Song G W, Robertson B, Curstedt T, Gan X Z, Huang W X
Capital Institute of Pediatrics, Beijing, China.
Acta Anaesthesiol Scand. 1996 Oct;40(9):1154-60. doi: 10.1111/j.1399-6576.1996.tb05580.x.
Deterioration of lung function in bacterial pneumonia may in part be due to inactivation of endogenous surfactant. We investigated the effects of surfactant treatment on gas exchange and lung morphology in an experimental model of pneumonia caused by Escherichia coli.
A total of 117 adult rats received via the trachea 2 ml/kg body weight of a standard suspension of Escherichia coli (4 x 10(9) bacteria/ml). After 2-3 days, 31 of the infected animals showed symptoms of respiratory failure with PaO2 < 27 kPa during ventilation with 100% O2. All these animals were kept in a multi-plethysmograph system and ventilated for 45 min with a tidal volume of 6 ml/kg, a frequency of 30/min, an inspiration/expiration ratio of 1:1, and a positive end-expiratory pressure of 0.2 kPa. After 15 min of mechanical ventilation, animals were divided in three treatment groups, receiving via the airways (1) no material, (2) normal saline (2 ml/kg), or (3) Curosurf, 80 mg/ml (2 ml/kg). Ten healthy animals served as controls. Lung-thorax compliance and blood gases were measured 15 and 30 min after surfactant treatment. After the period of ventilation, animals were killed, and the left lung was weighed and fixed in formalin for histological examination. The right lung was washed in situ with normal saline via the tracheal tube. Total phospholipids, and levels of phosphatidylcholine (PC) and protein in lavage fluid were determined.
In comparison with pre-treatment values, average PaO2 at 30 min was increased by 76% in animals receiving Curosurf (P < 0.01), but did not improve in the other groups. The left lung weight/body weight ratio showed a nearly 3-fold increase in infected animals in comparison with normal controls. There was also a 3-fold increase in the protein content of lung lavage fluid from infected rats, but values for total phospholipids and PC content were unchanged in animals not receiving surfactant. Histological examination of the lungs showed wide-spread non-specific pneumonia in infected animals, but no difference in alveolar air expansion between surfactant-treated and non-treated ones.
Surfactant replacement significantly improves oxygenation in rats with E. coli pneumonia, without affecting lung-thorax compliance during mechanical ventilation or alveolar expansion pattern in lungs fixed by conventional methods.
细菌性肺炎中肺功能的恶化可能部分归因于内源性表面活性剂的失活。我们在大肠杆菌所致肺炎的实验模型中研究了表面活性剂治疗对气体交换和肺形态的影响。
117只成年大鼠经气管给予2 ml/kg体重的标准大肠杆菌悬液(4×10⁹细菌/ml)。2至3天后,31只感染动物在100%氧气通气时出现呼吸衰竭症状,动脉血氧分压(PaO₂)<27 kPa。所有这些动物被置于多体积描记系统中,以潮气量6 ml/kg、频率30次/分钟、吸呼比1:1和呼气末正压0.2 kPa通气45分钟。机械通气15分钟后,将动物分为三个治疗组,经气道给予:(1)无物质,(2)生理盐水(2 ml/kg),或(3)固尔苏,80 mg/ml(2 ml/kg)。10只健康动物作为对照。在表面活性剂治疗后15分钟和30分钟测量肺胸顺应性和血气。通气期结束后,处死动物,称取左肺重量并固定于福尔马林中用于组织学检查。右肺经气管插管原位用生理盐水冲洗。测定灌洗液中的总磷脂、磷脂酰胆碱(PC)和蛋白质水平。
与治疗前值相比,接受固尔苏的动物在30分钟时平均PaO₂增加了76%(P<0.01),但其他组未改善。与正常对照相比,感染动物的左肺重量/体重比增加了近3倍。感染大鼠肺灌洗液中的蛋白质含量也增加了3倍,但未接受表面活性剂的动物的总磷脂和PC含量值未改变。肺组织学检查显示感染动物存在广泛的非特异性肺炎,但表面活性剂治疗组和未治疗组之间肺泡气扩张无差异。
表面活性剂替代可显著改善大肠杆菌肺炎大鼠的氧合,不影响机械通气期间的肺胸顺应性或传统方法固定的肺的肺泡扩张模式。