Nishina K, Mikawa K, Takao Y, Maekawa N, Obara H
Department of Anaesthesiology, Kobe University School of Medicine, Japan.
Anesthesiology. 1999 Jul;91(1):240-52. doi: 10.1097/00000542-199907000-00033.
An animal experimental model of acute lung injury after intratracheal instillation of acidified milk products has been recently demonstrated. Exogenous administration of surfactant has proved to be successful treatment for acute lung injury induced by many causes including acid aspiration. The authors conducted this study to investigate whether exogenous surfactant can reduce the magnitude of lung damage induced in rabbits by acidified milk products.
The lung injury was induced by intratracheal instillation of acidified human breast milk or acidified infant formula (0.8 ml/kg, pH 1.8). Thirty minutes after the insult, some animals were treated with intratracheal surfactant 100 or 200 mg/kg. Lung compliance and alveolar-to-arterial oxygen gradient were recorded during ventilation. After 4 or 12 h, the lungs were excised to determine physiologic and histologic lung damage. Albumin, interleukin-8, and eicosanoids in bronchoalveolar lavage fluid and superoxide production by neutrophils were measured.
The acidified milk products increased A-aD(O2)(550+/-52 and 156+/-28 mmHg; mean+/-SD at 4 h in saline solution and infant formula groups, respectively), lung wet-to-dry weight ratio (6.6+/-0.5 and 5.6 +/- 0.2), %neutrophils in bronchoalveolar lavage fluid (84+/-4% and 8+/-20%), and decreased compliance (0.76+/-0.09 and 1.90+/-0.11 ml/cm H2O). Surfactant improved these variables in a dose-dependent manner (A-aDO2 = 363+/-50 and 237+/-55 mmHg in 100-mg/kg and 200-mg/kg surfactant groups). Surfactant attenuated extensive histologic changes caused by the milk products. Superoxide production was less in rabbits receiving surfactant than in those not receiving it.
Exogenous surfactant improved physiologic, histologic, and biochemical lung injury induced by acidified milk products in a dose-dependent manner. The effectiveness of surfactant may be caused, in part, by inhibition of neutrophils' sequestration and activation. These data indicate that intratracheal instillation of surfactant may be a promising therapeutic modality in acute lung injury resulting from aspiration of acidified milk products.
最近已证实经气管内滴注酸化奶制品可建立急性肺损伤的动物实验模型。外源性给予表面活性剂已被证明是治疗包括酸吸入在内的多种原因所致急性肺损伤的成功方法。作者进行本研究以探讨外源性表面活性剂是否能减轻酸化奶制品对兔造成的肺损伤程度。
经气管内滴注酸化人母乳或酸化婴儿配方奶粉（0.8 ml/kg，pH 1.8）诱导肺损伤。损伤后30分钟，部分动物经气管内给予100或200 mg/kg表面活性剂。通气过程中记录肺顺应性和肺泡 - 动脉氧梯度。4或12小时后，切除肺脏以确定生理和组织学肺损伤情况。检测支气管肺泡灌洗液中的白蛋白、白细胞介素 - 8、类二十烷酸以及中性粒细胞产生的超氧化物。
酸化奶制品使肺泡 - 动脉氧分压差（A - aD(O2)）升高（生理盐水组和婴儿配方奶粉组4小时时分别为550±52和156±28 mmHg；均值±标准差）、肺湿重与干重之比升高（6.6±0.5和5.6±0.2）、支气管肺泡灌洗液中中性粒细胞百分比升高（84±4%和8±20%），并使肺顺应性降低（0.76±0.09和1.90±0.11 ml/cm H2O）。表面活性剂以剂量依赖方式改善了这些指标（100 mg/kg和200 mg/kg表面活性剂组的A - aDO2分别为363±50和237±55 mmHg）。表面活性剂减轻了奶制品所致的广泛组织学改变。接受表面活性剂的兔超氧化物产生量低于未接受的兔。
外源性表面活性剂以剂量依赖方式改善了酸化奶制品所致的生理、组织学和生化性肺损伤。表面活性剂的有效性可能部分归因于对中性粒细胞的扣押和激活的抑制。这些数据表明经气管内滴注表面活性剂可能是治疗酸化奶制品吸入所致急性肺损伤的一种有前景的治疗方式。
