lungs of a similar group of horses to compare changes in the live animal with the previously reported post mortem findings. Thoracic radiography and ventilation/perfusion (V/Q) scintigraphy were performed on five racing Thoroughbreds with recent histories of EIPH. Parametric images of V/Q ratios for left and right lungfields were also generated from the scan images. In all horses, ventilation and perfusion deficits were demonstrated in the dorsocaudal areas of the lung corresponding closely to the observed radiographic lesions. In particular, the perfusion images and V/Q ratio displays indicated that, in affected areas of lung, pulmonary arterial perfusion was the more seriously impaired. This finding appears to confirm the post mortem evidence of reduced pulmonary arterial perfusion and bronchial arterial dominance in these areas. Ventilation deficits in the same areas also confirmed the likelihood of partial airway obstruction consistent with the small airway disease noted in previous post mortem observations. These results suggest that the vascular and airway lesions demonstrated in detailed post mortems of horses with EIPH are also functionally important in affected horses, even at rest. As a consequence of the apparent persistent, insidious and progressive nature of the lesions associated with EIPH there are serious long term implications for management of the condition.  相似文献   

4.
In the United States, more than 75% of equine athletes are reported to suffer from exercise-related haemorrhage of the respiratory tract (Voynick and Sweeney, 1986; Sweeney et al., 1990). Fiberoptic endoscopy has traced the source of blood to beyond the bifurcation of the trachea. In 1981, the term exercise-induced pulmonary haemorrhage (EIPH) was introduced (Pascoe et al., 1981). Racehorses of all breeds, polo ponies and three-day event horses of mixed heritage, even foxhunters, may bleed (Voynick and Sweeney, 1986; Pascoe et al., 1981; Sweeney and Soma, 1983; Hillidge, 1986). Any horse working at speeds greater than 240 m/min is at risk (Voynick and Sweeney, 1986).The impact of exercise-induced pulmonary haemorrhage is difficult to assess. Most attempts to demonstrate statistically a negative correlation between EIPH and performance have been unrewarding, largely due to the number of uncontrollable variables (Pascoe et al., 1981; Raphel and Soma, 1982). In racing thoroughbreds (Mason et al., 1983) and standard breeds (MacNamara et al., 1990) approximately half as many EIPH-positive as EIPH-negative horses were placed in their races. Based on extensive intrapulmonary haemorrhage, a 3-year prospective study of sudden deaths in exercising thoroughbreds concluded that 9 out of 11 deaths were attributable to EIPH (Gunson et al., 1988).By correlation of clinical signs, thoracic radiographs, ventilation/perfusion scintigraphy, gross and subgross pathology and histopathology in 26 affected thoroughbreds, EIPH has been associated with chronic small airway inflammation, proliferation of subpleural, peribronchial and septal bronchial arterioles, interstitial connective tissue fibrosis and alveolar septal disruption in the dorsocaudal lung lobes (O'Callaghan et al., 1987). From this work it was proposed that the initial insult of EIPH started as focal, dorsocaudal pulmonary peribronchial inflammation which resulted in bronchial arterial neovascularization. Haemorrhage then occurred when, during exercise, bronchial blood pressure increased in fragile capillary buds. The incidence of bronchitis/bronchiolitis, regardless of aetiology, has been estimated to be 30% in non-racing equine athletes and close to 100% in one group of racing thoroughbreds (Sweeney et al., 1989). Histological study of lungs from horses with mild, moderate and severe chronic small airway disease consistently revealed a greater density of lesions in the diaphragmatic lobes (Winder and von Fellenberg, 1988).To understand further the aetiology and/or pathophysiology of EIPH, we will first explore some aspects of general mammalian and specific equine pulmonary and bronchial vascular anatomy and physiology. Exercise-related changes in these systems in normal and EIPH-positive horses will be briefly reviewed. Finally, a look at the types of therapies applied to bleeders may shed further light on the subject.  相似文献   

