Mengistu A M, Wolf M W, Boldt J, Röhm K D, Suttner S W, Piper S N
Klinikum Ludwigshafen, Department of Anaesthesiology and Intensive Care Medicine, Bremserstrasse 79, D-67063 Ludwigshafen, Germany.
Eur J Anaesthesiol. 2007 Jun;24(6):529-34. doi: 10.1017/S0265021506002286. Epub 2007 Jan 23.
Atrial 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.
We 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.
Preoperative 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.
Controlled 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.
心房利钠肽和脑利钠肽由心肌细胞合成,是继发于心室容量扩张和充盈压升高而分泌的介质。本研究旨在评估接受控制性低血压的鼻内镜鼻窦手术患者的血清心房利钠肽和脑利钠肽浓度。
我们研究了45例无心血管病史、计划行择期鼻内镜鼻窦手术的患者。患者被分为三组之一:使用艾司洛尔(n = 15)或硝普钠(n = 15)诱导控制性低血压,平均动脉压维持在50 - 55 mmHg。对照组(n = 15)平均动脉压调整为70 - 80 mmHg。分别于术前(T1)、手术结束时(T2)、术后2小时(T3)、24小时(T4)和48小时(T5)测定心房利钠肽和脑利钠肽。
术前所有组的心房利钠肽和脑利钠肽血浆水平均在正常范围内且相似。与对照组相比,接受艾司洛尔治疗的患者(心房利钠肽:2.46 ± 0.75 μg mL⁻¹;脑利钠肽:4.34 ± 3.06 μg mL⁻¹)和硝普钠治疗的患者(心房利钠肽:2.48 ± 0.92 μg mL⁻¹;脑利钠肽:4.49 ± 3.21 μg mL⁻¹)在T2和T3时心房利钠肽和脑利钠肽浓度显著降低(对照组:心房利钠肽:5.31 ± 2.32 μg mL⁻¹;脑利钠肽:13.26 ± 8.98 μg mL⁻¹,P < 0.01),且出血量和手术时间减少。
控制性低血压可降低心血管健康患者利钠肽的释放。这种效应可能是由于全身阻力降低和灌注压降低导致心脏充盈压改变所致。