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.     

预测控制加智能控制用于七氟醚闭合环路定量麻醉的可行性

目的探讨自制的伺服控制闭合麻醉系统、预测控制加智能控制用于七氟醚定量麻醉的可行性。方法143例ASAⅠ-Ⅲ级病人,静脉注射芬太尼2-3μg·kg-1、咪唑安定0.12mg·kg-1、维库溴铵0.1mg·kg-1诱导插管后,使用由IBM计算机、氧气质量流量控制器、电控七氟醚注射泵组成的伺服控制全麻系统向呼吸环路中送入氧气和七氟醚,氧气的新鲜气流量为[体重(kg)3/4×10 20]ml·min-1。用预测控制加智能控制法控制七氟醚呼气末浓度为1.3MAC。结果洗入时间(5.2±2.4)min,麻醉洗入和维持期间的新鲜气流量为(0.22±0.04)L·min-1。七氟醚的累积摄取量为:5.16ml(30min)、7.74ml(60min)、9.17ml(90min)、11.08ml(120min)、12.47ml(150min)、13.00ml(180min)、14.18ml(210min)、15.60ml(240min)、18.56ml(300min)和24.60ml(420min)。在420min中,七氟醚注入速率的三指数方程为(0.2673e-0.0598t 0.2269e-0.0597t 0.1150e-0.0021t)ml·min-1。结论预测控制加智能控制可控制多因素干扰下的设定的七氟醚呼气末浓度,是一种安全有效的方法。     

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.     

地氟烷预先给药对大鼠前脑缺血再灌注时线粒体通透性转换孔和膜电位的影响

目的 研究地氟烷预先给药对大鼠前脑缺血再灌注时线粒体通透性转换孔(PTP)和膜电位的影响,以探讨其脑保护作用的机制.方法 雄性Wistar大鼠40只,体重250～300 g,随机分为4组(n=10):假手术组(Ⅰ组)、缺血再灌注组(Ⅱ组)、1.0 MAC地氟烷组(Ⅲ组)和1.5 MAC地氟烷组(Ⅳ组),采用夹闭双侧颈总动脉合并低血压的方法建立前脑缺血再灌注损伤模型,Ⅲ组和Ⅳ组在缺血前分别吸入地氟烷1.0 MAC和1.5 MAC 40 min.再灌注4 h行神经功能缺陷评分(NDS),迅速断头,密度梯度离心分离线粒体,采用分光光度计法分析Ca2+诱发的线粒体肿胀,荧光分光光度计法检测线粒体膜电位耗散.结果 再灌注4 h,与Ⅰ组相比,Ⅱ组、Ⅲ组和Ⅳ组线粒体PTP活性、NDS升高,Ⅱ组线粒体膜电位耗散增加(P＜0.05);与Ⅱ组相比,Ⅲ组和Ⅳ组线粒体PTP活性、NDS及线粒体膜电位耗散降低(P＜0.05).结论 地氟烷预先给药可减轻大鼠前脑缺血再灌注损伤,改善再灌注时神经功能,可能与其抑制线粒体的肿胀、减少线粒体膜电位的耗散有关.     

模拟紧闭环路内不同的碱石灰对地氟烷分解反应的比较

目的 研究模拟紧闭环路内三种成分不同的十燥碱石灰与地氟烷发生分解反应生成一氧化碳(CO)的差异。方法 选用钡石灰、国产钠石灰及Sofnolime。在麻醉机的Y-piece端接一贮气囊做为模拟肺。二氧化碳(CO_2)以200ml·min~(-1)的流速通入环路。设定分钟通气量6L·min~(-1),呼吸频率(RR)12次/min,使P_(ET)CO_2在35～45 mm Hg。根据碱石灰的种类不同将实验分为三组,每组实验重复三次。向环路内通入二氧化碳及氧气的同时开启蒸发罐,洗入期开始,当呼气未地氟烷浓度达9％时关闭蒸发罐及新鲜气流,紧闭环路,继续机械通气直至180min。监测 P_(ET)CO_2、重复吸入CO_2分压、地氟烷的吸入、呼出浓度及上下罐反应温度。用气相色谱仪测定CO浓度。结果 三种碱石灰分解地氟烷生成CO的峰浓度及平均浓度由高到低的顺序依次是钡石灰、Sofnolime及国产钠石灰。钡石灰组CO达峰浓度时间明显快于其它两组(P<0.05)。与上罐相比下罐温度上升时间延迟。国产钠石灰组洗入时间较其余两组短。在温度上升期钠石灰组上罐温度上升速度快而钡石灰组下罐温度上升速度快。结论 在模拟紧闭环路内,使用钡石灰发生CO中毒的危险性要高于钠石灰。但仅仅去除钠石灰中的KOH,不能减少吸入全麻药的分解,相反生成CO的量可能增多。     

吸入不同浓度一氧化碳对大鼠脑死亡致肺损伤的影响

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.     

内皮素与一氧化氮在2型糖尿病大鼠心肌缺血再灌注损伤中的变化及意义

目的 探讨血清内皮素(ET)-1、一氧化氮(NO)在2型糖尿病大鼠心肌缺血再灌注损伤过程中的变化及意义.方法 选择体重160 ～ 180 g的健康雄性Wistar大鼠,采用高脂饲养联合腹腔注射链脲佐菌素(STZ)的方法制备2型糖尿病模型,取造模成功后的糖尿病大鼠14只(D组),随机分为两组(n=7):糖尿病心肌缺血再灌注组(DI组)和糖尿病假手术组(DC组).年龄匹配的健康雄性Wistar大鼠14只作为对照(C组),随机分为两组(n=7):心肌缺血再灌注组(CI组)和假手术组(CC组).DI组和CI组采用结扎左冠状动脉前降支30 min再灌注120 min的方法制备心肌缺血再灌注模型.各组分别测定基础状态、再灌注120 min时血清NO、ET-1的含量.结果 与基础状态时比较,CI组、DI组在缺血再灌注120 min时血清NO水平降低、ET-1水平升高(t值分别为4.96、4.69、19.04和3.35,P＜0.05).与CC组比较,CI组NO水平降低、ET-1水平升高,差异具有统计学差异(F=18.07、11.97,P＜0.05);与DC组比较,DI组NO水平降低、ET-1水平升高具有统计学差异(F=4.15、8.04,P＜0.05).DC组基础状态时血清ET-1水平高于CC组,具有统计学差异(=9.47,P＜0.05).结论 血清中NO、ET-1在2型糖尿病大鼠心肌缺血再灌注损伤的病理生理过程中具有一定的意义.     

B型利钠肽对非心脏手术患者心血管事件预测

心血管并发症是手术患者围术期死亡的主要原因,对患者进行准确的围术期风险评估至关重要。B型利钠肽是心功能受损的可靠生物标志物。现主要对B型利钠肽预测非心脏手术围术期心血管事件的进展进行综述,探讨其作为预测指标的优点和前景。     

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.