Effects of furosemide, exercise, and atropine on tracheal mucus transport rate (TMTR) in horses were investigated. Atropine (0.02 mg/kg of body weight) administered IV or by aerosolization significantly (P < 0.05) decreased TMTR at 60, but not at 30 minutes after its administration in standing horses. Furosemide (1.0 mg/kg, IV) did not have any significant effect on TMTR when measured at 2 or 4 hours after its administration in standing horses. Exercise alone or furosemide (1.0 mg/kg, IV) administration followed 4 hours later by exercise did not alter TMTR, compared with values for standing control or exercised horses administered saline solution. Atropine (0.02 mg/kg, IV) administered after exercise significantly (P < 0.05) decreased TMTR, compared with values for no exercise standing controls, for exercise after administration of saline solution, and for furosemide and exercise.

The effect of premedication with phenylbutazone on systemic hemodynamic and diuretic effects of furosemide was examined in 6 healthy, conscious, mares. Mares were instrumented for measurement of systemic hemodynamics, including cardiac output and pulmonary arterial, systemic arterial, and intracardiac pressures, and urine flow. Each of 3 treatments was administered in a randomized, blinded study; furosemide (1 mg/kg of body weight, IV) only, phenylbutazone (8.8 mg/kg PO, at 24 hours and 4.4 mg/kg IV, 30 minutes before furosemide) and furosemide, or 0.9% NaCl. Phenylbutazone administration significantly attenuated, but did not abolish, the diuretic effect of furosemide. Phenylbutazone completely inhibited the immediate effect of furosemide on cardiac output, stroke volume, total peripheral resistance, and right ventricular peak pressure. Premedication with phenylbutazone did not inhibit equally the diuretic and hemodynamic effects of furosemide, indicating that some of furosemide's hemodynamic effects are mediated by an extrarenal activity of furosemide.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

OBJECTIVE To evaluate the diuretic effects and associated changes in hematologic and plasma biochemical values following SC furosemide administration to water-deprived inland bearded dragons (Pogona vitticeps). ANIMALS 9 bearded dragons. PROCEDURES In a crossover study design, furosemide (5 or 10 mg/kg) was administered SC every 12 hours for 4 doses or no treatment (control treatment) was provided for the same period. Food and water were withheld. Body weight was recorded before (baseline) and 12 hours after treatment sessions ended and then after 5 minutes of soaking in a water bath. Blood samples were collected at baseline and 12 hours after treatment sessions ended for various measurements. RESULTS Compared with control values, a significant decrease from baseline in body weight was detected after furosemide treatment at 5 and 10 mg/kg (mean ± SD percentage decrease, 5.5 ± 3.2% and 5.2 ± 4.1%, respectively). Soaking resulted in a significant increase in body weight after the 5- and 10-mg/kg furosemide treatments (mean ± SD percentage increase, 2.9 ± 1.8% and 5.6 ± 2.5%, respectively), compared with change in body weight after the control treatment (0.7 ± 0.7%). Plasma total solids and total protein concentrations increased significantly with both furosemide treatments, and PCV increased significantly with the 10 mg/kg treatment only. No significant or relevant differences were identified in plasma osmolarity or uric acid or electrolyte concentrations. CONCLUSIONS AND CLINICAL RELEVANCE Furosemide as administered resulted in hemoconcentration and weight loss in bearded dragons, most likely owing to its diuretic effects. With additional research, furosemide could be considered for treatment of congestive heart failure and other conditions requiring diuresis in bearded dragons.

OBJECTIVE To determine whether high doses of enalapril and benazepril would be more effective than standard doses of these drugs in suppressing the furosemide-activated renin-angiotensin-aldosterone system (RAAS). ANIMALS 6 healthy Beagles. PROCEDURES 2 experiments were conducted; each lasted 10 days, separated by a 2-week washout period. In experiment 1, all dogs received furosemide (2 mg/kg, PO, q 12 h) and enalapril (1 mg/kg, PO, q 12 h) for 8 days (days 0 through 7). In experiment 2, dogs received furosemide (2 mg/kg, PO, q 12 h) and benazepril (1 mg/kg, PO, q 12 h) for 8 days. Effects on the RAAS were determined by assessing serum angiotensin-converting enzyme (ACE) activity on days −1, 3, and 7; serum aldosterone concentration on days −2, −1, 1, 3, and 7; and the urinary aldosterone-creatinine ratio (UAldo:C) in urine collected in the morning and evening of days −2, −1, 1, 3, and 7. RESULTS High doses of enalapril and benazepril caused significant reductions in serum ACE activity on all days but were not more effective than standard doses used in other studies. Mean UAldo:C remained significantly higher on days 2 through 7, compared with baseline values. Serum aldosterone concentration also increased after drug administration, which mirrored changes in the UAldo:C. CONCLUSIONS AND CLINICAL RELEVANCE In this study, administration of high doses of enalapril and benazepril significantly inhibited ACE activity, yet did not prevent increases in mean urine and serum aldosterone concentrations resulting from furosemide activation of RAAS. This suggested that aldosterone breakthrough from ACE inhibition was a dose-independent effect of ACE inhibitors.

