Furosemide continuous rate infusion diluted with 5% dextrose in water or hypertonic saline in normal adult dogs: a pilot study

Adin, Darcy B.; Atkins, Clarke E.; Papich, Mark G.; DeFrancesco, Teresa C.; Griffiths, E.; Penteado, Marilene de Vuono Camargo; Kurtz, K. A.; Klein, A. M.

doi:10.1016/j.jvc.2016.09.004

Cited by 7 publications

(11 citation statements)

References 31 publications

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“…Fractional excretion of sodium and chloride was higher in CHF stages C and D, compared to preclinical stages (B1 and B2) but did not differentiate between stages C and D. This higher excretion in stages C and D was attributed to diuretic administration . Supportive of this conclusion, we observed increased potassium excretion in CHF stages.…”

Section: Discussionsupporting

confidence: 40%

“…One aliquot was immediately analyzed for blood urea nitrogen (BUN), creatinine, and electrolyte (sodium, potassium, chloride) concentrations using an automated analyzer (Roche Cobas C501, Indianapolis, Indiana) at the clinical pathology laboratory of North Carolina State University Veterinary Hospital. A second aliquot was sent to an outside laboratory for symmetric dimethylarginine (SDMA) analysis (IDEXX, Westbrook, Maine), and a third aliquot was stored at −80°C until analysis of either furosemide or torsemide concentrations at the North Carolina State University Veterinary Pharmacology Laboratory, as previously described using a validated reverse‐phase high‐pressure liquid chromatography and fluorescence detection method . A voided urine sample (5‐10 mL) was obtained at the time of the appointment, and urine specific gravity (USG) was measured.…”

Section: Methodsmentioning

confidence: 99%

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Role of electrolyte concentrations and renin‐angiotensin‐aldosterone activation in the staging of canine heart disease

Adin

Kurtz

Atkins

et al. 2019

Veterinary Internal Medicne

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Background: Refractory congestive heart failure (CHF) and associated diuretic resistance are not well defined.Objectives: To characterize renal function, electrolyte concentrations, indices of diuretic efficacy, and renin-angiotensin-aldosterone system (RAAS) activation in dogs with naturally occurring heart disease (HD) in American College of Veterinary Internal Medicine stages B1, B2, C, and D and to determine their usefulness in defining HD stages.Animals: Group 1:149 dogs with HD stages B1, B2, C, and D. Group 2:22 dogs with HD stages C and D.Methods: Group 1: Renal parameters, serum and urine electrolyte and diuretic concentrations, and urine aldosterone concentrations were measured. Medication dosages and measured variables were compared among stages. Correlation of furosemide dosages to serum concentrations was explored. Group 2: Angiotensin-converting enzyme activity and RAAS components were measured and compared among CHF stages.Results: Serum chloride concentration was the best differentiator of HD stage. Furosemide PO dosages (≤6 mg/kg/day) were weakly correlated with serum furosemide concentrations, whereas higher dosages were not significantly correlated.Angiotensin-converting enzyme inhibitor dosage and RAAS inhibition were greater in stage D, compared to stage C dogs.Conclusions and Clinical Importance: Hypochloremia is a useful marker for stage D HD in dogs. Poor furosemide dosage correlation to serum concentration may indicate variable and poor absorption, especially at higher dosages, advanced disease, or both.A small number of stage D dogs met proposed criteria for diuretic resistance. Greater RAAS inhibition in stage D versus stage C indicates effectiveness of RAASsuppressive treatments in this group of dogs with refractory CHF.

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Section: Discussionsupporting

confidence: 40%

Section: Methodsmentioning

confidence: 99%

Role of electrolyte concentrations and renin‐angiotensin‐aldosterone activation in the staging of canine heart disease

Adin

Kurtz

Atkins

et al. 2019

Veterinary Internal Medicne

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“…Furosemide in plasma was analyzed by reversed-phase high-pressure liquid chromatography using a method that was identical to the assay recently used for canine studies in our laboratory. 11,12 To validate the assay for this study in cats, blank (control) feline plasma was fortified with furosemide at three concentrations (high, medium and low) and measured to ensure that concentrations fell within the acceptance criteria for the assay. All calibration samples were made from fortified feline blank plasma.…”

Section: Plasma Drug Analysismentioning

confidence: 99%

Pharmacokinetics of furosemide after intravenous, oral and transdermal administration to cats

