The present study was designed to investigate the consequences of isol
ated unilateral lung contusion on local alveolar and systemic inflamma
tory responses in an animal model in the pig. Isolated unilateral lung
contusion was induced by bolt shot in eight mechanically ventilated a
nimals under general anesthesia (sham: n = 4). Plasma and bronchoalveo
lar ravage fluid were collected during a period of 8 h following lung
contusion. Leukocytes, leukocyte neutral protease inhibitor (LNPI), te
rminal complement complex (TCC), thrombin-antithrombin-complex (TAT) a
s well as pulmonary microvascular permeability and surfactant function
were determined. Within 30 min, lung contusion was found to cause a s
ignificant local and systemic increase in TCC and TAT concentrations a
nd a systemic increase in LNPI concentrations. The latter was accompan
ied by a sequestration of leukocytes in the contused lung. Complement
activation and leukocyte sequestration in the contused lung progressiv
ely increased during the investigation period. Although surfactant fun
ction decreased in the entire lung 30 min after contusion, TCC, TAT, a
nd leukocyte sequestration was unchanged in the contralateral lung. Th
e first indication of an involvement of the contralateral lung was obt
ained by an increase in leukocyte sequestration 8 h after lung contusi
on. Unilateral lung contusion initiates an early systemic activation o
f humoral and cellular defense systems. Involvement of the contralater
al lung appears to be a secondary event caused by a systemic inflammat
ory reaction.