5.
REASONS FOR PERFORMING STUDY: Exercise-induced pulmonary haemorrhage (EIPH) occurs in the majority of horses performing strenuous exercise. Associated pulmonary lesions include alveolar and airway wall fibrosis, which may enhance the severity of EIPH. Further work is required to understand the pulmonary response to blood in the equine airways. OBJECTIVES: To confirm that a single instillation of autologous blood into horse airways is associated with alveolar wall fibrosis, and to determine if blood in the airways is also associated with peribronchiolar fibrosis. METHODS: Paired regions of each lung were inoculated with blood or saline at 14 and 7 days, and 48, 24 and 6 h before euthanasia. Resulting lesions were described histologically and alveolar and airway wall collagen was quantified. RESULTS: The main lesion observed on histology was hypertrophy and hyperplasia of type II pneumocytes at 7 days after blood instillation. This lesion was no longer present at 14 days. There were no significant effects of lung region, treatment (saline or autologous blood instillation), nor significant treatment-time interactions in the amount of collagen in the interstitium or in the peribronchial regions. CONCLUSION: A single instillation of autologous blood in lung regions is not associated with pulmonary fibrosis. POTENTIAL RELEVANCE: Pulmonary fibrosis and lung remodelling, characteristic of EIPH, are important because these lesions may enhance the severity of bleeding during exercise. A single instillation of autologous blood in the airspaces of the lung is not associated with pulmonary fibrosis. Therefore the pulmonary fibrosis described in EIPH must have other causes, such as repetitive bleeds, or the presence of blood in the pulmonary interstitium in addition to the airspaces. Prevention of pulmonary fibrosis through therapeutic intervention requires a better understanding of these mechanisms.  相似文献   

6.
This study was initiated to determine if the extent and intensity of lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses could be predicted from thoracic radiographs. Sets of thoracic radiographs from 24 horses with varied histories of EIPH were subjectively coded for radiographic quality, and perceived extent and intensity of diffuse interstitial opacity by three radiologists who had no knowledge of the corresponding autopsy results. Codes assigned from radiographs for the chosen parameters were compared with coded estimates of lung surface staining assigned at post mortem and volume measurements of haemosiderin deposits and bronchial arterial neovascularisation recorded from lung slices in separate studies. The non-parametric Spearman rank correlation test was used to test for statistical significance. All radiographically coded estimates of lesion severity were positively correlated with post mortem measurements of actual lesion involvement, but only the correlation between coded estimates of lesion opacity versus haemosiderin deposits and bronchial artery neovascularisation were statistically significant (P less than 0.05). Correlations between radiographic codes for lesion extent versus haemosiderin deposits and neovascularisation were just beyond the level of significance (P greater than 0.05 less than 0.1). These findings indicate that there are graded, radiographically discernible increases in interstitial opacity related to actual lesion severity. However, under the conditions of the study, accurate prediction of lung pathology in individual cases based on radiographic criteria was precluded by the wide variance of the coded values. The authors believe that with good radiographic technique and careful criteria selection, satisfactory prediction of lesion severity in EIPH cases could be achieved.  相似文献   

7.
Detailed physical and clinical examinations were performed on 26 Thoroughbred racehorses which were used subsequently in a series of studies to investigate the contribution of the pulmonary and bronchial arterial circulations to the pathophysiology of exercise-induced pulmonary haemorrhage (EIPH). Twenty-five of the horses had been retired from race training in Hong Kong during the 1984-85 season, all but four raced that season; one horse had been retired the previous season. The average number of races for the group that season was 4.1 +/- 2 with an average distance of 1502 +/- 216 metres, mean racing speed 15.5 +/- 0.5 metres/sec. Time from last race to necropsy was 177 +/- 155 days, range 12 to 572 days. All but one horse had a known history of either EIPH or epistaxis. Time from last recorded incident of expistaxis (17 horses) to necropsy was 156 +/- 141 days, range 12 to 513 days, with a longer interval since last recorded endoscopic observation of EIPH. Focal abnormal lung sounds were detected in the dorsocaudal lungfields on auscultation during rebreathing in three horses and six had tracheobronchial cytology consistent with previous episodes of pulmonary haemorrhage (haemosiderophages). No other characteristics which might have allowed separation of this group of horses from other Thoroughbred horses recently in race training were identified.  相似文献   

8.
EIPH is a condition affecting virtually all horses during intense exercise worldwide. The hemorrhage originates from the pulmonary vasculature and is distributed predominantly bilaterally in the dorsocaudal lung lobes. As the condition progresses, the lung abnormalities extend cranially along the dorsal portions of the lung. An inflammatory response occurs in association with the hemorrhage and may contribute to the chronic sequela. Although conflicting opinions exist as to its affect on performance, it is a syndrome that is thought to increase in severity with age. The most commonly performed method to diagnose EIPH at the present time is endoscopy of the upper airway alone or in combination with tracheal wash analysis for the presence of erythrocytes and hemosiderophages. Because horses may not bleed to the same extent every time and the bleeding may originate from slightly different locations, these diagnostic procedures may not be extremely sensitive or quantitative. At this time, there is no treatment that is considered a panacea, and the currently allowed treatments have not proven to be effective in preventing EIPH. Future directions for therapeutic intervention may need to include limiting inflammatory responses to blood remaining within the lungs after EIPH.  相似文献   

