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J Appl Physiol (March 15, 2002). doi:10.1152/japplphysiol.01186.2001
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Articles in PresS, published online ahead of print March 15, 2002
J Appl Physiol, 10.1152/jap.01186.2001
Submitted on November 30, 2001
Accepted on March 11, 2002

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

Murli Manohar1*, Thomas E Goetz1, Aslam S Hassan1, Tracy DePuy1, and Sarah Humphrey1

1 Departments of Veterinary Biosciences & Clinical Medicine, University of Illinois College of Veterinary Medicine, Urbana, IL, USA

* To whom correspondence should be addressed. E-mail: mmanohar{at}uiuc.edu.

In view of the suggestion that pulmonary injury induced release of histamine and/or other chemical mediators from airway inflammatory/mast cells contributes to the exercise-induced arterial hypoxemia (EIAH) in human athletes, we examined the effects of pretreatment with a potent antiinflammatory 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 IV dexamethasone (0.11 mg/kg/day 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.




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