Arterial hypoxemia in exercising thoroughbreds is not affected by pre-exercise nedocromil sodium inhalation

被引:1
|
作者
Manohar, M
Goetz, TE
机构
[1] Univ Illinois, Coll Vet Med, Dept Vet Biosci, Large Anim Clin 212, Urbana, IL 61801 USA
[2] Univ Illinois, Coll Vet Med, Dept Clin Med, Large Anim Clin 212, Urbana, IL 61801 USA
关键词
exercise; arterial hypoxemia; exertion; exercise-induced hypoxemia; gas exchange; mammals; horse; pharmacological agents; nedocromil sodium;
D O I
10.1016/S1569-9048(02)00210-0
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
It has been reported that pulmonary injury (i.e. capillary stress failure) evoked histamine release from airway inflammatory/mast cells contributes to exercise-induced arterial hypoxemia (EIAH) and that pre-exercise inhalation of nedocromil sodium mitigated EIAH in human subjects 'Med. Sci. Sports Exercise 29, (1997) 10-16'. Because exercise-induced pulmonary hemorrhage due to capillary stress failure is routinely observed in racehorses, we examined whether nedocromil inhalation would similarly benefit EIAH and desaturation of hemoglobin in horses. Two sets of experiments, namely, placebo studies followed in 7 days by pre-exercise nedocromil sodium (30 puffs = 60 mg) inhalation experiments were carried out on 7 healthy, sound, exercise-trained thoroughbred horses. In both treatments, arterial and mixed-venous blood-gas/pH measurements were made at rest pre- and post-placebo/drug inhalation, as well as during incremental exercise leading to galloping at 14 m/sec on a 3.5%) uphill grade-a workload that elicited maximal heart rate and caused pulmonary hemorrhage in all horses in both treatments, thereby indicating capillary stress failure had occurred. In both treatments, significant (P < 0.0001) EIAH of a similar magnitude had developed by 30 sec of maximal exertion, and further significant changes in arterial O-2 tension did not occur as exercise duration progressed to 120 sec. Thus, pre-exercise inhalation of nedocromil sodium was ineffective in modifying the development and/or severity of EIAH in the present study. These findings argue against the airway inflammatory mediator(s) release hypothesis for causing arterial hypoxemia in racehorses. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:145 / 154
页数:10
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