Abstract
BACKGROUND: The mechanism between ventilator-induced lung injury (VILI) and multiple organ injury is unclear. The aim of our study was to investigate the mechanisms of VILI-induced distal organ injury.
METHODS: VILI was induced in rat lungs with high tidal volume (VT) ventilation of 40 mL/kg for 6 h. Rats with low VT ventilation of 6 mL/kg served as controls. Inflammatory and apoptotic indices in lung and distal organs were assessed.
RESULTS: VILI increased lung weight, airway pressure, inflammation, and apoptotic pathologic changes without hemodynamic changes. The white blood cell count and the levels of H2O2, interleukin-1β (IL-1β), tumor necrosis factor alpha, and macrophage inflammatory protein-2 in bronchoalveolar lavage fluid were higher in the VILI group compared with the control group. H2O2, IL-1β, and tumor necrosis factor alpha in blood from the left ventricle were up-regulated. H2O2, IL-1β, tumor necrosis factor alpha, macrophage inflammatory protein-2, c-Jun N-terminal kinase, p38, nuclear factor kappa B, and caspase-3 in lung, heart, liver, and kidney tissues in the VILI group were up-regulated. Furthermore, the apoptotic score for the kidneys was higher than those for other distal organs in the VILI group.
CONCLUSIONS: High VT ventilation induces VILI and is associated with inflammation and apoptosis in distal organs. Up-regulation of reactive oxygen species and cytokines in VILI is associated with systemic inflammatory responses. Kidney tissue appears to be more vulnerable than heart and liver tissues following VILI.
Footnotes
- Correspondence: Chi-Huei Chiang MD, Division of Pulmonary Immunology and Infectious Diseases, Chest Department, Taipei Veterans General Hospital, No. 201, Section 2, Shih-Pai Road, Taipei, Taiwan. E-mail: chiang01{at}vghtpe.gov.tw, chiang1990{at}gmail.com.
This work was supported by Taipei Veterans General Hospital grants 101DHA0100665, 101DHA0100079, 100DHA0100130, and 99DHA0100412 and National Science Council grants NSC97-2314-B-075-045, NSC98-2314-B-075-036, and NSC99-2314-B-075-034-MY2. The authors have disclosed no conflicts of interest.
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