Myles Paul S, Chan Matthew T V, Kaye David M, McIlroy David R, Lau Chung-Wai, Symons Joel A, Chen Shaohui
Department of Anaesthesia and Perioperative Medicine, Alfred Hospital, Melbourne, Victoria, Australia.
Anesthesiology. 2008 Oct;109(4):657-63. doi: 10.1097/ALN.0b013e31818629db.
Endothelial function is impaired with hyperhomocysteinemia. Plasma homocysteine is increased by nitrous oxide anesthesia. The current study was designed to determine whether endothelial function is impaired after surgery and whether this is made worse by exposure to nitrous oxide.
The authors studied 59 patients with cardiovascular disease undergoing noncardiac surgery. Patients were randomly allocated to nitrous oxide-based anesthesia (n = 25) or nitrous oxide-free anesthesia (control, n = 34). Endothelial function was measured by flow-mediated dilation of the brachial artery before and 24 h after surgery. In addition, blood was drawn at both time points for the measurements of plasma homocysteine, folate, L-arginine, L-citrulline, asymmetric dimethylarginine, and nitrate concentrations.
The median duration of general anesthesia was 4.5 h. Patients had significantly lower flow-mediated dilation after surgery (5.1 +/- 3.3 to 3.0 +/- 4.1%; P = 0.001). Duration of anesthesia affected endothelial function. In the nitrous oxide group, there was an inverse correlation with flow-mediated dilation (r = -0.60, P = 0.004), but in the control group, there was a positive correlation (r = 0.61, P < 0.001). When compared with control, nitrous oxide exposure was associated with a significant increase in postoperative homocysteine (mean difference, 4.9 microm; 95% confidence interval, 2.8-7.0 microm; P < 0.0005) and decrease in flow-mediated dilation (3.2%; 95% confidence interval, 0.1-5.3%; P = 0.001). Nitrous oxide exposure was not associated with change in nitric oxide substrates.
Nitrous oxide-based anesthesia increased plasma homocysteine and significantly impaired endothelial function in patients undergoing noncardiac surgery. Nitrous oxide-based anesthesia could be a risk factor for postoperative cardiovascular morbidity.
高同型半胱氨酸血症会损害内皮功能。氧化亚氮麻醉会使血浆同型半胱氨酸升高。本研究旨在确定手术后内皮功能是否受损，以及接触氧化亚氮是否会使其恶化。
作者研究了59例接受非心脏手术的心血管疾病患者。患者被随机分配至基于氧化亚氮的麻醉组（n = 25）或无氧化亚氮麻醉组（对照组，n = 34）。在手术前及术后24小时通过肱动脉血流介导的血管舒张来测量内皮功能。此外，在两个时间点采集血液以测量血浆同型半胱氨酸、叶酸、L-精氨酸、L-瓜氨酸、不对称二甲基精氨酸和硝酸盐浓度。
全身麻醉的中位持续时间为4.5小时。患者术后血流介导的血管舒张明显降低（从5.1±3.3降至3.0±4.1%；P = 0.001）。麻醉持续时间影响内皮功能。在氧化亚氮组中，与血流介导的血管舒张呈负相关（r = -0.60，P = 0.004），但在对照组中呈正相关（r = 0.61，P < 0.001）。与对照组相比，接触氧化亚氮与术后同型半胱氨酸显著升高（平均差异，4.9 μmol；95%置信区间，2.8 - 7.0 μmol；P < 0.0005）及血流介导的血管舒张降低（3.2%；95%置信区间，0.1 - 5.3%；P = 0.001）相关。接触氧化亚氮与一氧化氮底物的变化无关。
基于氧化亚氮的麻醉会增加接受非心脏手术患者的血浆同型半胱氨酸并显著损害内皮功能。基于氧化亚氮的麻醉可能是术后心血管发病的一个危险因素。