9.
Gross post mortem examinations were performed on the lungs of 26 Thoroughbred horses of known exercise-induced pulmonary haemorrhage (EIPH) status. The most consistent finding was a variable degree of bilaterally symmetrical, dark discolouration of the dorsocaudal regions of the caudal lung lobes. In more severely affected lungs, the stained areas extended cranially along the dorsal surfaces of the lungs, and in some cases affected approximately one third of the lung surface. Discoloured areas of lung were denser than normal, collapsed less readily, often contained trapped air and were slow to inflate. The subpleural bronchial arteries were more prominent in the discoloured regions. Pleural adhesions were noted in two horses but were not related to the discoloured lung regions. It was concluded that the discoloured lesions have a complex pathogenesis and were related directly to previous bouts of EIPH. Associated with them were signs indicating probable partial small airway obstruction, decreased tissue compliance and direct involvement of the bronchial arterial circulation.  相似文献   

10.
Exercise induced pulmonary haemorrhage (EIPH) is a condition of uncertain aetiology. This article reviews the evidence relating to its incidence, clinical findings, radiological observations, histopathology and certain aspects of respiratory physiology. It is proposed that EIPH is primarily caused by mechanical stress in the dorsocaudal region of the lung.  相似文献   

11.
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.  相似文献   

12.
The stimulation of pulmonary beta2-adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol-a beta2-adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise-induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre-exercise)-control, and furosemide (250 mg i.v., 4 h pre-exercise)+clenbuterol (0.8 microg/kg i.v., 11 min pre-exercise) experiments. The sequence of these treatments was randomized 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, 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. In the control study, incremental exercise resulted in progressive significant (P<0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P<0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide-control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P<0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P<0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P<0.05), but these data were not different from the furosemide-control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood-gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.  相似文献   

13.
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.  相似文献   

14.
Reasons for performing study: Frusemide (Fru) is widely prescribed for management of racehorses experiencing EIPH. The effect of Fru in the lung appears to be a reduction in transcapillary pressures and inhibition of the erythrocyte anion exchange, which may lead to attenuation of transpulmonary fluid fluxes during exercise. Hypothesis: Treatment with Fru will attenuate transpulmonary fluid fluxes in horses during high intensity exercise. Methods: In a crossover study, 6 race‐fit Standardbred horses were treated with 250 mg of Fru i.v. (FruTr) or placebo (Con) 4 h before exercise on a high speed treadmill until fatigue. Arterial and central mixed venous blood, as well as CO2 elimination and O2 uptake, were sampled. Volume changes across the lung and transvascular fluid fluxes were calculated from changes in haemoglobin, packed cell volume, plasma protein and cardiac output (Q). Results: During exercise, Q increased in both Con and FruTr, with Q being significantly lower in FruTr (mean ± s.e. 301.8 ± 8.5 l/min at fatigue) compared to Con (336.5 ± 15.6 l/min) (P<0.01). At rest frusemide had no effect on erythrocyte (JER) and transvascular (JV‐A) fluid fluxes across the lung. Exercise had a significant effect on JER and JV‐A (P≤0.02). During exercise, JER (at fatigue 14.6 ± 2.3 l/min and 11.6 ± 2.2 l/min in Con and FruTr, respectively) and JV‐A (at fatigue14.9 ± 2.3 l/min and 12.0 ± 2.2 l/min in Con and FruTr, respectively) were not significantly different between Con and FruTr (P = 0.6 and P = 0.8 for JER and JV‐A, respectively). Conclusions and clinical importance: Fru does not have a measurable effect on JER and JV‐A. Cardiac output was reduced in FruTr, suggesting that there were also smaller changes in the capillary recruitment and transvascular transmural hydrostatic pressures; however, this did not effect JV‐A. Therefore, Fru at the dose of 250 mg does not appear to be an effective treatment for regulating pulmonary transvascular forces during exercise in horses.  相似文献   

15.
A retrospective survey was carried out at a Florida racetrack in 1984, to determine the prevalence of exercise-induced pulmonary hemorrhage (EIPH) in Appaloosa horses. Of 94 horses examined endoscopically between 30 and 90 minutes after racing, forty-nine (52%) were found to exhibit some degree of EIPH. There was a significantly increased prevalence of EIPH with increasing age in this population. An increased prevalence of EIPH was noted with mares and geldings as compared with stallions, but this was not statistically significant. More horses bled from the right lung than from the left, but the difference was statistically insignificant. An increased prevalence of EIPH with distance run was evident, but this was not significant when animals of the same age were examined.  相似文献   

