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Tianxin Yang - One of the best experts on this subject based on the ideXlab platform.

Marco Guazzi - One of the best experts on this subject based on the ideXlab platform.

  • 948 52 paradoxical neurohumoral axis inhibition after Body Fluid Volume depletion in patients with congestive heart failure and water retention
    Journal of the American College of Cardiology, 1995
    Co-Authors: Marco Guazzi, Piergiuseppe Agostoni, Gianfranco Lauri, Battista G Perego, Francesco Giraldi, Marco Matturri, Marco Guazzi, Giancarlo Marenzl
    Abstract:

    Background Hypovolemia stimulates the sympathoadrenal and renin systems and water retention. In congestive heart failure (CHF) reduction of cardiac output (CO) and, to the extent that it occurs, decrease of blood pressure (BP), have been suggested to be perceived as a state of underfilling of the arterial compartment, and to promote and perpetuate neurohumoral activation and retention of Fluid. This study was aimed to probe whether intravascular Volume deficit accounts for patterns that largely exceed the limits of a homeostatic response, as sometimes observed in more advanced stages of the syndrome. We reduced the Body Fluid mass with a non-pharmacological method, ultrafiltration (UF), in patients with CHF and water retention, and monitored the neurohumoral reaction. Methods and Results In 22 patients, UF was performed with a diafilter, which was part of an external venous circuit, whose flow was regulated to produce 500 ml/hour of ultrafiltrate (average total amount = 3122 ± 1199 ml) until right atrial pressure was lowered to 50% of baseline. Hemodynamics, plasma renin activity (PRA), norepinephrine (NE) and aldosterone (AL) were evaluated before and in the 48 hours after UF. Soon after the procedure, associated with a 20% reduction of plasma Volume (PV) and a moderate decrease of CO and BP (consistent with a diminished degree of filling of the arterial compartment), there was an obvious fall of NE, PRA and AL. In the next 48 hours we recorded a) recovery of PV. CO and BP, b) increasing depression of the neurohumoral axis, c) striking enhancement of water and sodium excretion and resolution of peripheral edema and organ congestion. Changes of NE, PRA or AL were not related to changes of PV. CO and BP (variations in the state of arterial filling) and significantly correlated with the increase of urinary output and sodium excretion. Conclusions Arterial underlilling, as a the main mechanism for activation of the neurohumoral axis and retention of Fluid, does not apply to the more advanced stages of CHF. The parallelism observed between fall of circulating hormones and reabsorption of extravascular Fluid suggests that hypoperfusion and/or congestion of organ, like kidney and lung, may reduce the clearance of circulating norepinephrine and contribute to keep renin and aldosterone raised. A positive feedback loop between Fluid retention and plasma hormone levels appears to be a mechanism of progression of the syndrome.

  • apparent paradox of neurohumoral axis inhibition after Body Fluid Volume depletion in patients with chronic congestive heart failure and water retention
    Heart, 1994
    Co-Authors: Piergiuseppe Agostoni, Gianfranco Lauri, Battista G Perego, Francesco Giraldi, Marco Matturri, Marco Guazzi, A Salvioni, Giancarlo Marenzi
    Abstract:

    BACKGROUND--Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of Fluid. This study examined whether an intravascular Volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure. METHODS AND RESULTS--In 22 patients with congestive heart failure and water retention the Body Fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma Volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma Volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion. CONCLUSIONS--In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining Fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular Fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between Fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.

Hui Zhang - One of the best experts on this subject based on the ideXlab platform.

Giancarlo Marenzl - One of the best experts on this subject based on the ideXlab platform.

  • 948 52 paradoxical neurohumoral axis inhibition after Body Fluid Volume depletion in patients with congestive heart failure and water retention
    Journal of the American College of Cardiology, 1995
    Co-Authors: Marco Guazzi, Piergiuseppe Agostoni, Gianfranco Lauri, Battista G Perego, Francesco Giraldi, Marco Matturri, Marco Guazzi, Giancarlo Marenzl
    Abstract:

