Objective: To evaluate whether pulmonary surfactant (PS) impairment plays a role in the development of ventilator-induced lung injury (VILI).
Methods: Thirty-two healthy adult Sprague-Dawley rats were randomly allocated to four groups ( n = 8, each group ) and mechanically ventilated (MV). (1) P7 group: with settings [expressed as peak inspiratory pressure (PIP, cm H2O)/frequency (cpm)/inspiratory:expiratory ratio/positive end expiratory pressure (PEEP, cm H2O)] of 7/40/1:1/0, (2) P45 group: with settings of 45/ 20/1:1/0, (3) PS group: 100 mg/kg of a porcine PS administered intra-tracheally and with the same settings as P45 group, (4) PEEP group: with settings of 45/20/1: 1/10. After 20 minutes of MV, all animals were killed. Another 8 animals were killed immediately after surgical procedure to serve as nonventilated controls (CON group). Arterial blood O2 partial pressure (PaO2) and maximum thorax-lung compliance (C(max)) were measured, and total proteins (TP), total phospholipids (TPL), small and large aggregates (SA, LA), and minimum surface tension (ST min) of bronchoalveolar lavage fluid (BALF) were analyzed.
Results: P45 group had decreased PaO2, C(max), TPL/TP all P < 0.01), increased TP, SA/LA and ST min of ABLF (all P < 0.01) as compared with P7 group. Both PS group and PEEP group had improved PaO2, C(max), BALF analyses as compared with P45 group (P < 0.05 or P < 0.01). There was no significant difference between P7 group and CON group in any parameter described above.
Conclusions: A short period of mechanical ventilation with high PIP alone can cause VILI in rats that is associated with PS impairment; both exogenous PS and PEEP can restore or preserve alveolar space PS composition and function, attenuate abnormalities of lung oxygenation and mechanics, indicating PS impairment may play an important role in the development of VILI.