16.
OBJECTIVE: To determine whether exercise-induced pulmonary hemorrhage (EIPH) was associated with racing performance inThoroughbred horses not medicated with furosemide and not using nasal dilator strips. DESIGN: Observational cross-sectional study. ANIMALS: 744 two- to 10-year-old Thoroughbred horses racing in Melbourne, Australia. PROCEDURE: Horses were enrolled prior to racing, and a tracheobronchoscopic examination was performed after 1 race. Examinations were recorded on videotape, and presence and severity (grade 0 to 4) of EIPH were subsequently determined by 3 observers blinded to the horses' identity. Race records were abstracted for each horse examined. RESULTS: Overall, 52.1% of horses eligible for participation in the study were examined, and horses that were examined did not differ from horses that were not examined in regard to age, sex distribution, or proportion of horses that won or finished in the first 3 positions. Horses with EIPH grades < 1 were 4.0 times as likely to win, 1.8 times as likely to finish in the first 3 positions, and 3.03 times as likely to be in the 90th percentile or higher for race earnings as were horses with grades > 2. Horses with EIPH grades > 1 finished significantly farther behind the winner than did horses without EIPH. However, odds that horses with grade 1 EIPH would win or finish in the first 3 positions were not significantly different from odds for horses without EIPH. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that EIPH is associated with impaired performance in Thoroughbred racehorses not medicated with furosemide and not using nasal dilator strips.  相似文献   

17.
The purpose of this study was to use radiographic contrast techniques and special imaging methods to identify and high-light bronchial arterial involvement in lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses. The lungs from four horses with histories of EIPH were prepared for computerised tomographic scanning and microradiography by perfusing the broncho-oesophageal artery with a mixture of red latex and either barium or iodine contrast materials while the pulmonary supply received only blue latex. Computerised tomographic scan slices of the prepared inflated lungs were obtained from the caudal tip of the lung to the hilus. Microradiography of selected lung slices was also performed on a Faxitron. Diffuse areas of increased density, with preferential bronchial arterial supply noted on the computerised tomographic scans were confirmed by microradiography. Dense focal and diffuse plexuses of markedly hypertrophied and highly branched bronchial arterial networks were identified, centred around certain small airways. The vascular supply to these plexuses was recruited predominantly from neighbouring bronchial vessels, and in some cases, from the enlarged vasa vasorum of pulmonary arteries sending anastomoses to the affected areas. The authors conclude that bronchial vascular lesions in EIPH cases are the likely origin of haemorrhage; that small airway disease is the probable initiating stimulus for bronchial vascular proliferation in these lesions; and that the morphology and nature of the neovascular tissue in these lesions provides the conditions leading to haemorrhage in the lungs of horses with EIPH.  相似文献   

18.
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.  相似文献   

19.
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.  相似文献   

20.
Respiratory abnormalities are common causes of decreased performance in horses presumably because of impaired pulmonary gas exchange. The objectives of the present study were to describe respiratory abnormalities in poorly performing horses and to investigate the relationships between dynamic upper respiratory tract (URT) videoendoscopy, postexercising bronchoalveolar lavage (BAL) cytology, and exercising arterial blood gas analysis. Medical records of 93 horses with exercise intolerance, which presented for treadmill evaluation, were reviewed. Relationships between horse demographics, treadmill endoscopic findings, exercising blood gas values, and BAL cytology results were examined. A total of 25 (27%) horses had a URT obstruction and 91 (98%) horses had abnormal BAL cytology; 73 (78%) had evidence of inflammatory airway disease (IAD) and 83 (89%) had exercise-induced pulmonary hemorrhage (EIPH). In all, 39 (42%) horses had abnormal blood gas values. Dynamic URT obstruction was significantly associated with exercising hypoxemia (P = .036). There were no significant relationships between gas exchange and IAD or between EIPH. Out of 24 (26%) horses with combined URT obstruction and abnormal BAL, horses with URT obstruction and EIPH were more likely to be hypoxic during exercise (P = .037). It was concluded that horses with dynamic URT abnormalities are likely to have exercising hypoxemia. Although IAD and EIPH were commonly indentified in poor performers, they were not significantly associated with abnormal exercising blood gas analysis.  相似文献   

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