Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses

2001 ◽  
Vol 90 (6) ◽  
pp. 2371-2377 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
High Intensity ◽  
Structural Changes ◽  
Pulmonary Hemorrhage ◽  
Exercise Bout ◽  
Blood Gas ◽  
Gas Barrier ◽  
Arterial Hypoxemia ◽  
Pulmonary Capillaries ◽  
Thoroughbred Horses ◽  
Exercise Induced

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial Pco 2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial Po 2 values were significantly ( P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar Po 2, as arterial Pco 2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses

1997 ◽  
Vol 82 (5) ◽  
pp. 1584-1592 ◽  
Author(s):  
Eric K. Birks ◽  
Odile Mathieu-Costello ◽  
Zhenxing Fu ◽  
Walter S. Tyler ◽  
John B. West
Keyword(s):  
High Pressures ◽  
Autologous Blood ◽  
Pulmonary Hemorrhage ◽  
Capillary Endothelium ◽  
Gas Barrier ◽  
Thoroughbred Racehorses ◽  
Pulmonary Capillaries ◽  
Thoroughbred Horses ◽  
Exercise Induced ◽  
Very High

Birks, Eric K., Odile Mathieu-Costello, Zhenxing Fu, Walter S. Tyler, and John B. West. Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses. J. Appl. Physiol. 82(5): 1584–1592, 1997.—Thoroughbred horses develop extremely high pulmonary vascular pressures during galloping, all horses in training develop exercise-induced pulmonary hemorrhage, and we have shown that this is caused by stress failure of pulmonary capillaries. It is known that the capillary transmural pressure (Ptm) necessary for stress failure is higher in dogs than in rabbits. The present study was designed to determine this value in horses. The lungs from 15 Thoroughbred horses were perfused with autologous blood at Ptm values (midlung) of 25, 50, 75, 100 and 150 mmHg, and then perfusion fixed, and samples (dorsal and ventral, from caudal region) were examined by electron microscopy. Few disruptions of capillary endothelium were observed at Ptm ≤ 75 mmHg, and 5.3 ± 2.2 and 4.3 ± 0.7 breaks/mm endothelium were found at 100 and 150 mmHg Ptm, respectively. Blood-gas barrier thickness did not change with Ptm. At low Ptm, interstitial thickness was greater than previously found in rabbits but not in dogs. We conclude that the Ptm required to cause stress failure of pulmonary capillaries is between 75 and 100 mmHg and is greater in Thoroughbred horses than in both rabbits and dogs.

Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds

2002 ◽  
Vol 93 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan ◽  
Tracy Depuy ◽  
Sarah Humphrey
Keyword(s):  
Pulmonary Hemorrhage ◽  
Exercise Duration ◽  
Pulmonary Injury ◽  
Arterial Hypoxemia ◽  
Inflammatory Agent ◽  
Pulmonary Capillaries ◽  
Anti Inflammatory ◽  
Gas Measurements ◽  
Exercise Induced ◽  
Chemical Mediators

In view of the suggestion that pulmonary injury-induced release of histamine and/or other chemical mediators from airway inflammatory and mast cells contribute to the exercise-induced arterial hypoxemia (EIAH) in human athletes, we examined the effects of pretreatment with a potent anti-inflammatory agent, dexamethasone, on EIAH and desaturation of hemoglobin in horses. Seven healthy, sound, exercise-trained Thoroughbreds were studied in the control (no medications) experiments, followed in 7 days by intravenous dexamethasone (0.11 mg·kg−1·day−1for 3 consecutive days) studies. Blood-gas measurements were made at rest and during incremental exercise leading to maximal exertion at 14 m/s on a 3.5% uphill grade. Galloping at this workload induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that stress failure of pulmonary capillaries had occurred. In both treatments, significant EIAH, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but significant differences between the control and dexamethasone treatments were not discerned. The failure of pretreatment with dexamethasone to significantly affect EIAH suggests that pulmonary injury-evoked airway inflammatory response may not play a major role in EIAH in racehorses. However, our observations in both treatments that EIAH developed quickly (being evident at 30 s of exertion) and that its severity remained unaffected by increasing exercise duration (to 120 s) suggest that EIAH has a functional basis, probably related to significant shortening of the transit time for blood in the pulmonary capillaries as cardiac output increases dramatically.

