Published ahead of print on November 20, 2003, doi:10.1165/rcmb.2003-0279OC
Am. J. Respir. Cell Mol. Biol., Volume 30, Number 5, May 2004, 641-650
A more recent version of this article appeared on May 1, 2004
Submitted on July 25, 2003
Revised on November 14, 2003
Effect of Acute Lung Injury on Structure and Function of Pulmonary Surfactant Films
Amiya K Panda1, Kaushik Nag2, Robert R Harbottle2, Karina Rodriguez Capote3, Ruud A.W. Veldhuizen4, Nils O Petersen2, and Fred Possmayer5*
1 Chemistry, Behala College, Kolkata, India; Chemistry, University of Western Ontario, London, ON, Canada; Ob/Gyn and Biochemistry, University of Western Ontario, London, ON, Canada,
2 Chemistry, University of Western Ontario, London, ON, Canada,
3 Ob/Gyn and Biochemistry, University of Western Ontario, London, ON, Canada; Research Centre, Victoria de Giron Medical School, Habana, Cuba,
4 Physiology and Pharmacology and Medicine, Lawson Health Research Institute, London, ON, Canada,
5 Ob/Gyn and Biochemistry, University of Western Ontario, London, ON, Canada
* To whom correspondence should be addressed. E-mail: fpossmay{at}uwo.ca.
The structural and functional alterations in pulmonary surfactant which occur during acute lung injury were studied using rat lung surfactant large aggregates (LA) isolated from normal nonventilated lungs (N), and from standard ventilated (V) and injuriously ventilated (IV) excised lungs. N lungs inflated significantly better than IV lungs, with V lungs intermediate. Although IV LA phosphatidylcholine levels were unchanged, cholesterol and protein were elevated. N and V LA, but not IV LA, adsorbed rapidly and were able to generate surface pressures ( ) near 70 mNm-1 during surface area reduction at 37°C on a captive bubble tensiometer. Langmuir-Wilhelmy surface balance studies at 23°C showed N LA films consistently attained approaching 70 mN m-1 during ten compression-expansion cycles. IV films were less effective and failed to achieve high consistently after the 6th cycle. V films were intermediate. Epifluorescence studies revealed compression of adsorbed N LA films formed well-defined liquid-condensed (LC) domains, but fewer, smaller domains were observed with IV films and, to a lesser extent, V films. Atomic force microscopy on Langmuir-Blodgett N films transferred at = 30 mN m-1 showed high, well-defined LC domains. IV films showed thinner, intermediate height, possibly fluid domains, which contain large numbers of small higher domains with heights corresponding to LC domains. V films were intermediate. We conclude acute lung injury induced by hyperventilation, and to a lesser extent standard ventilation, of excised lungs alters surfactant surface activity and the ability of natural surfactant to form surface structures at the air-water interface.
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