Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses

Authors

  • M. MANOHAR,

    1. Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois, 212 Large Animal Clinic, 1102 W. Hazelwood Drive, Urbana, Illinois 61802, USA
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  • T. E. GOETZ,

    1. Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois, 212 Large Animal Clinic, 1102 W. Hazelwood Drive, Urbana, Illinois 61802, USA
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  • P. ROTHENBAUM,

    1. Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois, 212 Large Animal Clinic, 1102 W. Hazelwood Drive, Urbana, Illinois 61802, USA
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  • S. HUMPHREY

    1. Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois, 212 Large Animal Clinic, 1102 W. Hazelwood Drive, Urbana, Illinois 61802, USA
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Summary

The present study was carried out to ascertain whether β2-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 μg/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.

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