    Background Hypovolemia stimulates the sympathoadrenal and renin systems and water retention. In congestive heart failure (CHF) reduction of cardiac output (CO) and, to the extent that it occurs, decrease of blood pressure (BP), have been suggested to be perceived as a state of underfilling of the arterial compartment, and to promote and perpetuate neurohumoral activation and retention of Fluid. This study was aimed to probe whether intravascular Volume deficit accounts for patterns that largely exceed the limits of a homeostatic response, as sometimes observed in more advanced stages of the syndrome. We reduced the Body Fluid mass with a non-pharmacological method, ultrafiltration (UF), in patients with CHF and water retention, and monitored the neurohumoral reaction. Methods and Results In 22 patients, UF was performed with a diafilter, which was part of an external venous circuit, whose flow was regulated to produce 500 ml/hour of ultrafiltrate (average total amount = 3122 ± 1199 ml) until right atrial pressure was lowered to 50% of baseline. Hemodynamics, plasma renin activity (PRA), norepinephrine (NE) and aldosterone (AL) were evaluated before and in the 48 hours after UF. Soon after the procedure, associated with a 20% reduction of plasma Volume (PV) and a moderate decrease of CO and BP (consistent with a diminished degree of filling of the arterial compartment), there was an obvious fall of NE, PRA and AL. In the next 48 hours we recorded a) recovery of PV. CO and BP, b) increasing depression of the neurohumoral axis, c) striking enhancement of water and sodium excretion and resolution of peripheral edema and organ congestion. Changes of NE, PRA or AL were not related to changes of PV. CO and BP (variations in the state of arterial filling) and significantly correlated with the increase of urinary output and sodium excretion. Conclusions Arterial underlilling, as a the main mechanism for activation of the neurohumoral axis and retention of Fluid, does not apply to the more advanced stages of CHF. The parallelism observed between fall of circulating hormones and reabsorption of extravascular Fluid suggests that hypoperfusion and/or congestion of organ, like kidney and lung, may reduce the clearance of circulating norepinephrine and contribute to keep renin and aldosterone raised. A positive feedback loop between Fluid retention and plasma hormone levels appears to be a mechanism of progression of the syndrome.

Marco Matturri - One of the best experts on this subject based on the ideXlab platform.

  • 948 52 paradoxical neurohumoral axis inhibition after Body Fluid Volume depletion in patients with congestive heart failure and water retention
    Journal of the American College of Cardiology, 1995
    Co-Authors: Marco Guazzi, Piergiuseppe Agostoni, Gianfranco Lauri, Battista G Perego, Francesco Giraldi, Marco Matturri, Marco Guazzi, Giancarlo Marenzl
    Abstract:

    Background Hypovolemia stimulates the sympathoadrenal and renin systems and water retention. In congestive heart failure (CHF) reduction of cardiac output (CO) and, to the extent that it occurs, decrease of blood pressure (BP), have been suggested to be perceived as a state of underfilling of the arterial compartment, and to promote and perpetuate neurohumoral activation and retention of Fluid. This study was aimed to probe whether intravascular Volume deficit accounts for patterns that largely exceed the limits of a homeostatic response, as sometimes observed in more advanced stages of the syndrome. We reduced the Body Fluid mass with a non-pharmacological method, ultrafiltration (UF), in patients with CHF and water retention, and monitored the neurohumoral reaction. Methods and Results In 22 patients, UF was performed with a diafilter, which was part of an external venous circuit, whose flow was regulated to produce 500 ml/hour of ultrafiltrate (average total amount = 3122 ± 1199 ml) until right atrial pressure was lowered to 50% of baseline. Hemodynamics, plasma renin activity (PRA), norepinephrine (NE) and aldosterone (AL) were evaluated before and in the 48 hours after UF. Soon after the procedure, associated with a 20% reduction of plasma Volume (PV) and a moderate decrease of CO and BP (consistent with a diminished degree of filling of the arterial compartment), there was an obvious fall of NE, PRA and AL. In the next 48 hours we recorded a) recovery of PV. CO and BP, b) increasing depression of the neurohumoral axis, c) striking enhancement of water and sodium excretion and resolution of peripheral edema and organ congestion. Changes of NE, PRA or AL were not related to changes of PV. CO and BP (variations in the state of arterial filling) and significantly correlated with the increase of urinary output and sodium excretion. Conclusions Arterial underlilling, as a the main mechanism for activation of the neurohumoral axis and retention of Fluid, does not apply to the more advanced stages of CHF. The parallelism observed between fall of circulating hormones and reabsorption of extravascular Fluid suggests that hypoperfusion and/or congestion of organ, like kidney and lung, may reduce the clearance of circulating norepinephrine and contribute to keep renin and aldosterone raised. A positive feedback loop between Fluid retention and plasma hormone levels appears to be a mechanism of progression of the syndrome.

  • apparent paradox of neurohumoral axis inhibition after Body Fluid Volume depletion in patients with chronic congestive heart failure and water retention
    Heart, 1994
    Co-Authors: Piergiuseppe Agostoni, Gianfranco Lauri, Battista G Perego, Francesco Giraldi, Marco Matturri, Marco Guazzi, A Salvioni, Giancarlo Marenzi
    Abstract:

    BACKGROUND--Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of Fluid. This study examined whether an intravascular Volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure. METHODS AND RESULTS--In 22 patients with congestive heart failure and water retention the Body Fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma Volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma Volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion. CONCLUSIONS--In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining Fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular Fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between Fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.