This study aimed to investigate and compare the antagonistic effects of atipamezole, yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats. Five cats were repeatedly used in each of the 9 groups. One group was not medicated. Cats in the other groups received 2 mg/kg BW xylazine intramuscularly, and saline (as the control); 160 mg/kg BW prazosin; or 40, 160, or 480 mg/kg BW atipamezole or yohimbine intravenously 0.5 h later. Urine and blood samples were collected 10 times over 8 h. Urine volume, pH, and specific gravity; plasma arginine vasopressin (AVP) concentration; and creatinine, osmolality, and electrolyte values in both urine and plasma were measured. Both atipamezole and yohimbine antagonized xylazine-induced diuresis, but prazosin did not. The antidiuretic effect of atipamezole was more potent than that of yohimbine but not dose-dependent, in contrast to the effect of yohimbine at the tested doses. Both atipamezole and yohimbine reversed xylazine-induced decreases in both urine specific gravity and osmolality, and the increase in free water clearance. Glomerular filtration rate, osmolar clearance, and plasma electrolyte concentrations were not significantly altered. Antidiuresis of either atipamezole or yohimbine was not related to the area under the curve for AVP concentration, although the highest dose of both atipamezole and yohimbine increased plasma AVP concentration initially and temporarily, suggesting that this may in part influence antidiuretic effects of both agents. The diuretic effect of xylazine in cats may be mediated by a2-adrenoceptors but not a1-adrenoceptors. Atipamezole and yohimbine can be used as antagonistic agents against xylazine-induced diuresis in clinically normal cats.

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 compare the effects of 2 NSAIDs (phenylbutazone and meloxicam) on renal function in horses. Animals—9 Thoroughbred or Standardbred mares (mean ± SD age, 5.22 ± 1.09 years [range, 2 to 12 years]; mean body weight, 470 ± 25 kg [range, 442 to 510 kg]). Procedures—A randomized blinded placebo-controlled crossover study was conducted to examine the effects of treatment with phenylbutazone, meloxicam, or a placebo (control solution) on renal responses to the administration of furosemide, dobutamine, and exercise (15 minutes at 60% of maximum heart rate). Renal function was assessed by use of bilateral ureteral catheterization for simultaneous determination of creatinine clearance, sodium excretion, and urine flow rate. Results—Both phenylbutazone and meloxicam attenuated diuresis and natriuresis and reduced glomerular filtration rate, compared with results for the control solution, when horses were treated with furosemide. Mean arterial blood pressure, urine flow rate, and glomerular filtration rate were increased during or after (or both) dobutamine infusion. Both NSAIDs reduced urine flow rate and sodium excretion associated with dobutamine infusion and exercise but had no effect on glomerular filtration rate. Conclusions and Clinical Relevance—Responses to meloxicam, a cyclooxygenase (COX)-2 preferential agent, appeared comparable to those detected after phenylbutazone treatment, which suggested that COX-2 was the mediator of prostanoid-induced changes to renal function in horses and indicated that COX-2–preferential agents would be likely to have adverse renal effects similar to those for nonselective COX inhibitors in volume-depleted horses.

This study aimed to investigate and compare the antagonistic effects of atipamezole, yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats. Five cats were repeatedly used in each of the 9 groups. One group was not medicated. Cats in the other groups received 2 mg/kg BW xylazine intramuscularly, and saline (as the control); 160 μg/kg BW prazosin; or 40, 160, or 480 μg/kg BW atipamezole or yohimbine intravenously 0.5 h later. Urine and blood samples were collected 10 times over 8 h. Urine volume, pH, and specific gravity; plasma arginine vasopressin (AVP) concentration; and creatinine, osmolality, and electrolyte values in both urine and plasma were measured. Both atipamezole and yohimbine antagonized xylazine-induced diuresis, but prazosin did not. The antidiuretic effect of atipamezole was more potent than that of yohimbine but not dose-dependent, in contrast to the effect of yohimbine at the tested doses. Both atipamezole and yohimbine reversed xylazine-induced decreases in both urine specific gravity and osmolality, and the increase in free water clearance. Glomerular filtration rate, osmolar clearance, and plasma electrolyte concentrations were not significantly altered. Antidiuresis of either atipamezole or yohimbine was not related to the area under the curve for AVP concentration, although the highest dose of both atipamezole and yohimbine increased plasma AVP concentration initially and temporarily, suggesting that this may in part influence antidiuretic effects of both agents. The diuretic effect of xylazine in cats may be mediated by α2-adrenoceptors but not α1-adrenoceptors. Atipamezole and yohimbine can be used as antagonistic agents against xylazine-induced diuresis in clinically normal cats.

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.

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.

A study was undertaken to determine the toxic effects of cisplatin, an antineoplastic agent, on canine kidneys and bone marrow when administered during a 6-hour saline diuresis. Cisplatin (70 mg/m2 of body surface) was administered IV to 6 healthy dogs over a 20-minute period after 0.9% NaCl solution (saline) was administered IV for 4 hours at a rate of 18.3 ml/kg/hr. After cisplatin injection, saline diuresis was continued at the same rate for 2 hours. Each dog vomited within 8 hours after the drug was administered. Clinical status, weight gain, and food consumption were normal throughout the 27-day study. All measures of renal function remained unchanged and were within normal limits for 27 days after the drug was administered. Nadirs in the daily neutrophil count were observed on days 6 (3,240 +/- 404/microliter) and 15 (1,196 +/- 275/microliter). There were no important gross or histologic abnormalities referable to cisplatin administration when the dogs were necropsied at the conclusion of the study (day 27). We concluded that cisplatin can be administered safely at a dosage of 70 mg/m2 of body surface, using a shortterm diuresis protocol, and that the drug induces a ndair in the neutrophil count on days 6 and 15.

Objectives-To determine effects of commonly used diuretic treatments on glomerular filtration rate (GFR), renal blood flow (RBF), and urine output (UO) and compare 2 methods of GFR measurement in healthy awake cats. Animals-8 healthy cats. Procedure-In a randomized crossover design, cats were randomly allocated to 4 groups: control; IV administration of fluids; IV administration of fluids and mannitol; and IV administration of fluids, dopamine, and furosemide. Inulin and para-aminohippuric acid were used for determination of plasma clearance for GFR and RBF, respectively. Plasma clearance of technetium-Tc-99m-diethylenetriaminepentacetic acid (99mTc-DTPA) was also used for GFR determination. Results-Furosernide-dopamine induced the largest UO, compared with other groups. Both mannitol and fluid therapy increased RBF, compared with the control group. Mannitol, and not fluid therapy, increased RBF, compared with furosemide-dopamine. There were significant differences in GFR values calculated from 99mTc-DTPA and inulin clearances between the 2 groups. In all groups, use of 99mTc-DTPA caused underestimation of GFR, compared with use of inulin. Conclusions and Clinical Relevance-In healthy awake cats, administration of furosemide-dopamine did not increase GFR or RBF despite increased UO. Fluid therapy and fluid therapy plus mannitol improved RBF. Determination of GFR by use of 99mTc-DTPA cannot always be substituted for inulin clearance when accurate measurement is required.