Wrigge H, Zinserling J, Stüber F, von Spiegel T, Hering R, Wetegrove S, Hoeft A, Putensen C
Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Germany.
Anesthesiology. 2000 Dec;93(6):1413-7. doi: 10.1097/00000542-200012000-00012.
Mechanical ventilation with high tidal volumes (V(T)) in contrast to mechanical ventilation with low V(T) has been shown to increase plasma levels of proinflammatory and antiinflammatory mediators in patients with acute lung injury. The authors hypothesized that, in patients without previous lung injury, a conventional potentially injurious ventilatory strategy with high V(T) and zero end-expiratory pressure (ZEEP) will not cause a cytokine release into systemic circulation.
A total of 39 patients with American Society of Anesthesiologists physical status I-II and without signs of systemic infection scheduled for elective surgery with general anesthesia were randomized to receive mechanical ventilation with either (1) V(T) = 15 ml/kg ideal body weight on ZEEP, (2) V(T) = 6 ml/kg ideal body weight on ZEEP, or (3) V(T) = 6 ml/kg ideal body weight on positive end-expiratory pressure of 10 cm H2O. Plasma levels of proinflammatory and antiinflammatory mediators tumor necrosis factor, interleukin (IL)-6, IL-10, and IL-1 receptor antagonist were determined before and 1 h after the initiation of mechanical ventilation.
Plasma levels of all cytokines remained low in all settings. IL-6, tumor necrosis factor, and IL-1 receptor antagonist did not change significantly after 1 h of mechanical ventilation. IL-10 was below the detection limit (10 pg/ml) in 35 of 39 patients. There were no differences between groups.
Initiation of mechanical ventilation for 1 h in patients without previous lung injury caused no consistent changes in plasma levels of studied mediators. Mechanical ventilation with high V(T) on ZEEP did not result in higher cytokine levels compared with lung-protective ventilatory strategies. Previous lunge damage seems to be mandatory to cause an increase in plasma cytokines after 1 h of high V(T) mechanical ventilation.
与低潮气量(V(T))机械通气相比,高潮气量机械通气已被证明会增加急性肺损伤患者促炎和抗炎介质的血浆水平。作者推测,在既往无肺损伤的患者中,采用高潮气量和零呼气末正压(ZEEP)的传统潜在有害通气策略不会导致细胞因子释放到体循环中。
总共39例美国麻醉医师协会身体状况为I-II级且无全身感染迹象、计划接受全身麻醉择期手术的患者被随机分组,分别接受以下机械通气:(1)ZEEP模式下V(T)=15 ml/kg理想体重;(2)ZEEP模式下V(T)=6 ml/kg理想体重;或(3)呼气末正压为10 cm H2O时V(T)=6 ml/kg理想体重。在机械通气开始前和开始后1小时测定促炎和抗炎介质肿瘤坏死因子、白细胞介素(IL)-6、IL-10和IL-1受体拮抗剂的血浆水平。
在所有情况下,所有细胞因子的血浆水平均保持较低。机械通气1小时后,IL-6、肿瘤坏死因子和IL-1受体拮抗剂无明显变化。39例患者中有35例IL-10低于检测限(10 pg/ml)。各组之间无差异。
既往无肺损伤的患者进行1小时机械通气后,所研究介质的血浆水平未出现一致变化。与肺保护性通气策略相比,ZEEP模式下的高潮气量机械通气并未导致更高的细胞因子水平。既往肺部损伤似乎是高潮气量机械通气1小时后导致血浆细胞因子升高的必要条件。