H1-receptor antagonist, tripelennamine, does not affect arterial hypoxemia in exercising Thoroughbreds

2002 ◽  
Vol 92 (4) ◽  
pp. 1515-1523 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Sarah Humphrey ◽  
Tracy Depuy
Keyword(s):  
Histamine Release ◽  
Receptor Antagonist ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Pulmonary Injury ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Exercise Induced

It has been suggested that pulmonary injury and inflammation-induced histamine release from airway mast cells may contribute to exercise-induced arterial hypoxemia (EIAH). Because stress failure of pulmonary capillaries and EIAH are routinely observed in exercising horses, we examined whether preexercise administration of an H1-receptor antagonist may mitigate EIAH. Two sets of experiments, placebo (saline) and antihistaminic (tripelennamine HCl at 1.10 mg/kg iv, 15 min preexercise) studies, were carried out on seven healthy, exercise-trained Thoroughbred horses in random order 7 days apart. Arterial and mixed venous blood-gas and pH measurements were made at rest before and after saline or drug administration and during incremental exercise leading to maximal exertion at 14 m/s on 3.5% uphill grade for 120 s. Galloping at this workload elicited maximal heart rate and induced exercise-induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that capillary stress failure-related pulmonary injury had occurred. In both treatments, EIAH, desaturation of hemoglobin, hypercapnia, and acidosis of a similar magnitude developed during maximal exertion, and statistically significant differences between the placebo and antihistaminic studies could not be demonstrated. The failure of the H1-receptor antagonist to modify EIAH significantly suggests that pulmonary injury-induced histamine release may not play a major role in bringing about EIAH in Thoroughbred horses.

scholarly journals Nasal strips do not affect pulmonary gas exchange, anaerobic metabolism, or EIPH in exercising Thoroughbreds

2001 ◽  
Vol 90 (6) ◽  
pp. 2378-2385 ◽  
Author(s):  
Thomas E. Goetz ◽  
Murli Manohar ◽  
Aslam S. Hassan ◽  
Gordon J. Baker
Keyword(s):  
Blood Lactate ◽  
Anaerobic Metabolism ◽  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Mixed Venous Blood ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Exercise Induced ◽  
Mixed Venous

The present study was carried out to examine whether nasal strip application would improve the exercise-induced arterial hypoxemia and hypercapnia, diminish anaerobic metabolism, and modify the incidence of exercise-induced pulmonary hemorrhage (EIPH) in horses. Two sets of experiments, control and nasal strip experiments, were carried out on seven healthy, sound, exercise-trained Thoroughbred horses in random order, 7 days apart. Simultaneous measurements of core temperature, arterial and mixed venous blood gases/pH, and blood lactate and ammonia concentrations were made at rest, during submaximal and near-maximal exercise, and during recovery. In both treatments, whereas submaximal exercise caused hyperventilation, near-maximal exercise induced significant arterial hypoxemia, desaturation of Hb, hypercapnia, and acidosis. However, O2 content increased significantly with exercise in both treatments, while the mixed venous blood O2 content decreased as O2 extraction increased. In both treatments, plasma ammonia and blood lactate concentrations increased significantly with exercise. Statistically significant differences between the control and the nasal strip experiments could not be discerned, however. Also, all horses experienced EIPH in both treatments. Thus our data indicated that application of an external nasal dilator strip neither improved the exercise-induced arterial hypoxemia and hypercapnia nor diminished anaerobic metabolism or the incidence of EIPH in Thoroughbred horses performing strenuous exercise.

Intrapulmonary arteriovenous shunts of >15 μm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses

2005 ◽  
Vol 99 (1) ◽  
pp. 224-229 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Blood Oxygenation ◽  
Mixed Venous Blood ◽  
Arteriovenous Shunting ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Arteriovenous Shunts ◽  
Exercise Induced ◽  
Mixed Venous

