ten Oever J, Mandon J, Netea M G, van Deuren M, Harren F J M, Cristescu S M, Pickkers P
Department of Internal Medicine, Radboud University Nijmegen Medical Centre, The Netherlands.
J Breath Res. 2013 Sep;7(3):036003. doi: 10.1088/1752-7155/7/3/036003. Epub 2013 Jul 18.
Nitric oxide (NO) is a key mediator in the pathophysiology of septic shock that can be measured in exhaled breath. To assess whether a pulmonary infection itself or systemic inflammation is responsible for NO production, we determined exhaled NO in ventilated patients with respiratory and non-respiratory septic shock and compared it with the concentration in ventilated intensive care patients without systemic inflammation. In addition, the change of NO production over time and correlations with haemodynamic instability were evaluated. The controls without systemic inflammation, as witnessed by the absence of systemic inflammatory response syndrome criteria and low levels of interleukin-6, had similar concentrations of NO as the patients with non-respiratory septic shock. The respiratory sepsis patients exhaled more NO than the non-respiratory sepsis patients (p = 0.05), and a time dependent decline in time in both groups (p = 0.04). Exhaled NO did not correlate with markers of disease severity, systemic inflammation and haemodynamic instability. These data indicate that the infected lungs are the source of exhaled NO.
一氧化氮（NO）是脓毒性休克病理生理学中的关键介质，可在呼出气体中检测到。为了评估肺部感染本身或全身炎症是否是产生NO的原因，我们测定了患有呼吸性和非呼吸性脓毒性休克的通气患者呼出的NO，并将其与没有全身炎症的通气重症监护患者的浓度进行比较。此外，还评估了NO产生随时间的变化以及与血流动力学不稳定的相关性。没有全身炎症的对照组，通过缺乏全身炎症反应综合征标准和低水平的白细胞介素-6得以证实，其NO浓度与非呼吸性脓毒性休克患者相似。呼吸性脓毒症患者呼出的NO比非呼吸性脓毒症患者更多（p = 0.05），并且两组患者呼出的NO均随时间呈下降趋势（p = 0.04）。呼出的NO与疾病严重程度、全身炎症和血流动力学不稳定的标志物无关。这些数据表明，受感染的肺部是呼出NO的来源。
