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Roger M. Mills - One of the best experts on this subject based on the ideXlab platform.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:Background In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Hypothesis Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Methods Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 µg/kg intravenous bolus followed by a 0.01 µg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Results Plasma aldosterone increased by 2.2 ± 1.6 ng/dL after Furosemide alone, decreased by 3.9 ± 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 ± 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Conclusions Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone. Copyright © 2010 Wiley Periodicals, Inc.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 microg/kg intravenous bolus followed by a 0.01 microg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Plasma aldosterone increased by 2.2 +/- 1.6 ng/dL after Furosemide alone, decreased by 3.9 +/- 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 +/- 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone.
Domenic A. Sica - One of the best experts on this subject based on the ideXlab platform.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:Background In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Hypothesis Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Methods Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 µg/kg intravenous bolus followed by a 0.01 µg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Results Plasma aldosterone increased by 2.2 ± 1.6 ng/dL after Furosemide alone, decreased by 3.9 ± 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 ± 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Conclusions Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone. Copyright © 2010 Wiley Periodicals, Inc.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 microg/kg intravenous bolus followed by a 0.01 microg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Plasma aldosterone increased by 2.2 +/- 1.6 ng/dL after Furosemide alone, decreased by 3.9 +/- 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 +/- 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone.
Mark C Haigney - One of the best experts on this subject based on the ideXlab platform.
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Furosemide and the progression of left ventricular dysfunction in experimental heart failure
Journal of the American College of Cardiology, 2004Co-Authors: John M Mccurley, Stephen U Hanlon, Shaokui Wei, Erich F Wedam, Michael Michalski, Mark C HaigneyAbstract:Objectives We tested the hypothesis that Furosemide accelerates the progression of left ventricular systolic dysfunction in a tachycardia-induced porcine model of heart failure. Background Furosemide activates the renin-angiotensin-aldosterone system in patients with congestive heart failure (CHF). Such activation may contribute to CHF progression, but prospective data are lacking. Methods Thirty-two Yorkshire pigs were randomized to Furosemide (1 mg/kg intramuscularly daily, mean 16.1 ± 0.9 mg) or placebo. Thereafter, a pacing model of heart failure was utilized to produce systolic dysfunction in both sets of animals (fractional shortening Results Furosemide shortened the time to left ventricular dysfunction (35.1 ± 5.1 days in placebo versus 21.4 ± 3.2 days for Furosemide animals; p = 0.038, log-rank test). By day 14, aldosterone levels were significantly higher in Furosemide animals (43.0 ± 11.8 ng/dl vs. 17.6 ± 4.5 ng/dl; p Conclusions Tachycardic pigs given Furosemide had significant acceleration of both contractile and metabolic features of CHF, including left ventricular systolic dysfunction, elevated serum aldosterone levels, and altered calcium handling in a controlled experimental model of heart failure.
Warren Pavey - One of the best experts on this subject based on the ideXlab platform.
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does Furosemide increase oxidative stress in acute kidney injury
Antioxidants & Redox Signaling, 2017Co-Authors: Benjamin I Silbert, Jeffrey Lipman, Jason A Roberts, Tomas Corcoran, David J R Morgan, Warren PaveyAbstract:Abstract Furosemide, a loop diuretic, is used to increase urine output in patients with acute kidney injury (AKI). It remains uncertain whether the benefits of Furosemide in AKI outweigh its potential harms. We investigated if Furosemide influenced oxidative stress in 30 critically ill patients with AKI by measuring changes in F2-isoprostanes (F2-IsoPs), markers of in vivo oxidative stress, in plasma and urine following intravenous Furosemide. Urine F2-IsoPs were higher in sepsis (p = 0.001) and increased in proportion to urine Furosemide (p = 0.001). The Furosemide-induced increase in urine F2-IsoPs differed depending on AKI severity (p < 0.001) and was greatest in those with the most severe AKI. Furosemide had no effect on plasma F2-IsoPs. We demonstrate for the first time that Furosemide increases renal oxidative stress in AKI and find that patients with the most severe AKI—to whom the largest doses are likely to be administered—showed the greatest increase in oxidative stress. These findings lead to t...
