| Introduction:Blunt injury to the lung, or pulmonary contusion, is common after thoracic trauma. The damage is caused not only by direct tissue injury, but also by a posttraumatic inflammatory initiated immediately after contusion, which is charactered by granulocyte activation known as acute lung injury (ALI). In its extreme form acute respiratory distress syndrome (ARDS),it can lead to multiple organ failure(MOF). Yet now, therapy and current standard of care for the pulmonary contusion are limited due to this multifactorial and complicated disease processes, with no widely accepted and practical pharmacological intervention used in clinical. Leukocyte elastase (NE) is a serine protease synthesized by leukocytes and macrophages in the lung. NE has multiple and complicated potential mechanisms ,which contribute to the pathogenesis of lung injury. In normal physiological conditions, lung tissues are protected from unregulated proteolysis by NE. One of these includes alphal1-antitrypsin (α1-AT), the endogenous inhibitor of NE, which forms the inactive protease-antiprotease complex combined with NE. Increased activity of NE and decreased contents of α1-AT were described in ARDS ,which concluded that the imbalance between protease and antiprotease might be involved in the pathogenesis of ALI. Aprotinin is a nonspecific serine protease inhibitor used extensively in cardiac operation, to reduce postoperative bleeding since its efficacy was discovered initially. Many trials and findings suggested that aprotinin might modify the inflammatory response through many pathways. However,the role of NE and whether or not aprotinin take effects on inflammatory reaction remained unclear and have not been reported in the process of inflammatory in pulmonary contusion. Objective: To investigate the roles of NE and the experimental effects of aprotinin on inflammatory reaction in the early phase of pulmonary contusion induced by chest trauma.Mathods: Established the isolated lung contusion model of rabbits, which were subjected to chest impact trauma by bioimpact machine. Rabbits were divided into three groups: the normal control group (n=10), infusion of saline without trauma; traumatic group (n=10), isolated thoracic trauma without treatment; the aprotinin treatment group (n=10), infusion of aprotinin simultaneous and continuous after trauma. Bloodpressure(BP), respiratory rate(RR), arterial oxygen pressure (PаO2) and arterial partial pressure of carbon dioxide( PаCO2 ) were recorded.The value of PH,base excess(BE),peripheral leukocyte and platelet counts were assessed. The activity of NE and the contents of α1-AT, prostaglandins, thromboxane B2 (TXB2), tumor necrosis factor-α(TNF-α) and interleukin-8(IL-8) were detected both in plasma and in bronchalvelor lavage fluid (BALF).Data were collected at different time points of 0,0.5,1,2,4,6h after chest trauma. Rabbits were killed and collected BALF at the end of 6h,static lung compliance(Cst), cell fraction , the contents of TNF-α and IL-8, TXB2 and 6keto-PGF1αwere measured in the BALF. The albumin concentration in BALF and the wet/dry (W/D) weight ratios of the lung were analyzed. Malondialdehyde (MDA) and myeloperoxidase (MPO) were detected in lung tissues. The histological features of lung were examined by light microscope.Results: In traumatic group ,it was observed signs of shortness of breath and fast heart rate compared to the control group . PаO2 ,PаCO2 ,the value of PH and Cst were declined but RR and BE were rised gradually.Peripheral leukocyte count, the contents of TNF-α , IL-8, TXB2 and 6keto-PGF1α were increased both in plasma and BALF. The activity of NE was elevated progressively, but the concentrations of α1-AT were declineded initially within 1h then uplifted later. The activity of NE raised much more than that of α1-AT . Data support the changes of the imbalance between NE andα1-AT. The contents of MDA and MPO were elevated in the lung tissue. The ratio of W/D and albumin in BALF were higher .Examnations showed the augmented activ...
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