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Anesth Analg 2001;93:676-682
© 2001 International Anesthesia Research Society


CRITICAL CARE AND TRAUMA

Differential Secretion of Atrial and Brain Natriuretic Peptide in Critically Ill Patients

Elmar Berendes, MD*, Hugo Van Aken, MD, PhD, FRCA, FANZCA*, Carsten Raufhake, MD*, Christoph Schmidt, MD*, Gerd Assmann, MD, FRCP{dagger}, and Michael Walter, MD{dagger}

*Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin and {dagger}Institut für Klinische Chemie und Laboratoriumsmedizin, Westfälische Wilhelms-Universität Münster, Münster, Germany

Address correspondence and reprint requests to PD Dr. Elmar Berendes, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Westfälische Wilhelms-Universität Münster, Albert-Schweitzer-Strasse 33, 48149 Münster, Germany. Address e-mail to berenel{at}uni-muenster.de

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are cardiac hormones with natriuretic, vasorelaxant, and aldosterone-inhibiting properties. We analyzed the plasma of 178 critically ill patients for ANP, BNP, aldosterone, and serum sodium concentration, as well as serum and urine osmolality and sodium filtration fraction. Mean plasma concentrations of ANP and BNP were increased in critically ill patients compared with healthy controls (ANP, 14.3 ± 5.8 pmol/L versus 8.8 ± 3.2 pmol/L, P < 0.05; BNP, 26.2 ± 10.7 pmol/L versus 4.6 ± 2.8 pmol/L, P < 0.0001). The relative increases in ANP concentrations were comparable in all diseases. BNP concentrations, by contrast, showed a wider variation. The largest BNP concentrations were observed in patients who underwent cardiac surgical procedures and in patients with subarachnoid hemorrhage. ANP, but not BNP, was correlated with aldosterone levels (r = 0.4, P < 0.001), serum sodium (r = 0.42, P < 0.001), sodium filtration fraction (r = 0.3, P < 0.001), serum osmolality (r = 0.25, P < 0.01), urinary osmolality (r = -0.24, P < 0.01), and central venous pressure (r = 0.22, P < 0.01). ANP and BNP concentrations were increased in critically ill patients; however, this did not correlate with the severity of illness or mortality. Our data support a regulatory role for ANP in the maintenance of water and electrolyte balance. The physiologic role of BNP, by contrast, is less clear. ANP and BNP are not predictors for the severity of illness and mortality in critically ill patients.

IMPLICATIONS: The pathophysiologic role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in critically ill patients is not clear. It is generally assumed that ANP and BNP have similar physiologic effects. We found a different secretion pattern in our patients, and this finding suggests a distinct role for ANP and BNP in the postoperative and posttraumatic period.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2001 by the International Anesthesia Research Society.