Chi-Huei Chiang1, Hsin-I Pai, Shiou-Ling Liu. 1. Institute of Emergency and Critical Care Medicine, Medical School, National Yang-Ming University, Taipei, Taiwan. chiang01@vghtpe.gov.tw
Abstract
RATIONALE: Whether the ventilator-induced lung injury (VILI) superimposed on ischemia/reperfusion injury (I/R) causes synergistic damage has not been well explored. Whether nuclear factor-kappa B (NF-kappaB) antibody has protective effects for both injuries is also unknown. METHODS: I/R and VILI were produced in an isolated rat lung model. Hemodynamics, lung weight gain (LWG), capillary filtration coefficient (K(fc)), cytokines, and lung pathology were assessed. RESULTS: VILI or I/R produced similar permeability pulmonary edema which was reflected by increasing K(fc) and LWG. Cytokine (IL-1beta) up-regulation occurred in both injuries. Pathologic examination showed edema and inflammatory cell infiltration in VILI or I/R. In addition, the alveoli were overdistended and even ruptured because of marked inhomogeneity of inflation in VILI. Furthermore, combined I/R and VILI produced further increases in K(fc), LWG, IL-1beta, as well as more severe pathologic changes. Conversely, less permeability pulmonary edema, pathologic changes and IL-1 expression were found in groups pretreated with anti-NF-kappaB antibody. CONCLUSION: VILI and I/R cause synergistic damage on the lung. I/R or VILI alone or combined can be attenuated by NF-kappaB antibody. NF-kappaB plays an important role in both forms of lung injury. We propose anti-NF-kappaB antibody pretreatment to be beneficial for VILI, I/R and lung transplantation.
RATIONALE: Whether the ventilator-induced lung injury (VILI) superimposed on ischemia/reperfusion injury (I/R) causes synergistic damage has not been well explored. Whether nuclear factor-kappa B (NF-kappaB) antibody has protective effects for both injuries is also unknown. METHODS: I/R and VILI were produced in an isolated rat lung model. Hemodynamics, lung weight gain (LWG), capillary filtration coefficient (K(fc)), cytokines, and lung pathology were assessed. RESULTS: VILI or I/R produced similar permeability pulmonary edema which was reflected by increasing K(fc) and LWG. Cytokine (IL-1beta) up-regulation occurred in both injuries. Pathologic examination showed edema and inflammatory cell infiltration in VILI or I/R. In addition, the alveoli were overdistended and even ruptured because of marked inhomogeneity of inflation in VILI. Furthermore, combined I/R and VILI produced further increases in K(fc), LWG, IL-1beta, as well as more severe pathologic changes. Conversely, less permeability pulmonary edema, pathologic changes and IL-1 expression were found in groups pretreated with anti-NF-kappaB antibody. CONCLUSION: VILI and I/R cause synergistic damage on the lung. I/R or VILI alone or combined can be attenuated by NF-kappaB antibody. NF-kappaB plays an important role in both forms of lung injury. We propose anti-NF-kappaB antibody pretreatment to be beneficial for VILI, I/R and lung transplantation.
Authors: Moo Suk Park; Qianbin He; Michael G Edwards; Amen Sergew; David W H Riches; Richard K Albert; Ivor S Douglas Journal: Am J Respir Crit Care Med Date: 2012-05-10 Impact factor: 21.405