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作 者:周华成[1] 刘金锋[1] 李文志[1] 金笛[1] 潘鹏[1] 丁文刚[1]
机构地区:[1]黑龙江省麻醉与危重病学重点实验室,哈尔滨医科大学附属第二医院麻醉科,150086
出 处:《中华麻醉学杂志》2010年第8期976-979,共4页Chinese Journal of Anesthesiology
基 金:哈尔滨医科大学博士启动基金(BS2009-08)
摘 要:目的 评价吸入不同浓度一氧化碳(CO)对大鼠脑死亡(BD)致肺损伤的影响.方法 成年雄性Wistar大鼠32只,随机分为4组(n=8),假手术组(S组)向大鼠颅内置入Fogarty导管,吸入40%O2 150 min;BD组、C1组和C2组向大鼠颅内置入Fogarty导管,通过膨胀导管前端球囊诱导BD,膨胀球囊30 min后确认BD情况.发生BD后BD组吸入40%O2 120min,C1组和C2组分别吸入40%O2+0.025%CO和40%O2+0.050%CO混合气120 min.于麻醉前(基础状态)、吸入CO前即刻、吸入CO 30、60、90和120 min时采集动脉血样,进行动脉血气分析.吸入CO 120 min时采集动脉血样,测定血浆IL-6和TNF-α浓度;采集血样后,处死大鼠,取肺组织,测定髓过氧化物酶(MPO)活性;计算肺组织湿/干重比(W/D比),并进行肺组织损伤评分(LIS评分).结果 与S组比较,BD组、C1组和C2组PaO2/FiO2、BE和pH值降低,血浆IL-6和TNF-α的浓度、MPO活性、肺组织W/D比和LIS评分升高(P<0.05);与BD组比较,C1组和C2组PaO2/FiO2、BE和pH值升高,血浆IL-6和TNF-α的浓度、MPO活性、肺组织W/D比和LIS评分降低(P<0.05);与C1组比较,C2组血浆IL-6和TNF-α的浓度降低(P<0.05),血气分析指标、MPO活性、肺组织W/D比和LIS评分差异无统计学意义(P>0.05).结论 吸入0.025%和0.050%CO减轻大鼠BD致肺损伤的效应无差异.Objective To investigate the effects of inhalation of different concentrations of carbon monoxide (CO) on brain death (BD)-induced lung injury in rats. Methods Thirty-two pathogen free adult male Wistar rats weighing 250-300 g were randomly divided into 4 groups ( n= 8 each): group Ⅰ sham operation (group S);group Ⅱ brain death (group BD) and group Ⅲ and Ⅳ BD + CO 0.025% and 0.050% (group C1, C2 ). The animals were anesthetized and tracheally intubated. Fogarty catheter was inserted into the skull. BD was induced by inflating the balloon slowly at 20 μl/min until apnea developed. The animals were then mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O) with 40% O2 in N2 . In group Ⅲ and Ⅳ CO 0.025% and 0.050%were added to the air mixture respectively. In group S the balloon was not inflated. BD was confirmed by apnea,dilated pupils and flat EEG. In group BD,C1 and C2, MAP was maintained at 80-120 mm Hg by norepinephrine infusion. The arterial blood gas analysis was performed before (baseline) and immediately after BD was confirmed (T1) and at 30, 60, 90 and 120 min (T2-5) of CO inhalation. The animals were then sacrificed. The plasma concentrations of IL-6 and TNF-α and the activity of myeloperoxidase (MPO) in the lungs were measured. The W/D lung weight ratio and lung injury score (LIS) were recorded. Results BD significantly decreased PaO2/FiO2, BE and pH while increased plasma IL-6 and TNF-α concentrations, MPO activity in the lungs, the W/D ratio and lung injury score as compared with group S. CO inhalation ameliorated the deleterious effects induced by BD. The antiinfiammatory effect of 0.050% CO was better than that of 0.025 % CO. Conclusion Inhalation of 0.025 % or 0.050% CO can ameliorate BD-induced lung injury in rats, but there is no significant difference in the efficacy.
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