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Pulmonary Injury (pulmonary + injury)

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Medical Sciences	100%

Selected Abstracts

Role of interleukin-18 in the development of acute pulmonary injury induced by intestinal ischemia/reperfusion and its possible mechanism

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2007
Yong-jie Yang
Abstract Background and Aims:, Lung injury is an important target for the systemic inflammatory response associated with intestinal ischemia/reperfusion (I/R). In the present study, the role of interleukin (IL)-18 in the development of acute pulmonary injury induced by intestinal I/R and its possible mechanism in relation to the increased activity of inducible nitric oxide synthase and tumor necrosis factor (TNF)-, were investigated. Methods:, Mice were randomly divided into three groups: normal control group without operation; sham group with sham operation; and I/R group in which mice underwent superior mesenteric artery occlusion for 30 min followed by reperfusion for 3 h. Each group received pretreatment with exogenous IL-18, anti-IL-18 neutralizing antibody or L-NIL, the selective inhibitor of inducible nitric oxide synthase, 30 min before ischemia. The expression of TNF-, was detected by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Lung injury was evaluated by means of Evans blue dye (EBD) concentration, myeloperoxidase (MPO) activity and morphological analysis. Results:, The experimental results showed that both in the sham-operated and I/R groups of animals, pretreatment with exogenous IL-18 clearly enhanced pulmonary MPO activity, microvascular leakage and the expression of TNF-, mRNA and protein. In contrast, IL-18 did not increase the TNF-, level and degree of lung injury, although it clearly enhanced the pulmonary MPO activity in normal animals. Meanwhile, IL-18 antibody given prior to ischemia led to a reduction in the sequestration of neutrophils, extravasation of EBD and downregulation of the serum level of TNF-, in the I/R group of animals. In addition, selective inhibition of inducible nitric oxide synthase (iNOS) that inhibited plasma extravasation and pulmonary injury without affecting the MPO activity could be demonstrated in all treated animals. Conclusions:, These data suggested a role of IL-18 in the activation and sequestration of neutrophils in lungs. Our results were consistent with the hypothesis that increased sequestration of neutrophils and microvascular leakage might, respectively, relate to the increased IL-18 level and the elevation of TNF-,/iNOS activity, and these two aspects might synergically contribute to intestinal I/R-induced pulmonary dysfunction. [source]

Protective role of Coenzyme Q10 in two models of rat lung injury

ANZ JOURNAL OF SURGERY, Issue 4 2010
Hou-Kiat Lim
Abstract Background:, Ischaemia-reperfusion injury is a life-threatening complication of lung transplantation. Attempts to ameliorate this injury have included optimization of donor management and improving techniques of lung preservation. However, few investigators have sought to pretreat potential recipients. Coenzyme Q10 (CoQ10) is a potent antioxidant and cellular energizer that has been shown to protect the heart against injury. However, its protective effect in the lung is unknown. We therefore set out to study the impact of Coenzyme Q10 pretreatment in a model of mild and severe lung injury. Methods:, We evaluated the impact of CoQ10 in a two-stage laboratory study. In the first stage, in order to measure the magnitude of increase in tissue and plasma CoQ10 following oral therapy we administered high-dose oral CoQ10 to rats (n = 6). In the second stage we evaluated the impact of CoQ10 in the rat lung (n = 10) that was subjected to 230 min of normoxic lung injury or 90 min of warm ischaemia and 120 min of reperfusion in a model of lung transplantation. Results:, High-dose oral CoQ10 for 7 days produced a 15-fold increase in plasma and a 3-fold increase in lung CoQ10. In the normoxic lung, the injury-induced rise in peak airway pressure was reduced by CoQ10 treatment at 90 min (P = 0.037) and at 120 min (P = 0.005) without any change in arterial oxygen. In the lung subjected to severe ischaemia-reperfusion injury, CoQ10 did not reduce the injury-induced increase in peak airway pressure (P = 0.599) nor the decrease in arterial oxygen (P = 0.844). However, CoQ10 markedly reduced the increase in tumour necrosis factor-alpha in ischaemic compared with normoxic lung (P = 0.027). Conclusions:, The effect of CoQ10 pretreatment is insufficient to protect the lung against severe ischaemia-reperfusion as may occur in lung transplantation. However, in the setting of less severe pulmonary injury as in anaesthesia and non-transplant surgery, CoQ10 may have a protective role. [source]