• A M Mengistu, M W Wolf, J Boldt, K D Röhm, S W Suttner, and S N Piper.
• Klinikum Ludwigshafen, Department of Anaesthesiology and Intensive Care Medicine, Bremserstrasse 79, D-67063 Ludwigshafen, Germany. a.mengistu@gmx.de
• Eur J Anaesthesiol. 2007 Jun 1;24(6):529-34.

Background And ObjectiveAtrial and brain natriuretic peptide, synthesized by cardiac myocytes, are mediators secreted secondary to cardiac volume expansion and increased filling pressure. The study was designed to assess serum concentration of atrial and brain natriuretic peptide in patients undergoing endonasal sinus surgery receiving controlled hypotension.MethodsWe studied 45 patients without cardiovascular history, scheduled for elective endonasal sinus surgery. Patients were allocated to one of three groups: controlled hypotension was induced either by using esmolol (n = 15) or sodium nitroprusside (n = 15) with a mean arterial pressure of 50-55 mmHg. In the control group (n = 15), mean arterial pressure was adjusted to 70-80 mmHg. Atrial and brain natriuretic peptides were measured preoperatively (T1), at the end of surgery (T2), 2 h (T3), 24 h (T4) and 48 h (T5) postoperatively.ResultsPreoperative atrial and brain natriuretic peptide plasma levels were within normal ranges and similar between all groups. Patients treated with esmolol (atrial natriuretic peptide: 2.46 +/- 0.75 microg mL(-1) brain natriuretic peptide: 4.34 +/- 3.06 microg mL(-1)) and sodium nitropusside (atrial natriuretic peptide: 2.48 +/- 0.92 microg mL(-1); brain natriuretic peptide: 4.49 +/- 3.21 microg mL(-1)) showed significantly lower concentrations of atrial and brain natriuretic peptide at T2 and T3 compared with controls (atrial natriuretic peptide: 5.31 +/- 2.32 microg mL(-1); brain natriuretic peptide: 13.26 +/- 8.98 microg mL(-1)) , P < 0.01) as well as a reduction in blood loss and duration of surgery.ConclusionsControlled hypotension decreases the release of natriuretic peptides in cardiovascular healthy patients. This effect may be contributed to by changes in cardiac filling pressure due to lower systemic resistance and diminished perfusion pressure.

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