Furosemide attenuates the exercise-induced increase in pulmonary artery wedge pressure in horses

Right atrial (RA), right ventricular (RV), pulmonary artery (PA), and pulmonary artery wedge (Paw) pressures were examined, using catheter-mounted micromanometers, in 8 healthy horses at rest and during galloping on a treadmill at belt speeds of 8, 10, and 13 m/s. The in vivo signals from the micromanometers were matched with those from conventional fluid-filled catheter transducers leveled at the scapulohumeral joint. Thirty minutes after completing control exercise measurements, furosemide was administered IV at a dosage of 1 mg/kg of body weight, and resting, as well as exercise, measurements were repeated 4 hours later. Studies also were performed on a separate day, when only postfurosemide resting and exercise data were collected. Prefurosemide and postfurosemide heart rate values for rest (37 +/- 2 beats/min, mean +/- SEM), as well as for exercise (213 +/- 5 beats/min at 13 m/s), were similar. Prefurosemide mean RA, PA, and PAW pressures were increased significantly (P < 0.05) from resting values of 8 +/-2, 31 +/- 2, and 18 +/- 2 mm of Hg, respectively, to 44 +/- 4, 89 +/- 5, and 56 +/- 4 mm of Hg with exercise at 13 m/s. Furosemide administration resulted in marked diuresis, and resting mean RA, PA, and PAW pressures decreased significantly (P < 0.05) to 1 +/-1, 27 +/- 2, and 11 +/- 2 mm of Hg, respectively, 4 hours after furosemide administration. Although pressures increased markedly with exercise (corresponding values being 31 +/- 5, 79 +/- 6, and 44 +/- 4 mm of Hg), these 4-hour postfurosemide exercise values were significantly (P < 0.05) less than those recorded with prefurosemide exertion. Intravascular pulmonary capillary pressure, calculated as the average of mean PA and PAW pressures, during prefurosemide exercise (73 +/- 5 mm of Hg) significantly (P < 0.05) exceeded that during exercise performed 4 hours after furosemide administration (61 +/- 5 mm of Hg). Attenuation by furosemide of the exercise-induced increase in pulmonary capillary pressure may have a role in limiting or reducing the extent of exercise-induced pulmonary hemorrhage in horses.