Verbrugge S J, Uhlig S, Neggers S J, Martin C, Held H D, Haitsma J J, Lachmann B
Department of Anesthesiology, Erasmus University Rotterdam, The Netherlands.
Anesthesiology. 1999 Dec;91(6):1834-43. doi: 10.1097/00000542-199912000-00038.
Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma.
In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls.
Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls.
Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.
作者利用表面活性剂缺乏的体内动物模型，比较了不同通气策略对氧合及肺实质炎症介质释放的影响。
对成年大鼠用100%氧气进行机械通气，通过反复肺灌洗诱导急性肺损伤，使动脉血氧分压<85 mmHg（峰压/呼气末正压[PEEP]=26/6 cm H₂O）。然后将动物随机分组，分别接受外源性表面活性剂治疗、部分液体通气、高PEEP（16 cm H₂O）通气、低PEEP（8 cm H₂O）通气或吸气峰压增加（至32 cm H₂O；PEEP = 6 cm H₂O）的通气。两组健康未灌洗的大鼠分别以32/6和32/0 cm H₂O的峰压/PEEP进行通气。测定血气。在90分钟和240分钟后测定血清和支气管肺泡灌洗液（BALF）中的前列环素（PGI₂）和肿瘤坏死因子-α（TNF-α）浓度以及BALF中的蛋白质浓度，并与机械通气和自主呼吸的对照组进行比较。
表面活性剂、部分液体通气和高PEEP改善了氧合并降低了BALF蛋白水平。在高平均气道压水平下用高PEEP通气可增加BALF中PGI₂水平，而各组间BALF中TNF-α水平无差异。与自主呼吸对照组相比，机械通气未导致血清PGI₂和TNF-α水平升高。
在该急性肺损伤模型中，尽管不同通气策略下肺泡蛋白浓度和氧合有显著差异，但没有迹象表明通气会引起全身性PGI₂和TNF-α释放，也没有肺内TNF-α释放。在高平均气道压水平下进行机械通气可增加支气管肺泡灌洗可及空间内的PGI₂水平。
