吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

吸入一氧化碳对大鼠脑死亡致肺损伤的影响

Objective To investigate the effects of carbon monoxide (CO) inhalation on lung injury induced by brain death (BD) in rats. Methods Adult male Wistar rats weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg, tracheostomized and mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O). A balloon-tip catheter was placed in the cranium. Twenty-four rats in which Fogarty catheter was successfully placed in the cranium without complication were randomly divided into 3 groups ( n = 8 each) : group I sham operation (group S) ; group II BD and group Ⅲ BDCO. BD was induced by increase in intracranial pressure produced by inflating the balloon at the tip of the catheter. In group S the balloon of the catheter was not inflated. The animals inhaled 40% O2 for 150 min. In group BD, BD was induced and confirmed at 30 min after inflation of the balloon. Then 40% O2 was inhaled for 120 min. In group BDCO, 40% O2 and 0.025% CO were inhaled for 120 min after BD was confirmed at 30 min after balloon inflation. At the end of the experiment the animals were killed. Arterial blood samples were obtained for blood gas analysis before anesthesia (basline), immediately after confirmation of BD, and at 30, 60, 90 and 120 min of CO inhalation. Blood was collected for determination of plasma TNF-α, IL-6 and IL-10 concentrations at 120 min of CO inhalation. The lungs were obtained for determination of W/D lung weight ratio, and MPO activity in the lung tissue and microscopic examination. Lung injury scores were calculated. Results PaO2/FiO2 was stable during the 150 min in group S. Brain death significantly decreased PaO2/FiO2 at 30 min after balloon inflation. PaO2/FiO2 was gradually decreasing during the 120 min in group BD. CO inhalation prevented PaO2/FiO2 from decreasing further. W/D lung weight ratio and MPO activity were significantly higher in group BD than in group S and BDCO. The lung injury score (1 = normal, 4= severely injured) and plasma TNF-αα IL-6 and IL-10 concentrations were significantly higher in group BD than in group S. CO inhalation ameliorated the BD-induced lung injury and attenuated the increase in plasma TNF-a and IL-6 concentration. Plasma IL-10 concentration was significantly higher in group BDCO than in group BD. Conclusion CO inhalation can ameliorate acute lung injury induced by BD through decreasing the local and systemic inflammatory response.     

立足基线,改进质量 ——记黑龙江省麻醉质控工作的开展

国际标准化组织(ISO)颁布的《质量管理体系——业绩改进指南》(ISO 9004)指出,质量管理不仅要着眼于产品和服务的质量,也需关注实现质量目标的方法和路径。这一质量管理理念不仅适用于产品,也同样适用于医疗行为。然而医疗行为不同于产品,它是一个动态的、多方参与的过程。因此,医疗行为质量控制工作的开展必须确保建立一个知识共享、具有协调和组织能力的系统,同时要营建一个鼓励并追求质量改进的意识和文化体系。     

烟碱对大鼠移植肺NF-κB表达和细胞因子的影响

目的评价外源性烟碱对大鼠移植肺损伤以及NF-κB表达和细胞因子的影响。方法雄性Wistar大鼠40只,随机分为3组,假手术组(S组;8只);肺移植组(C组;16只,供体、受体各8只);肺移植+烟碱处理组(N组;16只,供体、受体各8只)。S组只进行开胸等操作不进行肺移植;N组于肺移植术后15min时腹腔注射烟碱2 mg/kg。肺移植术后2 h取移植肺组织,进行肺组织病理损伤(LIS)评分,测定肺组织湿/干重比(W/D),采用免疫组化染色测定肺组织NF-κB表达,ELISA法测定血浆TNF-α、IL-1β和IL-6的浓度。结果 C组NF-κB的表达明显高于N组和S组,S组NF-κB的表达最低。与C组比较N组和S组血浆IL-6、IL-1β和TNF-α浓度降低。与C组比较,N组和S组W/D和LIS评分降低;但N组仍比S组W/D和LIS评分高。结论外源性烟碱可能通过激活胆碱能抗炎通路减少NF-κB的表达及随后TNF-α、IL-1β和IL-6的合成,减轻大鼠移植肺损伤。     

肝胆手术后胆漏的临床治疗分析

目的 探讨肝胆手术后胆漏的临床治疗方法及效果.方法 选取2008年3月至2020年3月我院收治的54例肝胆手术后胆漏患者,随机分为两组,对照组进行常规治疗,研究组进行针对性治疗.比较两组治疗结果、生活质量、炎性因子水平、总胆红素、谷氨酰转肽酶、白细胞计数.结果 与对照组比较,研究组手术、下床活动、住院天数、肛门排气时间...     

