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.     

神经介入治疗带状疱疹引发尿潴留2例

带状疱疹 (herpes zoster, HZ) 是由潜伏在体内的水痘-带状疱疹病毒 (varicella zoster virus, VZV) 再次激活所致,主要症状为病人皮肤出现沿神经分布的成簇状疱疹及相应皮损区疼痛等.此外,因为发病部位不同,临床症状表现各异,如发生在面神经分布区可出现亨特综合征,累及眼神经可能出...     

地氟烷对大鼠脑缺血再灌注时线粒体呼吸链复合体活性的影响

目的 评价地氟烷对大鼠脑缺血再灌注时线粒体呼吸链复合体活性的影响,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(S组)、缺血再灌注组(I/R组)、1.0 MAC地氟烷组(D1.0组)和1.5 MAC地氟烷组(D1.5组).采用前脑缺血再灌注损伤模型,D1.0组和D1.5组缺血前分别吸入1.0 MAC和1.5 MAC地氟烷40 min.再灌注4 h时,迅速断头取前脑,密度梯度离心,分离线粒体,分光光度计法测定线粒体呼吸链复合体Ⅰ+Ⅲ、Ⅱ+Ⅲ和Ⅳ的活性,透射电子显微镜观察线粒体病理学结果.结果 与S组比较,I/R组复合体Ⅰ+Ⅲ和Ⅳ的活性降低(P＜0.05);与I/R组比较,D1.0组和D1.5组复合体Ⅰ+Ⅲ和Ⅳ的活性升高(P＜0.05);各组复合体Ⅱ+Ⅲ、D1.0组及D1.5组复合体Ⅰ+Ⅲ和Ⅳ的活性差异均无统计学意义(P＞0.05).前脑缺血再灌注后,线粒体体积增大、基质电子密度降低、嵴间隙增宽、破裂、膜崩解;D1.0组和D1.5组线粒体超微结构改变不明显.结论 地氟烷可减轻大鼠脑缺血再灌注损伤,机制与提高线粒体呼吸链复合体Ⅰ+Ⅲ和Ⅳ的活性有关.     

电针对大鼠神经病理性疼痛及背根神经节中p38 MAPK蛋白表达的影响

目的:观察电针刺激“足三里”穴位对大鼠神经病理性疼痛的影响,及电针治疗对大鼠背根神经节中p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)信号转导途径的影响.方法:40只雄性Wistar大鼠随机均分为4组(n=10):空白对照组(Con组);坐骨神经结扎组(CCI组);假电针治疗组(CCI+A组);电针治疗组(CCI+EA组).分别于实验前及坐骨神经结扎后第7、14、21 d,观察并记录大鼠的热缩足反射潜伏期(paw withdrawal latency,PWL)和机械缩足反应阈值(paw withdrawal threshold,PWT)变化和大鼠受累后肢的运动功能评分.在实验结束(即第21 d)时,处死大鼠,取出右侧L4～6节段的背根神经节,之后采用免疫组化的方法检测大鼠背根神经节中p38MAPK蛋白的表达.结果:PWT和PWL在Con组中没有变化,而在CCI组和CCI+A组中显著降低,并持续至实验结束.CCI+EA组在电针治疗后PWT和PWL与CCI组和CCI+A组相比显著升高(P＜0.05).电针治疗后,CCI+EA组大鼠受累后肢的运动评分显著低于CCI+A组和CCI组(P＜0.05).免疫组化结果显示:CCI+EA组大鼠背根神经节中的磷酸化p38MAPK (phosphor-p38 MAPK,p-p38 MAPK)阳性细胞表达均显著低于CCI组和CCI+A组(P＜0.05).结论:电针刺激“足三里”穴位能够减轻神经病理性疼痛大鼠的热痛和机械痛,改善大鼠受累后肢的运动功能评分;电针抑制CCI大鼠背根神经节中p38MAPK的表达.     

桡动脉穿刺置管对甲襞微循环的影响

目的观察桡动脉置管对甲襞微循环的影响。方法选14例心脏直视手术病人为观察对象,在手术前,术后,离开ICU前经桡动脉输入硝酸甘油、利多卡因和肝素时,及动脉导管拔除后第7d,观察无名指甲襞微循环。结果离开ICU前,甲襞血管襻的输入枝、输出枝和襻顶管径,均较手术前和导管拔除后显著减少(P<0.05);经桡动脉输入硝酸甘油和利多卡因可以显著扩张血管襻管径(P<0.01);动脉导管拔除7d后甲襞血管襻的管径和微循环加权积分与手术前比较无显著差异(P>0.05)。结论本实验结果显示桡动脉有创监测不会引起末梢微循环长期显著改变;通过桡动脉输入扩血管药物可以显著改善末梢微循环状态。     

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.     

红外热成像在神经病理性疼痛诊疗中的应用进展

红外热成像是一种无创测量和可视化红外辐射的功能成像技术,已被证实可用于辅助诊断疼痛、肿瘤和炎症等疾病.神经病理性疼痛是疼痛科的常见疾病,因缺乏精准、高效、客观的辅助检查工具,在诊疗过程中面临许多难题.近年来,研究报道红外热成像可通过客观地反映人体表温度的改变和分布特点在神经病理性疼痛的诊疗中发挥作用.随着研究的深入,红...     

失血性休克对猪一氧化氮与内皮素的影响

目的 探讨内源性一氧化氮（NO）与内皮素（ET）在失血性休克中的变化及其意义。方法 14头体重为14～17kg的健康雄性家猪,随机均分为失血性休克组（H组）和对照组（C组）。H组按照Wigger’s改良法制作失血性休克模型,经股动脉快速放血使MAP降至40mmHg,维持90min,然后回输血液及等量的复方氯化钠。C组处理同H组,但未放血。各组分别在休克前、休克末、复苏末、复苏后30、60、120、240min记录MAP、HR、CVP、肺动脉压（PAP）、肺动脉楔压（PCWP）的变化,同时测定血浆NO与ET水平以及动脉血乳酸盐浓度（Lac）的变化。结果 H组休克末MAP、PAP和CVP降低而HR升高,PCWP无显著变化。血浆NO水平在休克后逐渐升高,复苏后60min显著高于休克前和C组水平（P〈0．05）,此后一直维持较高水平,240min时达到高峰;休克后ET水平显著增加,并显著高于C组及休克前（P〈0．05）,复苏后逐渐下降。结论 失血性休克后血浆NO、ET水平增加,在失血性休克的病理生理过程可有一定意义。     

无心跳家兔呼出气中CO变化

目的检测无心跳兔呼出气中一氧化碳(CO)浓度变化。方法根据肺脏原位热缺血时间不同,随机分为A~E组(n=8):分别为心跳停止后0、30、60、90和120 min。在相应时间点测量呼出气中CO浓度;同时检测传统的肺损伤指标。结果 A~E组呼出气中CO浓度[中位数(四分位区间)]分别为4.41(3.36~4.79)ppm、4.52(4.14~4.97)ppm、4.65(4.17~5.48)ppm、4.90(4.24~6.00)ppm和5.59(4.55~6.64)ppm,其中D、E组显著高于A组,而E组显著高于D组(P0.05)。而传统的肺损伤指标呈逐渐恶化趋势。结论兔心跳停止后120 min内,呼出气中CO浓度逐渐升高。