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Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801
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·day1
for 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.
blood-gas tensions in exercise; adrenoglucocorticoids; airway inflammation; corticosteroids; horses
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