The present study examined whether Thoroughbred horses performing strenuous exercise exhibit intrapulmonary arteriovenous shunting that may contribute to the observed arterial hypoxemia. Experiments were carried out on seven healthy, exercise-trained Thoroughbreds at rest, maximal exercise (galloping at 14 m/s on a 3.5% uphill grade for 120 s), and submaximal exertion (8 m/s on a 3.5% uphill grade for 150 s). Along with blood gas/hemodynamic parameters, intrapulmonary arteriovenous shunting was studied by injecting 15-μm-diameter microspheres, labeled with different stable isotopes, into the right atrium while simultaneous blood samples were being withdrawn at a constant rate from the pulmonary artery and the aorta. Arterial hypoxemia was observed only during maximal exercise. Also, despite significant pulmonary arterial hypertension during submaximal and maximal exertion, 15-μm microspheres did not traverse the pulmonary microcirculation to appear in the aortic blood. Thus our findings did not support a role for intrapulmonary arteriovenous shunts of >15 μm in diameter in the exercise-induced arterial hypoxemia in racehorses. Interestingly, our observation that, in going from 30 to 120 s of maximal exertion, arterial O2 tension had remained unchanged despite significant reductions in mixed venous blood O2 tension, hemoglobin-O2 saturation, and O2 content also discounts the importance of intrapulmonary arteriovenous shunts in causing arterial hypoxemia. This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30–120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.

NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds

2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Physiological Saline ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Exercise Induced ◽  
Mixed Venous

The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.

scholarly journals Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution

2009 ◽  
Vol 297 (6) ◽  
pp. R1625-R1634 ◽  
Author(s):  
John B. West
Keyword(s):  
Gas Exchange ◽  
Complete Separation ◽  
External Support ◽  
Blood Gas ◽  
Large Area ◽  
Gas Barrier ◽  
Type Iv ◽  
Pulmonary Capillaries ◽  
The Face ◽  
Flow Through

Two opposing selective pressures have shaped the evolution of the structure of the blood-gas barrier in air breathing vertebrates. The first pressure, which has been recognized for 100 years, is to facilitate diffusive gas exchange. This requires the barrier to be extremely thin and have a large area. The second pressure, which has only recently been appreciated, is to maintain the mechanical integrity of the barrier in the face of its extreme thinness. The most important tensile stress comes from the pressure within the pulmonary capillaries, which results in a hoop stress. The strength of the barrier can be attributed to the type IV collagen in the extracellular matrix. In addition, the stress is minimized in mammals and birds by complete separation of the pulmonary and systemic circulations. Remarkably, the avian barrier is about 2.5 times thinner than that in mammals and also is much more uniform in thickness. These advantages for gas exchange come about because the avian pulmonary capillaries are unique among air breathers in being mechanically supported externally in addition to the strength that comes from the structure of their walls. This external support comes from epithelial plates that are part of the air capillaries, and the support is available because the terminal air spaces in the avian lung are extremely small due to the flow-through nature of ventilation in contrast to the reciprocating pattern in mammals.

Pulmonary capillaries are more resistant to stress failure in dogs than in rabbits

1995 ◽  
Vol 79 (3) ◽  
pp. 908-917 ◽  
Author(s):  
O. Mathieu-Costello ◽  
D. C. Willford ◽  
Z. Fu ◽  
R. M. Garden ◽  
J. B. West
Keyword(s):  
Autologous Blood ◽  
Transmural Pressure ◽  
Blood Gas ◽  
Barrier Thickness ◽  
Rabbit Lung ◽  
Gas Barrier ◽  
Athletic Ability ◽  
Pulmonary Capillaries ◽  
Glutaraldehyde Solution

We previously showed that stress failure of pulmonary capillaries occurs at transmural pressures of approximately 50 cmH2O (40 mmHg) and above in rabbit lung. In this study, we examined whether pulmonary capillaries are more resistant to failure in dogs than in rabbits. This might be expected because of the greater athletic ability of dogs and therefore their presumably greater tolerance to large cardiac outputs and higher pulmonary vascular pressures. The lungs of 12 anesthetized mongrel dogs [22.1 +/- 5.2 (SD) kg] were perfused in situ with autologous blood and then with saline-dextran (5 min) and glutaraldehyde solution (10 min), all three perfusions at the same preset transmural pressure of 32.5, 72.5, 92.5, or 112.5 cmH2O. In dogs, the stress failure curves relating break number per millimeter of epithelium and endothelium were right shifted by approximately 40 cmH2O compared with rabbits. Blood-gas barrier thickness was significantly greater than in rabbits at 32.5 cmH2O, and unlike in rabbits, neither total nor interstitial thickness increased significantly with increasing pressure. These results indicate that pulmonary capillaries are more resistant to stress failure in dogs than rabbits.