A 6 year-old, spayed female, Maltese dog was presented with precordial thrill and mild coughing. Thoracic auscultation revealed a grade V/VI systolic murmur with maximal intensity over the left apex characterized by musical murmur. Echocardiography revealed mild myxomatous degeneration of mitral valve and ruptured chordae tendineae. Musical murmur was produced due to the vibration of ruptured piece of chordae tendineae along with regurgitant flow. After treatment with furosemide and ramipril, clinical signs resolved and precordial thrill reduced. This case report describes typical clinical signs and phonocardiogram of musical murmur in a dog with acute chordae tendineae rupture.

Objective—To evaluate the effect of administration of the labeled dosage of pimobendan to dogs with furosemide-induced activation of the renin-angiotensin-aldosterone system (RAAS). Animals—12 healthy hound-type dogs. Procedures—Dogs were allocated into 2 groups (6 dogs/group). One group received furosemide (2 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). The second group received a combination of furosemide (2 mg/kg, PO, q 12 h) and pimobendan (0.25 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). To determine the effect of the medications on the RAAS, 2 urine samples/d were obtained for determination of the urinary aldosterone-to-creatinine ratio (A:C) on days 0 (baseline), 5, and 10. Results—Mean ± SD urinary A:C increased significantly after administration of furosemide (baseline, 0.37 ± 0.14 µg/g; day 5, 0.89 ± 0.23 µg/g) or the combination of furosemide and pimobendan (baseline, 0.36 ± 0.22 µg/g; day 5, 0.88 ± 0.55 µg/g). Mean urinary A:C on day 10 was 0.95 ± 0.63 µg/g for furosemide alone and 0.85 ± 0.21 µg/g for the combination of furosemide and pimobendan. Conclusions and Clinical Relevance—Furosemide-induced RAAS activation appeared to plateau by day 5. Administration of pimobendan at a standard dosage did not enhance or suppress furosemide-induced RAAS activation. These results in clinically normal dogs suggested that furosemide, administered with or without pimobendan, should be accompanied by RAAS-suppressive treatment

Effects of furosemide, exercise, and atropine on tracheal mucus transport rate (TMTR) in horses were investigated. Atropine (0.02 mg/kg of body weight) administered IV or by aerosolization significantly (P < 0.05) decreased TMTR at 60, but not at 30 minutes after its administration in standing horses. Furosemide (1.0 mg/kg, IV) did not have any significant effect on TMTR when measured at 2 or 4 hours after its administration in standing horses. Exercise alone or furosemide (1.0 mg/kg, IV) administration followed 4 hours later by exercise did not alter TMTR, compared with values for standing control or exercised horses administered saline solution. Atropine (0.02 mg/kg, IV) administered after exercise significantly (P < 0.05) decreased TMTR, compared with values for no exercise standing controls, for exercise after administration of saline solution, and for furosemide and exercise.

High-intensity exercise results in a dramatic increase in mean pulmonary capillary blood pressure of horses, and administration of furosemide 4 hours before exertion significantly attenuates this exercise-induced increment. To test whether this effect of furosemide is mediated via release of prostaglandins, right atrial and pulmonary vascular pressures were measured in 8 healthy, sound, exercise-trained Thoroughbreds at rest and during incremental-step exercise on a treadmill. Horses were studied on 3 separate occasions: after IV administration of saline (0.9% NaCl) solution, after administration of furosemide (250 mg, iv, 4 hours before exercise) alone, and after administration of flunixin meglumine (1.1 mg/kg, IV, q 8 h for 3 days) and furosemide (250 mg, IV, 4 hours before exercise; last dose of flunixin meglumine was administered 90 seconds after furosemide injection). Experiments on each horse were separated by at least 7 days and were performed in random order. At rest and at the highest workload (14.5 m/s on a 5% uphill incline), mean pulmonary capillary blood pressure recorded after administration of furosemide alone was not significantly different from that recorded after administration of flunixin meglumine and furosemide. However, these values were significantly (P < 0.05) less than corresponding values of mean pulmonary capillary blood pressure recorded after administration of saline solution. Thus, it was concluded that furosemide-induced attenuation of the increment in pulmonary capillary blood pressure during strenuous exercise is probably not mediated via prostaglandin production.

Effects of furosemide administration on exertion-induced changes in plasma renin activity and plasma concentrations of atrial natriuretic peptide and aldosterone in horses during sustained submaximal exertion were examined. Furosemide (1 mg/kg of body weight) or heparinized saline solution was administered IV to each of 6 mares not conditioned to exercise, either 4 hours or 2 minutes before 60 minutes of sustained submaximal running on a treadmill. Horses ran at a speed that induced heart rate approximately 65% of maximal after saline treatment. After 15 minutes of running, furosemide suppressed the exertion-induced increase in plasma concentrations of atrial natriuretic peptide (mean [95% confidence interval] values of 63.9 [9.9 to 421] pg/ml vs 100 [15.4 to 652] pg/ml after furosemide or saline treatment, respectively), and enhanced the response of plasma renin activity to exertion (18.6 [5.7 to 60.4] ng/ml/h vs 6.0 [1.8 to 19.4] ng/ml/h, respectively). An effect of furosemide on the exertion-induced increase in plasma aldosterone concentration was not detected.