非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

星状神经节阻滞治疗植物神经功能紊乱的甲襞微循环改变

目的观察星状神经节阻滞 (stellateganglionicblock,SGB)治疗植物神经功能紊乱前后甲襞微循环的变化情况。方法按照CCMD诊断标准选取39例植物神经功能紊乱患者作为观察对象 ,均为女性 ,年龄(40.72±10.29)岁。用1.5 %利多卡因6ml进行SGB治疗 ,在治疗前30min和治疗后10min分别测量甲襞血管襻管径及流速的变化 ,并对甲襞微循环的血管形态、血液流态和管周状态进行评分。结果SGB治疗后 ,甲襞血管襻的输入枝管径、输出枝管径、襻顶管径及输入枝襻长均较治疗前显著增加(P<0.05) ,血液流速与治疗前比较无显著差异 (P>0.05) ,血管形态积分增加(P<0.01),血液流态积分减少(P<0.05),管周状态积分和总积分无显著改变。结论本实验结果显示植物神经功能紊乱患者治疗前的甲襞微循环总积分大于2 ,提示甲襞微循环障碍 ;SGB可以增加甲襞微循环血流量。     

低压复苏对非控制出血性休克抢救效果的探讨

目的建立非控制性脾大部损伤出血性休克模型,比较低压复苏与常压复苏抢救的效果。方法脾部分切除模拟人失血低压状态下,建立类似人休克的模型后,将动物随机分成4组。1组,假手术组;2组,休克未处理组;3组,正常血压复苏组;4组,低压复苏组。观察其成活率及对内脏的损伤程度。结果动物失血低压抢救比常压抢救存活时间长。结论低压可改善组织代谢,提高生存时间,是更为理想的复苏方法。低压复苏非控制性脾大部损伤出血性休克模型的建立,为临床急性大出血提供新的抢救方法。     

试论“五经推拿法”的临床运用

一、概述“五经推拿法”即是医者用各种特定的手法在患者督脉、膀胱经、华佗夹脊的五条经脉上自上而下地选择性地进行推拿操作,通过手法作用产生的良性刺激而达到治疗某些疾病的一种疗法。笔者通过十年的临床观察及研究发现,五经推拿法具     

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.     

低压复苏对非控制性出血性休克的作用

目前国内外的动物实验和部分临床研究结果显示，低压复苏是治疗非控制性出血性休克较为合理的方案，但还没有人从增加血容量，减少应激反应引起的血管收缩、改善组织微循环氧供方面进行研究。本研究拟观察低压及低压扩容复苏对腹腔实质脏器损伤非控制性出血性休克的治疗效果。     

自制可调式异型气管导管固定器在小儿扁桃腺摘除术中的应用

异型气管导管适用于口咽部手术病人的呼吸道管理,导管一般采用医用胶布固定于面颊。但导管的口咽部分靠近扁桃腺,直接影响手术的操作,同时手术过程中,由于导管固定胶布粘帖不牢、手术操作调整气管导管位置、麻醉过浅、病人呛咳等原因,可能导致导管脱出声门,发现和处理不及时将危及病人生命。本课题设计了可调式异型气管导管固定器,目的是既可牢固固定气管导管,又可根据需要在术中调整导管在口腔内的位置,便于手术操作。现将本固定器的结构、操作方法以及其在慢性扁桃腺摘除术中的应用情况介绍如下。     

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.