Effect of furosemide and weight carriage on energetic responses of horses to incremental exertion

K. W. Hinchcliff From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon Tharp St, Columbus, OH 43210.

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K. H. McKeever From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon Tharp St, Columbus, OH 43210.

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W. W. Muir III From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon Tharp St, Columbus, OH 43210.

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R. Sams From the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon Tharp St, Columbus, OH 43210.

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Summary

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, iv, 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, fl), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, fu). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (Vco2) and carbon dioxide production (Vco2) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < 0.001) greater weight loss than did saline administration; mean ± sem weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (sem = 2.0) for C, fl, and fu trials, respectively. The speed at which peak Vo2 was achieved was 9.31, 9.56, and 9.50 (sem = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (sem = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (sem = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (sem = 1.9) ml/min/kg, respectively. There was a significant (P = 0.070) group × speed interaction for Vco2; during trial fu, horses had significantly (P < 0.05) lower rate of CO2 production at speed of 9 m/s and at the speed that caused peak Vo2, than during trial C. The respiratory exchange ratio during the fu trial was significantly (P < 0.05) less than that during the C trial at the speed that caused peak Vo2. Plasma lactate concentration at speed of 9 m/s for C, fl, and fu trials was 15.4, 16.5, and 13.3 (sem = 0.8) mmol/L, respectively; values for the fl and C trials were not significantly different, whereas the mean value for the fu trial was significantly (P < 0.05) less than that for the C trial. Thus, administration of furosemide to horses altered the energetic response to exertion. Replacement of the furosemide-induced weight loss resulted in Vco2, plasma lactate, and respiratory exchange values indistinguishable from those during the control trial.

Summary

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, iv, 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, fl), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, fu). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (Vco2) and carbon dioxide production (Vco2) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < 0.001) greater weight loss than did saline administration; mean ± sem weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (sem = 2.0) for C, fl, and fu trials, respectively. The speed at which peak Vo2 was achieved was 9.31, 9.56, and 9.50 (sem = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (sem = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (sem = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (sem = 1.9) ml/min/kg, respectively. There was a significant (P = 0.070) group × speed interaction for Vco2; during trial fu, horses had significantly (P < 0.05) lower rate of CO2 production at speed of 9 m/s and at the speed that caused peak Vo2, than during trial C. The respiratory exchange ratio during the fu trial was significantly (P < 0.05) less than that during the C trial at the speed that caused peak Vo2. Plasma lactate concentration at speed of 9 m/s for C, fl, and fu trials was 15.4, 16.5, and 13.3 (sem = 0.8) mmol/L, respectively; values for the fl and C trials were not significantly different, whereas the mean value for the fu trial was significantly (P < 0.05) less than that for the C trial. Thus, administration of furosemide to horses altered the energetic response to exertion. Replacement of the furosemide-induced weight loss resulted in Vco2, plasma lactate, and respiratory exchange values indistinguishable from those during the control trial.

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