From the Dipartimento di Fisiopatologia Medico-chirurgica e dei Trapianti, Università degli Studi di Milano, Milan, Italy (M.P., A.M., and E.D.); 1st Department of Respiratory Medicine, Sotiria Hospital, University of Athens Medical School, Athens, Greece (A.K.); Servizio di Coagulazione e Unità di Ricerca sulla Trombosi, Istituto di Ricovero e Cura a Carattere Scientifico, San Raffaele, Milan, Italy (P.D.V.); and Dipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, Milan, Italy (G.G.).
Anesthesiology. 2014 Apr;120(4):943-50. doi: 10.1097/ALN.0000000000000075.
Recent studies in healthy mice and rats have reported that positive pressure ventilation delivered with physiological tidal volumes at normal end-expiratory volume worsens lung mechanics and induces cytokine release, thus suggesting that detrimental effects are due to positive pressure ventilation per se. The aim of this study in healthy animals is to assess whether these adverse outcomes depend on the mode of mechanical ventilation.
Rats were subjected to 4 h of spontaneous, positive pressure, and whole-body or thorax-only negative pressure ventilation (N = 8 per group). In all instances the ventilatory pattern was that of spontaneous breathing. Lung mechanics, cytokines concentration in serum and broncho-alveolar lavage fluid, lung wet-to-dry ratio, and histology were assessed. Values from eight animals euthanized shortly after anesthesia served as control.
No evidence of mechanical ventilation-dependent lung injury was found in terms of lung mechanics, histology, or wet-to-dry ratio. Relative to control, cytokine levels and recruitment of polymorphonuclear leucocytes increased slightly, and to the same extent with spontaneous, positive pressure, and whole-body negative pressure ventilation. Thorax-only negative pressure ventilation caused marked chest and lung distortion, reversible increase of lung elastance, and higher polymorphonuclear leucocyte count and cytokine levels.
Both positive and negative pressure ventilation performed with tidal volumes and timing of spontaneous, quiet breathing neither elicit an inflammatory response nor cause morpho-functional alterations in normal animals, thus supporting the notion of the presence of a critical volume threshold above which acute lung injury ensues. Distortion of lung parenchyma can induce an inflammatory response, even in the absence of volotrauma.
最近的研究表明,在正常呼气末容积下,使用生理潮气量对健康的小鼠和大鼠进行正压通气会加重肺力学并诱导细胞因子释放,这表明有害影响是由于正压通气本身引起的。本研究旨在健康动物中评估这些不良后果是否取决于机械通气模式。
将大鼠置于自主、正压和全身或仅胸腔负压通气 4 小时(每组 8 只)。在所有情况下,通气模式均为自主呼吸。评估肺力学、血清和支气管肺泡灌洗液中细胞因子浓度、肺湿干比和组织学。麻醉后立即处死的 8 只动物的数值作为对照。
在肺力学、组织学或湿干比方面,没有发现与机械通气相关的肺损伤的证据。与对照组相比,细胞因子水平和多形核白细胞的募集略有增加,且与自主、正压和全身负压通气的程度相同。仅胸腔负压通气导致明显的胸廓和肺变形、肺弹性增加、多形核白细胞计数和细胞因子水平升高。
使用与自主、安静呼吸的潮气量和时间相匹配的正压和负压通气,既不会引起炎症反应,也不会导致正常动物的形态功能改变,从而支持存在一个临界容量阈值的观点,超过该阈值后会导致急性肺损伤。即使没有容积性创伤,肺实质的变形也会引起炎症反应。