Surfactant dysfunction in lung contusion with and without superimposed gastric aspiration in a rat model.
This study investigates surfactant dysfunction in rats with lung contusion (LC) induced by blunt chest trauma. Rats at 24 h postcontusion had a decreased percent content of large surfactant aggregates in cell-free bronchoalveolar lavage (BAL) and altered large-aggregate composition with decreased phosphatidylcholine (PC), increased lyso-PC, and increased protein compared with uninjured controls. The surface activity of large aggregates on a pulsating bubble surfactometer was also severely impaired at 24 h postcontusion. Decreases in large surfactant aggregate content and surface activity were improved, but still apparent, at 48 and 72 h postcontusion compared with uninjured control rats and returned to normal by 96 h postcontusion. The functional importance of surfactant abnormalities in LC injury was documented in pilot studies showing that exogenous surfactant replacement at 24 h postcontusion improved inflation/deflation lung volumes. Additional experiments investigated a clinically relevant combination of LC plus gastric aspiration (combined acid and small gastric food particles) and found reductions in large surfactant aggregates in BAL similar to those for LC. However, rats given LC + combined acid and small gastric food particles versus LC had more severe surfactant dysfunction based on decreases in surface activity and alterations in large aggregate composition. Combined data for all animal groups had strong statistical correlations between surfactant dysfunction (increased minimum surface tension, decreased large aggregates in BAL, decreased aggregate PC, and increased aggregate lyso-PC) and the severity of inflammatory lung injury (increased total protein, albumin, protein/phospholipid ratio, neutrophils, and erythrocytes in BAL plus increased whole lung myeloperoxidase activity). These results show that surfactant dysfunction is important in the pathophysiology of LC with or without concurrent gastric aspiration and provides a rationale for surfactant replacement therapy in these prevalent clinical conditions.
Raghavendran
Krishnan
K
Department of Surgery, State University of New York at Buffalo, New York 14214, USA. kr25@buffalo.edu
Davidson
Bruce A
BA
Knight
Paul R
PR
Wang
Zhengdong
Z
Helinski
Jadwiga
J
Chess
Patricia R
PR
Notter
Robert H
RH
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D003288:Contusions / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D055370:Lung Injury / Q000503:physiopathology; D008297:Male; D010713:Phosphatidylcholines / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D011015:Pneumonia, Aspiration / Q000276:immunology / Q000378:metabolism*; D011663:Pulmonary Surfactants / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D013500:Surface Tension
D010713:Phosphatidylcholines; D010743:Phospholipids; D011663:Pulmonary Surfactants