Coker P J, Hernandez L A, Peevy K J, Adkins K, Parker J C
Department of Physiology, University of South Alabama College of Medicine, Mobile 36688.
Crit Care Med. 1992 May;20(5):635-40. doi: 10.1097/00003246-199205000-00015.
To study the individual and combined effects of surfactant inactivation and mechanical ventilation on pulmonary microvascular permeability and lung compliance.
Prospective, controlled trial. An isolated, perfused, lung model of surfactant inactivation and mechanical ventilation at 15, 30, and 45 cm H2O peak inspiratory pressure was developed in young (4 to 6 wks) New Zealand white rabbits.
Laboratory of a university-affiliated medical school.
Isolated, perfused lungs were prepared for measurement of the capillary filtration coefficient before and after one of four interventions: instillation of dioctyl succinate, a surfactant inactivator, without ventilation (group 1); ventilation without dioctyl succinate at 15, 30, or 45 cm H2O peak inspiratory pressure (group 2); ventilation after dioctyl succinate pretreatment at 15, 30, or 45 cm H2O peak inspiratory pressure (group 3); and control lungs without dioctyl succinate or ventilation (group 4). A significant increase in the capillary filtration coefficient was noted after dioctyl succinate treatment alone, after ventilation alone at 45 cm H2O peak inspiratory pressure, and after dioctyl succinate plus ventilation at 15, 30, and 45 cm H2O peak inspiratory pressure. Dioctyl succinate plus ventilation produced a significantly greater increase in the capillary filtration coefficient than ventilation alone at 15 and 45 cm H2O peak inspiratory pressure.
These data suggest that ventilation after surfactant inactivation is more injurious to the pulmonary microvasculature than ventilation alone, and that generalized lung overdistention is not the primary mechanism for microvascular injury in the diseased, noncompliant lung. The increases seen in the capillary filtration coefficient in postventilated surfactant inactivated lungs, even at low-ventilation pressures, suggest that low peak inspiratory pressures do not overdistend the dioctyl succinate-treated lung.
研究表面活性剂失活和机械通气对肺微血管通透性和肺顺应性的单独及联合作用。
前瞻性对照试验。在年轻(4至6周)的新西兰白兔中建立了一个在15、30和45 cm H₂O吸气峰压下进行表面活性剂失活和机械通气的离体灌注肺模型。
一所大学附属医学院的实验室。
制备离体灌注肺以测量四种干预之一前后的毛细血管滤过系数:滴注二辛基琥珀酸酯(一种表面活性剂失活剂)且不通气(第1组);在15、30或45 cm H₂O吸气峰压下通气但不使用二辛基琥珀酸酯(第2组);在15、30或45 cm H₂O吸气峰压下用二辛基琥珀酸酯预处理后通气(第3组);以及不使用二辛基琥珀酸酯或通气的对照肺(第4组)。单独使用二辛基琥珀酸酯处理后、在45 cm H₂O吸气峰压下单独通气后以及在15、30和45 cm H₂O吸气峰压下二辛基琥珀酸酯加通气后,毛细血管滤过系数均显著增加。在15和45 cm H₂O吸气峰压下,二辛基琥珀酸酯加通气比单独通气使毛细血管滤过系数增加得更显著。
这些数据表明,表面活性剂失活后通气对肺微血管的损伤比单独通气更严重,并且广泛性肺过度膨胀不是病变、顺应性差的肺微血管损伤的主要机制。即使在低通气压力下,通气后的表面活性剂失活肺中毛细血管滤过系数的增加表明,低吸气峰压不会使经二辛基琥珀酸酯处理的肺过度膨胀。