BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: Gustavo Matute-Bello; Gregory Downey; Bethany B Moore; Steve D Groshong; Michael A Matthay; Arthur S Slutsky; Wolfgang M Kuebler Journal: Am J Respir Cell Mol Biol Date: 2011-05 Impact factor: 6.914
Authors: James Devaney; Gerard F Curley; Mairead Hayes; Claire Masterson; Bilal Ansari; Timothy O'Brien; Daniel O'Toole; John G Laffey Journal: Crit Care Date: 2013-04-27 Impact factor: 9.097