Sleeper

O’Donnell

Fitzgerald

et al. 2018

Journal of Feline Medicine and Surgery

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Objectives The aim of this study was to determine the pharmacokinetics of furosemide in cats following intravenous (IV), oral and transdermal administration. Methods This study used six healthy adult cats in a three-phase design to compare plasma furosemide concentrations in cats that received one IV 2 mg/kg dose of furosemide, one oral 2 mg/kg dose of furosemide and 3 days of q12h dosing with 2 mg/kg furosemide transdermally applied to the ear pinna. Results After IV administration the elimination half-life was (mean and coefficient of variation) 2.25 h (72%), systemic clearance was 149 ml/kg/h (27.4%) and volume of distribution was 227 ml/kg (22%). After oral administration the terminal half-life was 1.2 h (18.7%), peak concentration was 3.4 μg/ml (51.7%) and bioavailability was 48.4%. The transdermal plasma concentrations were undetectable or very low at most time points, and pharmacokinetics were not determined from the transdermal dose. Conclusions and relevance Furosemide was rapidly eliminated in cats after oral and IV administration and is probably best administered orally at least q12h in cats with heart failure. The oral dose absorbed was approximately 50%, but the absorption from transdermal administration was negligible.

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“…Previous studies in our laboratory have shown that braking occurs despite continued furosemide presence in the urine. 2,4 In the current study, diuretic braking occurred despite significant suppression of ACE activity for treatments B and C, both of which included benazepril. It is unknown whether a higher benazepril dosage or frequency of administration would have suppressed ACE activity more or would have affected urine production.…”

Section: Discussionmentioning

confidence: 64%

“…aldosterone antagonist, angiotensin-converting enzyme inhibitor, continuous rate infusion, diuretic resistance, neurohormone, urine production 1 | INTRODUCTION Furosemide continuous rate infusion (FCRI) has been shown to cause more urine production than bolus administration of the same dose in normal dogs and normal horses [1][2][3] but, these studies found that urine production decreased after several hours of the infusion (so-called "diuretic braking"). Renin-angiotensin-aldosterone system (RAAS) activation has been proposed as a mechanism to explain diuretic braking in these acute models.…”

Section: Introductionmentioning

confidence: 99%

Effect of spironolactone and benazepril on furosemide‐induced diuresis and renin‐angiotensin‐aldosterone system activation in normal dogs

Adin

Atkins

Wallace

et al. 2021

Veterinary Internal Medicne

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Background: Diuretic braking during furosemide continuous rate infusion (FCRI) curtails urine production.Hypothesis: Renin-angiotensin-aldosterone system (RAAS) activation mediates braking, and RAAS inhibition will increase urine production.Animals: Ten healthy purpose-bred male dogs. Methods: Dogs received placebo, benazepril, or benazepril and spironolactone PO for 3 days before a 5-hour FCRI (0.66 mg/kg/h) in a 3-way, randomized, blinded, cross-over design. Body weight (BW), serum creatinine concentration (sCr), serum electrolyte concentrations, PCV, and total protein concentration were measured before PO medications, at hours 0 and 5 of FCRI, and at hour 24. During the FCRI, water intake, urine output, urine creatinine concentration, and urine electrolyte concentrations were measured hourly. Selected RAAS components were measured before and after FCRI. Variables were compared among time points and treatments.Results: Diuretic braking and urine production were not different among treatments.Loss of BW, hemoconcentration, and decreased serum chloride concentration occurred during FCRI with incomplete recovery at hour 24 for all treatments.Although unchanged during FCRI, sCr increased and serum sodium concentration decreased at hour 24 for all treatments. Plasma aldosterone and angiotensin-II concentrations increased significantly at hour 5 for all treatments, despite suppressed angiotensin-converting enzyme activity during benazepril background treatment. Conclusions:The neurohormonal profile during FCRI supports RAAS mediation of diuretic braking in this model. Background treatment with benazepril with or without spironolactone did not mitigate braking, but was well tolerated. Delayed changes in

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Furosemide continuous rate infusion diluted with 5% dextrose in water or hypertonic saline in normal adult dogs: a pilot study

Cited by 7 publications

References 31 publications

Role of electrolyte concentrations and renin‐angiotensin‐aldosterone activation in the staging of canine heart disease

Role of electrolyte concentrations and renin‐angiotensin‐aldosterone activation in the staging of canine heart disease

Pharmacokinetics of furosemide after intravenous, oral and transdermal administration to cats

Effect of spironolactone and benazepril on furosemide‐induced diuresis and renin‐angiotensin‐aldosterone system activation in normal dogs

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