| IntroductionOxygen deprivation from ischemia or nonventilation leads to cellular hypoxic injury.Paradoxically, reperfusion of hypoxic tissues may result in further cellular damage. There is an abundantevidence that reperfusion injury is the structural damage caused by the interaction of reactive oxygenspecies (ROS), endothelial factors and neutrophils. Lung is a critical organ in oxidative stress process ofeither systematic or pulmonary origin. Pulmonary parenchyma is one of the largest reservoirs forneutrophils, monocytes and macrophages. Moreover atelectasis leads to hypoxic vasoconstriction.Reexpansion along with oxygen reentrance through the airways causes reactive pulmonaryvascular dilatation commencing reperfusion of the lungs. Ischemia-reperfusion sequence develops ROS.These are highly reactive species due to the unpaired electrons which contain to their outer orbits. Theyinteract with cellular structural molecules provoking dysfunction mostly to endothelial cells. Lipidperoxidation is one of the most important metabolic consequences of oxidative stress. Under normalcircumstances, these reactions are counteracted by the action of endogenous antioxidant defensemechanisms. This balance is disturbed during reperfusion. A tremendous cascade of events developsextremely reactive molecules that outnumber the reserves of antioxidant systems. During one lungventilation the operated lung remains completely atelectatic for a period of time. It is well known thatnon-ventilated lung is also hypoperfused due to hypoxic vasoconstriction. Besides, the postresectionalremaining pulmonary tissue has been subjected to considerable manipulation during the conductedlobectomy or segmentectomy. When bronchial block is ended the following immediate lung reexpansionalong with tissue reperfusion might generate ROS through a fairly well described mechanism. Althoughone lung is a resistant tissue to hypoxia because of its dual blood flow and the use of oxygen reserves inalveolar spaces reexpansion injury detected after pneumothorax management and reperfusion injury afterlung transplantation are two examples for possible oxidative damage. We conducted a prospective analysisin order to investigate the generation of ROS through lipid peroxidation metabolites after one-lungventilation (OLV) pulmonary resections. Dexmedetomidine is a new set of α2-adrenergic receptor agonist. Studies have shown thatdexmedetomidine is given by anti-sympathetic can inhibit apoptosis, oxidative stress in a variety of waysand inflammatory reactions to vital organs such as the brain, heart, kidneys, liver and lungs, which plays aprotective role.ObjectiveProtective effect of expression and one-lung ventilation (OLV) oxygen free radical-mediatedoxidative research OLV lower part of the stress response of inflammatory cytokines and through animalexperiments testing dexmedetomidine for one-lung ventilation.Methods1. Clinical Research: Oxidation of one-lung ventilation (OLV) oxygen free radical-mediatedstress response. From2010to2003,221patients were prospectively studied for lungreexpansion/reperfusion injury. They were classified in six groups. Group A, non-OLV lobectomy group; B,OLV pneumonectomy group; C–E, OLV lobectomy of60,90, and120min duration, respectively; F,normal subjects as baseline group. Preoperative, intraoperative and postoperative strict blood samplingprotocol was followed. Malondialdehyde (MDA) plasma levels were measured. The recorded values wereanalyzed and statistically compared between groups and within each one.2. Animal experiments: the male New Zealand white rabbits were randomly selected10as thesham group (control group), only puncture operate and maintain non-OLV. Another group of two simpleone-lung ventilation group, another group of one-lung ventilation plus dexmedetomidine. The third set ofexperiments to estimate the protective effect of dexmedetomidine for single lung ventilation By detectingTNF-α and IL-6differences between these two factors.Results1. Clinical research results: Comparison of groups C–E (OLV) to all other documented significant(P<0.001) increase of MDA levels during lung reexpansion and for the following12h. The magnitude ofoxidative stress was related to OLV duration (group E>D>C, all P<0.001). The removal ofcancer-associated parenchyma led to MDA level decrease postoperatively (P<0.001) especially afterpneumonectomy (A vs. B, P<0.001).2. The results of animal experiments: Detected by immunoblotting and some inflammatory cytokines, staining results indicate that dexmedetomidine can effectively play a protective role followingthe lung injury.Conclusions1. One-lung ventilation (OLV) provoked severe oxidative stress.2. The volume of TNF-α and IL-6in dexmedetomidine in the experimental group are reduced,note dexmedetomidine can reduce pulmonary inflammation, can play a protective role on the unilaterallung ventilation.3. Experiments found that join dexmedetomidine in the experimental group reduces the bodylevel of oxidative stress, reduce the lung tissue--to instill damage. |
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