DiRocco Joseph D, Pavone Lucio A, Carney David E, Lutz Charles J, Gatto Louis A, Landas Steve K, Nieman Gary F
Department of Surgery, Upstate Medical University, 750 E Adams Street, Syracuse, NY 13210, USA.
Intensive Care Med. 2006 Jan;32(1):140-8. doi: 10.1007/s00134-005-2854-3. Epub 2005 Dec 2.
To determine whether pathological alterations in alveolar mechanics (i.e., the dynamic change in alveolar size and shape with ventilation) at a similar level of lung injury vary depending on the cause of injury.
Prospective controlled animal study in a university laboratory.
30 male Sprague-Dawley rats (300-550 g).
Rats were separated into one of four lung injury models or control (n=6): (a) 2% Tween-20 (Tween, n=6), (b) oleic acid (OA, n=6), (c) ventilator-induced lung injury (VILI, PIP 40/ZEEP, n=6), (d) endotoxin (LPS, n=6). Alveolar mechanics were assessed at baseline and after injury (PaO2/FIO2 <300 mmHg) by in vivo microscopy.
Alveolar instability (proportional change in alveolar size during ventilation) was used as a measurement of alveolar mechanics.
Alveoli were unstable in Tween, OA, and VILI as hypoxemia developed (baseline vs. injury: Tween, 7+/-2% vs. 67+/-5%; OA: 3+/-2% vs. 82+/-9%; VILI, 4+/-2% vs. 72+/-5%). Hypoxemia after LPS was not associated with significant alveolar instability (baseline vs. injury: LPS, 3+/-2 vs. 8+/-5%).
These data demonstrate that multiple pathological changes occur in dynamic alveolar mechanics. The nature of these changes depends upon the mechanism of lung injury.
确定在相似肺损伤程度下，肺泡力学的病理改变（即通气时肺泡大小和形状的动态变化）是否因损伤原因而异。
大学实验室中的前瞻性对照动物研究。
30只雄性Sprague-Dawley大鼠（300 - 550克）。
将大鼠分为四种肺损伤模型之一或对照组（n = 6）：（a）2%吐温-20（吐温，n = 6），（b）油酸（OA，n = 6），（c）呼吸机诱导的肺损伤（VILI，气道峰压40/呼气末正压0，n = 6），（d）内毒素（LPS，n = 6）。通过体内显微镜在基线和损伤后（动脉血氧分压/吸入氧分数值<300 mmHg）评估肺泡力学。
肺泡不稳定性（通气期间肺泡大小的比例变化）用作肺泡力学的测量指标。
随着低氧血症的发展，吐温、OA和VILI组的肺泡不稳定（基线与损伤后：吐温，7±2%对67±5%；OA：3±2%对82±9%；VILI，4±2%对72±5%）。LPS诱导低氧血症后，肺泡无明显不稳定（基线与损伤后：LPS，3±2对8±5%）。
这些数据表明，动态肺泡力学中会出现多种病理变化。这些变化的性质取决于肺损伤的机制。
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