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.     

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.     

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.     

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.     

超声评估围手术期胃内容物的研究进展

围手术期饱胃患者发生反流和误吸的风险很大,可引起气道梗阻和吸入性肺炎等严重并发症。准确及时地判断胃内容量非常重要,然而目前还缺乏可靠的诊断工具。近年来的研究表明超声可较为准确地用于胃内容物容量及性质的判断,该方法也逐渐在临床实践中普及。     

丙泊酚对2型糖尿病大鼠心肌缺血再灌注损伤内皮细胞功能的影响

目的 探讨丙泊酚(propofol)对2型糖尿病大鼠心肌缺血再灌注损伤期间内皮细胞功能的影响.方法 雄性Wistar大鼠48只,随机分为糖尿病组(D组)和非糖尿病对照组(N组),两组各24只.N组随机分为三组(每组8只),即心肌缺血再灌注组(NI组)、心肌缺血再灌注+丙泊酚组(NP组)、假手术组(NS组);D组随机分为三组(每组8只),即糖尿病心肌缺血再灌注组(DI组)、糖尿病心肌缺血再灌注+丙泊酚组(DP组)、糖尿病假手术组(DS组).采用高脂高糖饮食联合腹腔注射链脲佐菌素(STZ)方法制备2型糖尿病模型.DI组和NI组采用结扎左冠状动脉前降支30 min再灌注2h的方法制备心肌缺血再灌注模型.DP组、NP组在缺血前10 min开始静脉泵注丙泊白酚6 mg· kg-1·h-1至再灌注2h结束,DI组、NI组给予等容量的生理盐水;DS组、NS组仅穿线不结扎.再灌注结束后,取部分病变心肌,光镜下观察缺血心肌形态学改变,测定基础状态、再灌注结束后血清中一氧化氮(NO)、内皮素-1(ET-1)的含量.结果 NI组与NS组比较,NI组NO水平降低、ET-1水平升高(F=12.18、14.37,P ＜0.05).与NI组比较,NP组NO水平升高、ET-1水平降低(F=14.99、15.521,P＜0.05).DI组与DS组比较,DI组NO水平降低、ET-1水平升高(F=4.76、4.94,P＜0.05),与DI组比较,DP组NO水平明显升高、ET-1水平降低显著(F=6.40、8.80,P＜0.05).结论 丙泊酚能改善心肌内皮细胞功能,减轻2型糖尿病大鼠心肌缺血再灌注损伤.     

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。     

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...