The objective of this controlled experimental animal study was to evaluate whether
acute hepatic failure (AHF) can cause
acute lung injury (ALI) and to investigate possible pathophysiologic mechanisms. Seventeen domestic pigs were randomly assigned to AHF and
sham groups. AHF was induced by surgical devascularization of liver in 10 animals. Seven animals were
sham operated. Hemodynamics, lung mechanics, extravascular lung water (EVLW), and intracranial pressure, blood gas, liver function tests, and serum
endotoxin levels were measured. Cells count, total
protein, and
phospholipids and
phospholipases A(2) were determined in the bronchoalveolar lavage (BAL) fluid. Measurements were obtained after the insertion of central lines and 4 hours and 7 hours after the completion of the
surgical procedure. Hemodynamic, biochemical, neuromonitoring, and histologic data confirmed the development of
liver failure. Seven hours after devascularization, EVLW was higher in AHF (13.7 +/- 1.8 mL/kg) compared with the
sham group (5.9 +/- 0.7 mL/kg) (P <.05); in AHF, increase of neutrophils (5% +/- 8% to 25% +/- 8%, P <.001), total
protein (6.2 +/- 3.7 to 11.2 +/- 6.5 microg/mL, P <.048), and
phospholipase A(2) (1.43 +/- 0.56 to 2.38 +/- 1.38 nmoL/mL/h, P <.03) and decrease in
PAF-acetylhydrolase (0.114 +/- 0.128 to 0.039 +/- 0.038 nmol/mL/h, P <.01) compared with baseline were observed; total
phospholipids decreased in AHF and increased in the
sham model. Histologic examination confirmed lesions compatible with
acute lung injury. In conclusion, AHF due to hepatic devascularization induced
acute lung injury, confirmed by the increase of inflammatory cells in the alveoli as well as by histologic findings. The decreased PAF-AcH and the increased
phospholipase A(2) may play a significant role in the perpetuation of
inflammation accompanied by
surfactant disorders.