RATIONALE Ventilator management in acute respiratory distress syndrome usually focuses on setting parameters, but events occurring at ventilator disconnection are not well understood. OBJECTIVES To determine if abrupt deflation after sustained inflation causes lung injury. METHODS Male Sprague-Dawley rats were ventilated (low Vt, 6 ml/kg) and randomized to control (n = 6; positive end-expiratory pressure [PEEP], 3 cm H2O; 100 min) or intervention (n = 6; PEEP, 3-11 cm H2O over 70 min; abrupt deflation to zero PEEP; ventilation for 30 min). Lung function and injury was assessed, scanning electron microscopy performed, and microvascular leak timed by Evans blue dye (n = 4/group at 0, 2, 5, 10, and 20 min after deflation). Hemodynamic assessment included systemic arterial pressure (n = 6), echocardiography (n = 4), and right (n = 6) and left ventricular pressures (n = 6). MEASUREMENTS AND MAIN RESULTS Abrupt deflation after sustained inflation (vs. control) caused acute lung dysfunction (compliance 0.48 ± 1.0 vs. 0.82 ± 0.2 m/cm H2O, oxygen saturation as measured by pulse oximetry 67 ± 23.5 vs. 91 ± 4.4%; P < 0.05) and injury (wet/dry ratio 6.1 ± 0.6 vs. 4.6 ± 0.4; P < 0.01). Vascular leak was absent before deflation and maximal 5-10 minutes thereafter; injury was predominantly endothelial. At deflation, left ventricular preload, systemic blood pressure, and left ventricular end-diastolic pressure increased precipitously in proportion to the degree of injury. Injury caused later right ventricular failure. Sodium nitroprusside prevented the increase in systemic blood pressure and left ventricular end-diastolic pressure associated with deflation, and prevented injury. Injury did not occur with gradual deflation. CONCLUSIONS Abrupt deflation after sustained inflation can cause acute lung injury. It seems to be mediated by acute left ventricular decompensation (caused by increased left ventricular preload and afterload) that elevates pulmonary microvascular pressure; this directly injures the endothelium and causes edema, which is potentiated by the surge in pulmonary perfusion.

中文翻译：

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持续充气后突然放气会导致肺部受伤。

急性呼吸窘迫综合征的呼吸机管理通常着重于设置参数，但是对呼吸机断开时发生的事件了解得很少。目的确定持续通气后突然放气是否会导致肺损伤。方法将雄性Sprague-Dawley大鼠通气（低Vt，6 ml / kg），并随机分为对照组（n = 6；呼气末正压[PEEP]，3 cm H2O； 100分钟）或干预（n = 6； PEEP） ，在70分钟内达到3-11厘米水柱；突然放气至零PEEP；通风30分钟）。评估肺功能和损伤，执行扫描电子显微镜检查，并通过伊文思蓝染料（在放气后0、2、5、10和20分钟，n = 4 /组）对微血管渗漏计时。血液动力学评估包括全身动脉压（n = 6），超声心动图（n = 4），右（n = 6）和左心室压力（n = 6）。测量和主要结果持续通气后（与对照相比）突然放气引起急性肺功能不全（顺应性0.48±1.0对0.82±0.2 m / cm H2O，通过脉搏血氧饱和度法测得的氧饱和度67±23.5对91±4.4％； P <0.05）和伤害（干/湿比6.1±0.6 vs. 4.6±0.4; P <0.01）。放气前无血管渗漏，此后最多5-10分钟。损伤主要是内皮。放气时，左心室的预紧力，全身血压和左心室舒张末期压力与损伤程度成比例地急剧增加。受伤导致后来的右心室衰竭。硝普钠预防了与放气相关的全身性血压升高和左心室舒张末期压力的升高，并防止受伤。逐渐放气不会造成伤害。结论持续通气后突然放气可导致急性肺损伤。似乎是由急性左心室代偿失调（由左心室前负荷和后负荷增加引起）介导的，从而引起肺微血管压力升高。这直接伤害了内皮并引起水肿，这是由于肺灌注激增所致。