Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure

Carlo M. Cipolla, Sergio Grazi, Andrea Rimondini, Giuseppe Susini, Marco Guazzi, Paolo Della Bella, Maurizio D. Guazzi

Research output: Contribution to journalArticle

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Abstract

In congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 ± 1,228 ml) lowered plasma norepinephrine by 515 ± 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 ± 415 ml; changes were prompt and correlated inversely (r = -0.7; p <0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.

Original languageEnglish
Pages (from-to)987-994
Number of pages8
JournalThe American Journal of Cardiology
Volume66
Issue number12
DOIs
Publication statusPublished - Oct 15 1990

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Hemofiltration
Norepinephrine
Heart Failure
Diuresis
Kidney
Neural Inhibition
Renin
Cardiac Output
Vascular Resistance
Pulmonary Artery
Arterial Pressure
Perfusion
Pressure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure. / Cipolla, Carlo M.; Grazi, Sergio; Rimondini, Andrea; Susini, Giuseppe; Guazzi, Marco; Bella, Paolo Della; Guazzi, Maurizio D.

In: The American Journal of Cardiology, Vol. 66, No. 12, 15.10.1990, p. 987-994.

Research output: Contribution to journalArticle

Cipolla, Carlo M. ; Grazi, Sergio ; Rimondini, Andrea ; Susini, Giuseppe ; Guazzi, Marco ; Bella, Paolo Della ; Guazzi, Maurizio D. / Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure. In: The American Journal of Cardiology. 1990 ; Vol. 66, No. 12. pp. 987-994.
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N2 - In congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 ± 1,228 ml) lowered plasma norepinephrine by 515 ± 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 ± 415 ml; changes were prompt and correlated inversely (r = -0.7; p <0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.

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