Mechanical ventilation increases microvascular permeability in oleic acid-injured lungs.
Mechanical ventilation increases microvascular permeability in oleic acid-injured lungs.
复制标题
机械通气增加油酸损伤肺部的微血管通透性。
DOI：
10.1152/jappl.1990.69.6.2057
复制
发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Parker,JC
中科院分区：
文献类型：
--
作者：
Hernandez,LA;Coker,PJ;May,S;Thompson,AL;Parker,JC
患者接受呼吸支持的肺部病理可能会增加发生气压伤的风险，因为潜在的疾病过程可能会削弱血管系统，使肺更容易受到机械通气的损伤。本实验观察了油酸（OA）损伤后离体幼兔肺对机械通气的反应。用戊巴比妥钠（30 mg/kg）麻醉新西兰白色家兔（0.7-1.3 kg），切开气管并放血。分离心脏和肺，并以恒定流量用自体血液灌注。在油酸给药（OA组; 0.2 ml注入静脉储液器）、单独通气（Vent组;吸气峰压= 25 cmH 2 O）或油酸联合通气（OA + Vent组）之前和之后30 min和60 min测定毛细血管滤过系数（Kf，c，单位：ml.min-1.cmH2O-1.100 g wet wt-1）以及肺动脉压（Ppa）和静脉压。OA给药后Ppa短暂增加4.21 +/- 0.822 cmH 2 O，但随后恢复至约对照值。OA组（0.288 +/- 0.042）、Vent组（0.296 +/- 0.035）或OA + Vent组（0.276 +/- 0.028）的基线Kf，c值彼此之间无显著差异。OA给药（0.45 +/- 0.066）或Vent给药（0.35 +/- 0.75）后的Kf，c彼此之间或与基线测量值相比均无显著差异。在OA给药后通气组（OA + Vent）中，Kf，c（0.883 +/- 0.148）较基线显著增加（P <0.001），与所有其他治疗组显著不同。我们的结论是，最小OA损伤和通气的组合是更有害的肺比任何一个单独。
The pulmonary pathology for which a patient receives ventilatory support may increase the risk of developing barotrauma, because an underlying disease process may weaken the vasculature and render the lung more susceptible to damage by mechanical ventilation. We determined the response of isolated young rabbit lungs to mechanical ventilation after oleic acid (OA) injury. New Zealand White rabbits (0.7-1.3 kg) were anesthetized with pentobarbital sodium (30 mg/kg), tracheotomized, and exsanguinated. The heart and lungs were isolated and perfused with autologous blood at a constant flow. The capillary filtration coefficient (Kf,c, in ml.min-1.cmH2O-1.100 g wet wt-1) and pulmonary arterial (Ppa) and venous pressures were determined before and 30 and 60 min after oleic acid administration (OA group; 0.2 ml into the venous reservoir), ventilation alone (Vent group; peak inspiratory pressure = 25 cmH2O), or oleic acid combined with ventilation (OA + Vent group). Ppa transiently increased by 4.21 +/- 0.822 cmH2O after OA administration but then returned to approximately control values. Baseline Kf,c values for OA (0.288 +/- 0.042), Vent (0.296 +/- 0.035), or OA + Vent (0.276 +/- 0.028) groups were not significantly different from each other. Kf,c after either OA administration (0.45 +/- 0.066) or Vent (0.35 +/- 0.75) were not significantly different from each other or from baseline measurements. In the group ventilated after OA administration (OA + Vent), Kf,c (0.883 +/- 0.148) increased significantly from baseline (P less than 0.001) and was significantly different from all other treatment groups. We conclude that the combination of minimal OA injury and ventilation was more deleterious to the lung than either one alone.