Meredith J W, Martin M B, Poole G V, Kon N D, Breyer R H, Mills S A
Am Surg. 1983 Dec;49(12):637-41.
The pathophysiology of pulmonary inhalation injury, a major cause of morbidity and mortality from fires, is poorly understood. To examine the effects of colloid and crystalloid resuscitation on extravascular lung water (EVLW) during a standard smoke inhalation injury, we subjected 12 sheep to 8 minutes of cool pine smoke inhalation. The animals were then resuscitated to a pulmonary capillary wedge pressure (PCWP) of 10 +/- 1.5 mm Hg with either lactated Ringer's solution or plasma protein derivative. EVLW, cardiac output, vascular resistance, colloid oncotic pressure (COP), arterial and pulmonary artery pressures, PCWP, and blood gases were monitored during 4 hours of resuscitation. In colloid-treated animals, EVLW increased from 8.3 +/- 1.2 to 11.1 +/- 0.9 ml/kg with injury; it increased only to 12.5 +/- 1.3 ml/kg during resuscitation. In crystalloid-treated animals, EVLW increased from 8.0 +/- 1.0 to 10.3 +/- 0.8 ml/kg with injury and further increased to 17.4 +/- 1.6 ml/kg during resuscitation, a level significantly higher than that in the colloid group (P less than 0.05). The increases in EVLW were associated with progressive hypoxia, which was worse in the crystalloid group. In the crystalloid group, COP decreased from 27.3 +/- 0.9 to 14.2 +/- 0.4 mm Hg and intravascular driving force (COP-PCWP) dropped from 17.6 to 3.26 +/- 1.5 mm Hg; COP and COP-PCWP were maintained in the colloid group. These data demonstrate that supporting serum COP minimizes the increase in EVLW with smoke inhalation injury and suggests that smoke inhalation does not lead to a dramatic increase in alveolar capillary membrane permeability to protein.
肺部吸入性损伤是火灾导致发病和死亡的主要原因，但其病理生理学仍知之甚少。为了研究在标准烟雾吸入性损伤期间胶体和晶体复苏对血管外肺水（EVLW）的影响，我们对12只绵羊进行了8分钟的冷松烟吸入。然后用乳酸林格氏液或血浆蛋白衍生物将动物复苏至肺毛细血管楔压（PCWP）为10±1.5 mmHg。在复苏的4小时内监测EVLW、心输出量、血管阻力、胶体渗透压（COP）、动脉和肺动脉压、PCWP以及血气。在接受胶体治疗的动物中，EVLW在受伤时从8.3±1.2增加到11.1±0.9 ml/kg；在复苏期间仅增加到12.5±1.3 ml/kg。在接受晶体治疗的动物中，EVLW在受伤时从8.0±1.0增加到10.3±0.8 ml/kg，并在复苏期间进一步增加到17.4±1.6 ml/kg，这一水平显著高于胶体组（P<0.05）。EVLW的增加与进行性缺氧相关，晶体组的缺氧情况更严重。在晶体组中，COP从27.3±0.9降至14.2±0.4 mmHg，血管内驱动力（COP-PCWP）从17.6降至3.26±1.5 mmHg；胶体组的COP和COP-PCWP得以维持。这些数据表明，维持血清COP可使烟雾吸入性损伤导致的EVLW增加最小化，并表明烟雾吸入不会导致肺泡毛细血管膜对蛋白质的通透性急剧增加。
