Cox C S, Zwischenberger J B, Traber D L, Traber L D, Haque A K, Herndon D N
University of Texas Medical Branch, Galveston 77550.
Surg Gynecol Obstet. 1993 Apr;176(4):339-49.
Inhalation injury is one of the main causes of mortality in burn victims. The tracheobronchial epithelium sloughs and combines with a protein rich exudate to form casts of the airways that can lead to obstruction. We studied the effects of a continuous infusion of heparin on the acute pulmonary injury that occurs after smoke inhalation injury in sheep. Twelve ewes with vascular catheters received a standardized smoke inhalation injury and mechanical ventilation according to protocol for 72 hours. The heparin group (n = 6) received a 400 unit per kilogram bolus of heparin followed by a continuous infusion to maintain the activated clotting time between 250 to 300 seconds. The control group (n = 6) received a saline solution vehicle. Hemodynamics, blood gases and plasma samples for conjugated dienes were taken every six hours. At necropsy, pulmonary tissue was collected for histologic findings, polymorphonuclear neutrophil leukosequestration, wet-to-dry weight ratios and conjugated dienes. PaO2 to FIO2 ratios were improved in the heparin group compared with the control group at 12 to 72 hours after injury, and peak airway pressures were higher in the control group compared with the heparin group. Positive end expiratory pressure requirements were higher in the control group compared with the heparin group. There were significantly fewer airway tracheobronchial casts as determined by our tracheobronchial casts scoring system (2.4 +/- 0.4 versus 0.67 +/- 0.21) and confirmed by histologic examination. Pulmonary blood-free wet-to-dry weight ratios were higher in the control group compared with the heparin group (6.4 +/- 0.5 versus 5.2 +/- 0.1; p < 0.05). There were no differences in pulmonary tissue or plasma conjugated dienes; likewise, pulmonary leukosequestration was unaffected by heparin. Heparin decreases tracheobronchial cast formation, improves oxygenation, minimizes barotrauma and reduces pulmonary edema in an ovine model of severe smoke inhalation injury. Heparin does not reduce oxygen free radical activity after smoke inhalation injury.
吸入性损伤是烧伤患者死亡的主要原因之一。气管支气管上皮脱落并与富含蛋白质的渗出物结合形成气道铸型，可导致气道阻塞。我们研究了持续输注肝素对绵羊烟雾吸入性损伤后发生的急性肺损伤的影响。12只带有血管导管的母羊按照方案接受标准化烟雾吸入性损伤并机械通气72小时。肝素组（n = 6）静脉推注每千克400单位的肝素，随后持续输注以维持活化凝血时间在250至300秒之间。对照组（n = 6）接受生理盐水载体。每6小时采集血流动力学、血气和血浆共轭二烯样本。尸检时，收集肺组织用于组织学检查、多形核中性粒细胞滞留、湿重与干重比值以及共轭二烯检测。与对照组相比，肝素组在损伤后12至72小时的氧合指数（PaO2/FIO2）得到改善，且对照组的气道峰压高于肝素组。对照组的呼气末正压需求高于肝素组。根据我们的气管支气管铸型评分系统确定，气道气管支气管铸型明显减少（2.4±0.4对0.67±0.21），并经组织学检查证实。对照组的肺无血湿重与干重比值高于肝素组（6.4±0.5对5.2±0.1；p<0.05）。肺组织或血浆共轭二烯无差异；同样，肺白细胞滞留不受肝素影响。在严重烟雾吸入性损伤的绵羊模型中，肝素可减少气管支气管铸型形成，改善氧合，使气压伤最小化并减轻肺水肿。肝素不会降低烟雾吸入性损伤后的氧自由基活性。
