Mechanical diuresis: a novel treatment for patients with decompensated heart failure
Mitchell SaltzbergMaria Rosa CostanzoMary C. O'NeillJoAnne PouillotMarilyn ArnoldNancy J. BurkeHoward S. RothAngelo Makris
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Intravascular volume status
The mechanism by which the nondiuretic mercurial, p -chloromercuribenzoic acid ( p -CMB), prevents and reverses mercurial diuresis has been studied in different types of experiments. Histochemical data are presented which indicate that the reduction in protein-bound sulfhydryl concentrations in cells of the renal tubules in rats produced by p -CMB is not additive with that produced by diuretic mercurials, while the effects of two diuretic mercurials are additive. Measurement in dogs of the mercury 203 content of plugs of renal cortex, before and after injection of p -CMB, indicates that p -CMB displaces diuretic mercury from the kidney in proportion to the dose administered. This renal loss of mercury is due to an increased loss of mercury in the urine and to the blood which leaves the kidney. The dose-response relationship between diuretic mercuric glutathione and p -CMB has been studied in acidotic and alkalotic dogs and indicates that the 50% blocking dose is not related to the diuretic dose in a simple or direct way. The reasons for this are discussed. The experiments provide evidence that only a small amount of mercury is involved in the production of the diuresis, and that mercaptide formation is not per se the cause of diuresis, but is an essential part of the interaction between mercury and its renal receptor.
Mercury
Renal cortex
Dose dependence
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Congestive heart failure is a complex clinical hemodynamic disorder characterized by chronic and progressive pump failure and fluid accumulation. Although the overall impact of diuretic therapy on congestive heart failure mortality remains unknown, diuretics remain a vital component of symptomatic congestive heart failure management. Over time, sodium and water excretion are equalized before adequate fluid elimination occurs. This phenomenon is thought to occur in one out of three patients with congestive heart failure on diuretic therapy and is termed diuretic resistance. In congestive heart failure, both pharmacokinetic and pharmacodynamic alterations are thought to be responsible for diuretic resistance. Due to disease chronicity, symptomatic management is vital to improved quality of life and enhancing diuretic response is therefore pivotal.
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Loop diuretics are recommended to treat congestive symptoms in patients with heart failure. However, observational studies have indicated that loop diuretic treatment in heart failure is associated with increased mortality. Therefore, loop diuretic discontinuation or dose reduction, when clinically possible, is recommended. Our aim was to study nationwide temporal trends in loop diuretic treatment from 2005 to 2014 in real-life patients with chronic heart failure.Data from the nationwide Swedish National Patient, Prescribed Drug and Cause of Death Registers were linked. The annual proportions of patients with chronic heart failure treated with loop diuretics from 2005 to 2014 were calculated. In addition, the annual median loop diuretic doses (DDD) in patients with chronic heart failure treated with loop diuretics from 2005 to 2014 were calculated.The proportion of real-life patients with chronic heart failure treated with loop diuretics decreased from 73.2% in 2005 to 65.7% in 2014 (p for trend < 0.001). The median loop diuretic DDD in real-life patients with chronic heart failure decreased from 2.13 (IQR 1.09-2.77) in 2005 to 1.63 (IQR 1.09-2.25) in 2014 (p = 0.001 for trend).Loop diuretic treatment decreased from 2005 to 2014 in real-life patients with chronic heart failure. The prognostic impact of changes in loop diuretic treatment in patients with heart failure remains unclear.
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Renal medulla
Red Cell
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Abstract Three preparations of Satureja montana subsp. montana leaves were tested for diuretic activity in rats: an infusion, a water‐alcohol extract and essential oil. In 1‐day experiments, the cumulative volume of urine was collected during the first 5 h after oral administration of 5 mL/100 g body weight of plant preparation. It was established that all the preparations tested initially caused a decrease in diuresis and subsequently a mild stimulation of diuresis. 0.1% solution of essential oil was considered to be a therapeutic dose, whereas 0.5% and 1% solutions caused toxic symptoms in the animals. A further experiment involving treatment of rats for 3 days with a 10% drug infusion and 0.1% essential oil solution demonstrated the considerable diuretic activity of winter savory.
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Congestive heart failure is a disease state distinguished by the regular presence of both renal and hepatic abnormalities in drug handling. One such abnormality involves flaws in the process of drug absorption. In most instances, congestive heart failure‐related abnormalities in drug absorption are of inconsequential significance. However, this is not the case with loop diuretics. Loop diuretic action ordinarily tracks the rate and extent of absorption if a sufficient amount of diuretic has been given to exceed the threshold for diuretic effect. In congestive heart failure, both the rate and absolute amount of loop diuretic absorbed can be reduced as a function of the heart failure state itself. In this setting, drug dissolution characteristics can assume added significance. Furosemide is the loop diuretic with the widest intra‐ and interpatient variability of absorption. Alternatively, the loop diuretic torsemide is rapidly and fairly completely absorbed independent of the heart failure state. This pattern of absorption establishes it as the preferred loop diuretic in the otherwise diuretic‐resistant heart failure patient. However, the exact role of torsemide in the outpatient management of congestive heart failure remains to be determined.
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Lack of diuretic efficiency (but not low diuresis) early in an acutely decompensated heart failure episode is associated with increased 180-day mortality: CO-008 J Ferreira;N Girerd;F Zannad;P Rossignol; Fundamental and Clinical Pharmacology
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Diuretic therapy entails decreased plasma concentrations of thiamine and riboflavine. Vitamins eliminated with urine more rapidly when diuresis accelerates. This process is not related to diuresis cause. A linear relationship exists between diuresis intensity and amount of eliminated thiamine and riboflavine. Thus it is shown that diuretic therapy provokes thiamine and riboflavine elimination from the body.
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SummaryTHA administered subcutaneously caused a dose-related diuresis in rats. This diuretic response was probably not due to a muscarinic action of THA, as the diuresis was not blocked by atropine. Preliminary experiments in the dog and the chicken indicate that in these species there was little if any direct renal effect. The diuretic response to THA in rats does not appear to involve release of a pituitary hormone since hypophysectomy did not abolish the diuretic effect of THA.
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