| Long-term smoking can cause chronic bronchitis, emphysema and chronic obstructive pulmonary disease (COPD) and other lung damages. Approximately two thirds of the patients with COPD show airway hyperresponsiveness, and clinical observations suggest that patients of this kind are prone to airway spasm under the strong stimulation of anesthesia induction and intubation. Chronic obstructive pulmonary disease (COPD) is a disease characterized by airflow limitation airflow limitation that is not fully reversible, showing progressive development, associated with the abnormal inflammatory response of lungs to the harmful gases or particles. Long-term smoking can cause COPD that increases various inflammatory mediators attracting inflammatory cells in the circulation, aggravating the inflammatory response and leading to the structural changes of the airway wall. Meanwhile the malfunction of the autonomic nerve and the hyperfunction of the parasympathetic nerve cause so higher airway response than normal and weak stimulation can result in bronchoconstriction spasm. Most of the patients with lung cancer surgery have a long smoking history (20to50years), needing double-lumen endobronchial intubation single lung ventilation in anesthesia and surgery. That studies this kind of patients under the strong stimulus of anaesthesia and intubation, leading to the release of inflammatory mediators and the relationship with bronchospasm and performing effective prevention and drug application, to a great extent should be completed by animal experiments. Preliminary work has successfully constructed a COPD rabbit model caused by simple smudging. LTB4is mainly secreted by the alveolar macrophage cells and neutrophils, which is a potent inflammatory mediators. Leukotriene B4(LTB4) has a strong effect in causing the bronchial smooth muscle contraction.Previous studies mainly focused its participation on the airway inflammation and its significant role in the formation and development of COPD. Vitro experiments showed that its contraction effect to human bronchial smooth muscle was1000times stronger than that of histamine and platelet activating factor (PAF). LTB4combing with the target tissue receptors can cause smooth muscle contraction, capillary exudation, edema and chemotactic response while acting on the bronchial wall can cause bronchial smooth muscle contraction, bronchial luminal narrowing, significantly higher resistance of the airway, increasing permeability and exudation of the trachea and bronchial wall and mucosal edema caused by protein and water leakage. The airway of COPD patients is hyperresponsive, whether the airway spasm under strong stimulation of bronchial intubation, anesthesia induction and single lung ventilation has something to do with LTB4concentration changes in vivo and few domestic and international research in seeking effective prevention and treatment strategies has been done.The experiment is to observe the effects of Salbutamol on leukotriene B4concentration during endobronchial intubatioin and one-lung ventilation in COPD Rabbits.30new zealand white rabbits were divided into3groups, including control group (group A n=6), COPD group (group B n=6) and salbutamol COPD group (group C n=6). A smoke-induced chronic obstructive pulmonary disease rabbit model was established successfully in group B and C.3groups were performed one-lung ventilation by right endobronchial intubation after anesthesia, and group C was promptly given salbutamol atomizing solution through ventilator tube. Serum leukotriene B4concentration was respectively determined before intubation (To), the moment after intubation (Ti),30minutes after one-lung ventilation (T2), and60minutes after one-lung ventilation (T3). The rabbits were sacrificed after60minutes. Double little upper lungs were then removed for microscopic examination and the LTB4concentration in bronchoalveolar lavage fluid was determined. The results of this study showed that one hour after bronchial intubation and one-lung ventilation, the LTB4concentration of lavage fluid in COPD group was much higher than that of the control group (p<0.05). The LTB4concentration of Salbutamol group was much lower than that of COPD group (p<0.05) but had no statistical significance comparing with the control group (p>0.05). Morphological examination of lung tissue showed that in the COPD group alveolar septum widened, neutrophil and lymphocyte infiltrated, the capillary expanded and congested, lymphoid nodules could be seen around the bronchials, alveolar fracture and fusion in some region and bullae were also visable while in the Salbutamol group bronchioles dilated slightly and telangiectasia and congestion of the capillary improved. Salbutamol is a kind of selective β2agonist, which can selectively agitate the bronchial smooth muscle β2receptor and has a strong effect of bronchiectasis. It can also promote mucociliary swing, increase mucociliary clearance function, reduce vascular permeability, inhibit inflammatory exudation and edema, which can promote airway patency and lung function. Bronchial intubation and single lung ventilation could promote the release of LTB4that the bronchial smooth muscle contraction factor of the COPD rabbit, and some sensitive individuals may lead to airway spasm. Prophylactic inhalation of Salbutamol could inhibit the release of LTB4, which had a preventive effect on airway spasm that may occur in the process of bronchial intubation and one-lung ventilation, and had a protective effect on lung tissues.The differences of LTB4concentration of blood serum of each group had no statistical significance, and by morphological examination of lung tissue, three groups had no differences obviously between ventilation side and non-ventilation side, which was related to the short duration of one-lung ventilation. The changes of LTB4concentration in long-time one-lung ventilation and the effects of Salbutamol remained to be further research. |
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