Raghavendran Krishnan, Davidson Bruce A, Helinski Jadwiga D, Marschke Cristi J, Manderscheid Patricia, Woytash James A, Notter Robert H, Knight Paul R
Departments of *Surgery, †Anesthesiology, and ‡Pathology, State University of New York (SUNY) at Buffalo, Buffalo; and §Department of Pediatrics, University of Rochester, Rochester, New York.
Anesth Analg. 2005 Nov;101(5):1482-1489. doi: 10.1213/01.ANE.0000180201.25746.1F.
Lung contusion affects 17%-25% of adult blunt trauma patients, and is the leading cause of death from blunt thoracic injury. A small animal model for isolated bilateral lung contusion has not been developed. We induced lung contusion in anesthetized rats by dropping a 0.3-kg weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs. Lung injury was characterized as a function of chest impact energy (1.8-2.7 J) by measurements of arterial oxygenation, bronchoalveolar lavage (BAL) albumin and cytology, pressure-volume mechanics, and histopathology. Histology confirmed bilateral lung contusion without substantial cardiac muscle trauma. Rats receiving 2.7 J of chest impact energy had 33% mortality that exceeded prospectively defined limits for sublethal injury. Hypoxemia in rats with maximal sublethal injury (2.45 J) met criteria for acute lung injury at < or =24 h, improving by 48 h. BAL albumin levels were highest at < or =24 h, and remained elevated along with increased BAL leukocytes and decreased lung volumes at 48 h. We concluded that an impact energy of 2.45 J induces isolated, bilateral lung contusion and provides a useful model for future mechanistic pathophysiological assessments.
肺挫伤影响17%-25%的成年钝性创伤患者,是钝性胸部损伤致死的主要原因。目前尚未建立孤立性双侧肺挫伤的小动物模型。我们通过将一个0.3千克的重物落在心前区保护罩上,使冲击力远离心脏并朝向肺部,从而在麻醉的大鼠中诱导肺挫伤。通过测量动脉氧合、支气管肺泡灌洗(BAL)白蛋白和细胞学、压力-容积力学以及组织病理学,将肺损伤表征为胸部撞击能量(1.8-2.7焦耳)的函数。组织学证实为双侧肺挫伤,无明显心肌损伤。接受2.7焦耳胸部撞击能量的大鼠死亡率为33%,超过了预先定义的亚致死性损伤限度。最大亚致死性损伤(2.45焦耳)的大鼠低氧血症在≤24小时时符合急性肺损伤标准,48小时时有所改善。BAL白蛋白水平在≤24小时时最高,48小时时随着BAL白细胞增加和肺容积减少而持续升高。我们得出结论,2.45焦耳的撞击能量可诱导孤立性双侧肺挫伤,并为未来的机制性病理生理学评估提供了一个有用的模型。