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determinants of urinary output response to iv Furosemide in acute kidney injury a pharmacokinetic pharmacodynamic study
Critical Care Medicine, 2016Co-Authors: Benjamin I Silbert, Jeffrey Lipman, Jason A Roberts, Tomas Corcoran, David J R Morgan, Warren PaveyAbstract:Objectives: This study assessed the determinants of urinary output response to Furosemide in acute kidney injury; specifically, whether the response is related to altered pharmacokinetics or pharmacodynamics. Design: Prospective cohort. Setting: Tertiary ICU. Patients: Thirty critically ill patients with acute kidney injury without preexisting renal impairment or recent diuretic exposure. Intervention: A single dose of IV Furosemide. Measurements and Main Results: Baseline markers of intravascular volume status were obtained prior to administering Furosemide. Six-hour creatinine clearance, hourly plasma/urinary Furosemide concentrations, and hourly urinary output were used to assess Furosemide pharmacokinetics/pharmacodynamics parameters. Of 30 patients enrolled, 11 had stage-1 (37%), nine had stage-2 (30%), and 10 had stage-3 (33%) Acute Kidney Injury Network acute kidney injury. Seventy-three percent were septic, 47% required norepinephrine, and 53% were mechanically ventilated. Urinary output doubled in 20 patients (67%) following IV Furosemide. Measured creatinine clearance was strongly associated with the amount of urinary Furosemide excreted and was the only reliable predictor of the urinary output after Furosemide (area under the receiver-operating-characteristic curve, 0.75; 95% CI, 0.57-0.93). In addition to an altered pharmacokinetics (p < 0.01), a reduced pharmacodynamics response to Furosemide also became important when creatinine clearance was reduced to less than 40 mL/min/1.73 m 2 (p = 0.01). Acute kidney injury staging and markers of intravascular volume, including central venous pressure, brain-natriuretic-peptide concentration, and fractional urinary sodium excretion were not predictive of urinary output response to Furosemide. Conclusions: The severity of acute kidney injury, as reflected by the measured creatinine clearance, alters both pharmacokinetics and pharmacodynamics of Furosemide in acute kidney injury, and was the only reliable predictor of the urinary output response to Furosemide in acute kidney injury.
Ron M. Oren - One of the best experts on this subject based on the ideXlab platform.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:Background In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Hypothesis Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Methods Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 µg/kg intravenous bolus followed by a 0.01 µg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Results Plasma aldosterone increased by 2.2 ± 1.6 ng/dL after Furosemide alone, decreased by 3.9 ± 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 ± 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Conclusions Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone. Copyright © 2010 Wiley Periodicals, Inc.
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Natriuretic and neurohormonal responses to nesiritide, Furosemide, and combined nesiritide and Furosemide in patients with stable systolic dysfunction.
Clinical cardiology, 2010Co-Authors: Domenic A. Sica, Ron M. Oren, Mildred D. Gottwald, Roger M. MillsAbstract:In patients with heart failure, few data describe the neurohormonal response to nesiritide and Furosemide either alone or in combination. This study systematically compared the effects of nesiritide, Furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Natriuretic, diuretic, and neurohormonal responses to Furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) Furosemide, 40 mg intravenous bolus; (2) nesiritide, 2 microg/kg intravenous bolus followed by a 0.01 microg/kg/min infusion for 6 hours; (3) both Furosemide and nesiritide, with Furosemide given at least 15 minutes after initiation of nesiritide. Plasma aldosterone increased by 2.2 +/- 1.6 ng/dL after Furosemide alone, decreased by 3.9 +/- 1.6 ng/dL after nesiritide alone (P = 0.005 vs Furosemide alone and P = 0.56 vs Furosemide plus nesiritide), and decreased by 2.8 +/- 1.6 ng/dL after Furosemide plus nesiritide (P = 0.02 vs Furosemide alone). Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis, but decreased plasma aldosterone values. When Furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with Furosemide alone, without the anticipated increase in plasma aldosterone observed with Furosemide alone.