脑死亡供体吸入一氧化碳对肺移植后细胞凋亡的影响

目的观察脑死亡(brain death,BD)肺移植供体吸入一氧化碳(carbon monoxide,CO)对移植肺细胞凋亡的影响。方法将24只大鼠随机分为3组,对照组(sham组)供体鼠颅内置入Fogarty导管,但不膨胀前端球囊;脑死亡组(BD组)和脑死亡CO治疗组(BDCO组)供体鼠颅内置入Fogarty导管,并膨胀前端球囊建立BD模型。sham组和BD组吸入氧气浓度为40%的氧氮混合气150 min,BDCO组在开始BD诱导后30 min,确认BD后,吸入氧气浓度为40%的氧氮混合气和250 ppm的CO2 h。然后进行肺移植,移植后2 h取移植肺组织切片进行TUNEL染色观察移植肺中细胞凋亡情况,使用RT-PCR和免疫组化技术观察Caspase-3 mRNA和蛋白表达情况。使用免疫组化评分(immunohistoche micas scores,IHS)对细胞凋亡和Caspase-3蛋白表达进行评估。结果BD组细胞凋亡程度,Caspase-3蛋白和mRNA表达显著高于sham组(P0.05),BDCO组与BD组相比,上述指标显著降低(P0.05)。结论供体BD过程增加了移植肺细胞凋亡比率,BD供体吸入CO对移植肺再灌注后细胞凋亡有拮抗效应。     

SLIPA喉罩在老年人全身麻醉中的应用

我国已接近进入老龄社会,老年患者全麻下手术治疗的数量逐年增多,此类患者多采用气管插管全麻,麻醉诱导后喉镜置入和气管导管插入容易引起明显的心血管应激反应。由于老年人多存在高血压、血管硬化、心血管代偿机能减弱,血压骤升和心动过速将加重心脏负担,容易发生心肌缺氧、缺血、心律紊乱以及心脑血管意外等。     

脑死亡供体鼠吸入一氧化碳对受体鼠移植肺损伤的影响

目的 评价脑死亡供体鼠吸入一氧化碳(CO)对受体鼠移植肺损伤的影响.方法 雄性Wistar大鼠24只,体重250～300 g,随机分为3组(n=8),接受非脑死亡供体肺组(NBD组)供体鼠颅内置入Fogarty导管,但不诱导脑死亡,观察2.5 h;接受吸入氧气的脑死亡供体肺组(BDO2组)供体鼠确认脑死亡后吸入40%氧气2 h;接受吸入CO的脑死亡供体肺组(BDCO组)供体鼠确认脑死亡后吸入40%氧气和0.025%CO混合气2 h.处理结束后取供体左肺,进行原位异体肺移植,受体鼠每30 min进行一次动脉血气分析.肺移植成功后2 h处死受体鼠,采集右股动脉血样,采用嘌呤氧化酶法测定血浆超氧化物歧化酶(SOD)活性;采用硫代巴比妥酸法测定丙二醛(MDA)浓度;采用ELISA法测定血浆白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α和IL-10浓度.计算移植肺组织湿/干重比(W/D);测定移植肺组织髓过氧化物酶(MPO)活性,并进行移植肺组织损伤评分.结果 与C组比较,BDO2组和BDCO组PaO2/FiO2、BE、pH值和血浆SOD活性、IL-10浓度降低,移植肺组织W/D、MPO活性、损伤评分和血浆MDA、IL-6、TNF-α浓度升高(P<0.05);与BD02组比较,BDCO组PaO2/FiO2、BE、pH值和血浆SOD活性、IL-10浓度升高,移植肺组织W/D、MPO活性、损伤评分和血浆MDA、IL-6、TNF-α浓度降低(P<0.05).结论 脑死亡供体鼠吸入CO 2 h可减轻受体鼠移植肺损伤,其机制可能是吸入CO提高了移植肺的抗氧化能力,减轻了移植后局部和全身炎性反应.