Stress failure of pulmonary capillaries in racehorses with exercise-induced pulmonary hemorrhage

1993 ◽  
Vol 75 (3) ◽  
pp. 1097-1109 ◽  
Author(s):  
J. B. West ◽  
O. Mathieu-Costello ◽  
J. H. Jones ◽  
E. K. Birks ◽  
R. B. Logemann ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Soft Tissues ◽  
Pulmonary Hemorrhage ◽  
Ultrastructural Changes ◽  
Radius Of Curvature ◽  
Alveolar Wall ◽  
Ultrastructural Studies ◽  
Pulmonary Capillaries ◽  
Exercise Induced

Bleeding into the lungs in thoroughbreds is extremely common; there is evidence that it occurs in essentially all horses in training. However, the mechanism is unknown. We tested the hypothesis that exercise-induced pulmonary hemorrhage (EIPH) is caused by stress failure of pulmonary capillaries. Three thoroughbreds with known EIPH were galloped on a treadmill, and after the horses were killed with intravenous barbiturate the lungs were removed, inflated, and fixed for electron microscopy. Ultrastructural studies showed evidence of stress failure of pulmonary capillaries, including disruptions of the capillary endothelial and alveolar epithelial layers, extensive collections of red blood cells in the alveolar wall interstitium, proteinaceous fluid and red blood cells in the alveolar spaces, interstitial edema, and fluid-filled protrusions of the endothelium into the capillary lumen. The appearances were consistent with the ultrastructural changes we have previously described in rabbit lungs at high capillary transmural pressures. Actual breaks in the endothelium and epithelium were rather difficult to find, and they were frequently associated with platelets and leukocytes that appeared to be plugging the breaks. The paucity of breaks was ascribed to their reversibility when the pressure was lowered and to the fact that 60–70 min elapsed between the gallop and the beginning of lung fixation. Capillary wall stress was calculated from pulmonary vascular pressures measured in a companion study (Jones et al. FASEB J. 6: A2020, 1992) and from measurements of the thickness of the blood-gas barrier and the radius of curvature of the capillaries. The value was as high as 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2), which exceeds the breaking stress of most soft tissues. We conclude that stress failure of pulmonary capillaries is the mechanism of EIPH.

Morphometry of the extremely thin pulmonary blood-gas barrier in the chicken lung

2007 ◽  
Vol 292 (3) ◽  
pp. L769-L777 ◽  
Author(s):  
Rebecca R. Watson ◽  
Zhenxing Fu ◽  
John B. West
Keyword(s):  
Type I Collagen ◽  
Arithmetic Mean ◽  
Type I ◽  
Blood Gas ◽  
Gas Barrier ◽  
Structural Support ◽  
Pulmonary Capillaries ◽  
Mammalian Lung ◽  
Avian Lung ◽  
To Come

The gas exchanging region in the avian lung, although proportionally smaller than that of the mammalian lung, efficiently manages respiration to meet the high energetic requirements of flapping flight. Gas exchange in the bird lung is enhanced, in part, by an extremely thin blood-gas barrier (BGB). We measured the arithmetic mean thickness of the different components (endothelium, interstitium, and epithelium) of the BGB in the domestic chicken lung and compared the results with three mammals. Morphometric analysis showed that the total BGB of the chicken lung was significantly thinner than that of the rabbit, dog, and horse (54, 66, and 70% thinner, respectively) and that all layers of the BGB were significantly thinner in the chicken compared with the mammals. The interstitial layer was strikingly thin in the chicken lung (∼86% thinner than the dog and horse, and 75% thinner than rabbit) which is a paradox because the strength of the BGB is believed to come from the interstitium. In addition, the thickness of the interstitium was remarkably uniform, unlike the mammalian interstitium. The uniformity of the interstitial layer in the chicken is attributable to a lack of the supportive type I collagen cable that is found in mammalian alveolar lungs. We propose that the surrounding air capillaries provide additional structural support for the pulmonary capillaries in the bird lung, thus allowing the barrier to be both very thin and extremely uniform. The net result is to improve gas exchanging efficiency.

Sign in / Sign up

Export Citation Format

Share Document