Oleic acid-induced lung injury is an established experimental model of acute lung injury in pigs and is considered to reproduce the early exudative phase of acute respiratory distress syndrome. Ultrasound lung comets are an echographic sign of extravascular lung water, originating from thickened interlobular septa. The objective of this study was to evaluate the timing and relationship between the number of ultrasound lung comets, the Pao2/Fio2 ratio, and the static respiratory compliance in an experimental model of oleic acid-induced lung injury in pigs.
Ten anesthetized pigs.
Acute lung injury was induced by injection of oleic acid (0.1 mL/kg, intravenously). Ultrasound lung comets, Pao2/Fio2, and static respiratory compliance were measured at baseline and at 15, 30, 60, and 90 mins after the injection of oleic acid. We evaluated ultrasound lung comets by transthoracic echography (7.5-MHz vascular probe), scanning on right and left hemithoraxes at 12 predefined scanning sites.
Acute lung injury/acute respiratory distress syndrome was present in all pigs at 90 mins. The number of ultrasound lung comets increased over time and was consistently earlier than the decrease in Pao2/Fio2. At 15 mins, ultrasound lung comets were markedly increased, but no significant changes in Pao2/Fio2 were observed. Accordingly, static respiratory compliance was dramatically reduced at 15 mins compared with baseline (17.04 ± 1.82 vs. 34.84 ± 2.62 mL/cm H2O,p< .05).
Ultrasound lung comets, assessed by transthoracic echography, detected extravascular lung water accumulation very early in the course of the oleic acid lung injury in pigs, in the presence of a normal Pao2/Fio2. These results suggest that ultrasound lung comets could be a very early, noninvasive, and simple method to detect and quantify pulmonary edema in acute lung injury.
From the Institute of Clinical Physiology, National Research Council, Pisa, Italy (LG, VL, EP); Sector of Medicine, Scuola Superiore S. Anna, Pisa, Italy (VL, FAR); Department of Physiology, New York Medical College, Valhalla, New York, NY (FAR); and Division of Surgical, Molecular and Ultrastructural Pathology, Department of Oncology, University of Pisa, Pisa, Italy (CDC, GB). Drs. Gargani and Lionetti contributed equally to the project.
Supported, in part, by the institutional funds of the Institute of Clinical Physiology, National Research Council, Pisa, Italy and by a research fund from the Compagnia di San Paolo, Turin, Italy. Dr. Recchia is an Established Investigator of the American Heart Association.
The authors have not disclosed any potential conflicts of interest.
Address requests for reprints to: Luna Gargani, MD, CNR, Institute of Clinical Physiology, Via G. Moruzzi, 1, 56124, Pisa, Italy. E-mail: firstname.lastname@example.org
*See also p. 2869.