Amigoni Maria, Bellani Giacomo, Scanziani Margherita, Masson Serge, Bertoli Elisa, Radaelli Enrico, Patroniti Nicolò, Di Lelio Alessandro, Pesenti Antonio, Latini Roberto
Department of Experimental Medicine, University of Milano-Bicocca and Department of Perioperative Medicine and Intensive Care, San Gerardo Hospital, Monza, Italy.
Anesthesiology. 2008 Jun;108(6):1037-46. doi: 10.1097/ALN.0b013e318173f64f.
Acid aspiration is a complication of general anesthesia. Most animal models developed to define its pathophysiology have focused on the acute (< or =24 h) phase of the injury. The authors describe a model of acid aspiration allowing the study of this type of lung injury over time.
The authors instilled hydrochloric acid (0.1 m, 1.5 ml/kg) or normal saline in the right bronchus of mice. Lung injury was evaluated at 6 h, 12 h, 24 h, and 2 weeks by assessing arterial blood gases, respiratory system compliance, lung wet weight normalized by body weight, lung myeloperoxidase activity, and histology. Twelve hours and 2 weeks after injury, a computed tomography scan was obtained.
In the hydrochloric acid group, arterial oxygen tension decreased (P < 0.05) at 12 and 24 h, whereas it recovered at 2 weeks; respiratory system compliance was lower both at 24 h and 2 weeks (P < 0.05). Lung weight increased at 12 and 24 h (P < 0.05). Myeloperoxidase activity peaked between 6 and 12 h. Computed tomography at 12 h showed that almost 30% of the injured lung was abnormally aerated. Although reduced, the abnormalities were still present at 2 weeks as confirmed by a fibrotic scar well evident at histologic examination.
The authors characterized a murine model of regional acid aspiration allowing long-term survival. Despite a partial recovery, at 2 weeks the injury persisted, with evidence of fibrosis and lung compliance reduction. This long-term, low-mortality model seems suitable for assessment of the effects of different therapies on lung injury and repair.
误吸酸性物质是全身麻醉的一种并发症。大多数为明确其病理生理学而建立的动物模型都聚焦于损伤的急性期(≤24小时)。作者描述了一种误吸酸性物质的模型,可用于长期研究此类肺损伤。
作者将盐酸(0.1 m,1.5 ml/kg)或生理盐水注入小鼠右支气管。在6小时、12小时、24小时和2周时,通过评估动脉血气、呼吸系统顺应性、按体重标准化的肺湿重、肺髓过氧化物酶活性和组织学来评估肺损伤。在损伤后12小时和2周时,进行计算机断层扫描。
在盐酸组中,动脉血氧分压在12小时和24小时时降低(P < 0.05),而在2周时恢复;呼吸系统顺应性在24小时和2周时均较低(P < 0.05)。肺重量在12小时和24小时时增加(P < 0.05)。髓过氧化物酶活性在6至12小时之间达到峰值。12小时时的计算机断层扫描显示,近30%的损伤肺出现异常通气。尽管有所减轻,但2周时异常仍然存在,组织学检查清楚显示的纤维化瘢痕证实了这一点。
作者对一种可长期存活的局部误吸酸性物质的小鼠模型进行了特征描述。尽管有部分恢复,但在2周时损伤仍然存在,有纤维化和肺顺应性降低的证据。这种长期、低死亡率的模型似乎适合评估不同疗法对肺损伤和修复的影响。