Pulmonary surfactant is altered during mechanical ventilation of isolated rat lung.
OBJECTIVE
To test the hypothesis that the lung injury induced by certain mechanical ventilation strategies is associated with changes in the pulmonary surfactant system.


METHODS
Analysis of the pulmonary surfactant system from isolated rat lungs after one of four different ventilatory strategies.


METHODS
A research laboratory at a university.


METHODS
A total of 45 Sprague-Dawley rats.


METHODS
Isolated lungs were randomized to either no ventilation (0-TIME) or to ventilation at 40 breaths/min in a humidified 37 degrees C chamber for either 30 mins or 120 mins with one of the following four strategies: a) control (CON, 7 mL/kg, 3 cm H2O positive end-expiratory pressure); b) medium volume, zero end-expiratory pressure (MVZP, 15 mL/kg, 0 cm H2O end-expiratory pressure); c) medium volume, high positive end-expiratory pressure (MVHP, 15 mL/kg, 9 cm H2O positive end-expiratory pressure); and d) high volume, zero end-expiratory pressure (HVZP, 40 mL/kg, 0 cm H2O end-expiratory pressure).


METHODS
Pressure-volume curves were determined before and after the ventilation period, after which the lungs were lavaged for surfactant analysis.


RESULTS
Compared with 0-TIME, 30 mins of ventilation with the HVZP strategy or 120 mins of ventilation with CON and MVZP strategies caused a significant decrease in compliance. Groups showing a decreased compliance had significant increases in the amount of surfactant, surfactant large aggregates, and total lavage protein compared with 0-TIME.


CONCLUSIONS
A short period of injurious mechanical ventilation can cause a decrease in lung compliance that is associated with a large influx of proteins into the alveolar space and with alterations of the pulmonary surfactant system. The changes of surfactant in these experiments are different from those seen in acute lung injury, indicating that they may represent an initial response to mechanical ventilation.
Veldhuizen
R A
RA
Department of Medicine and the Lawson Research Institute, University of Western Ontario, London, Canada. rveldhui@julian.uwo.ca
Tremblay
L N
LN
Govindarajan
A
A
van Rozendaal
B A
BA
Haagsman
H P
HP
Slutsky
A S
AS
D000818:Animals; D011175:Positive-Pressure Respiration; D011663:Pulmonary Surfactants / Q000302:isolation & purification / Q000502:physiology*; D012333:RNA, Messenger / Q000302:isolation & purification; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000009:adverse effects*; D012128:Respiratory Distress Syndrome / Q000209:etiology*; D013990:Tidal Volume
D011663:Pulmonary Surfactants; D012333:RNA, Messenger