^192Ir脑胶质瘤间质内放疗的临床应用

我院神经外科自1997年1月至2000年3月与放疗科合作,采用~(192)Ir后装治疗机行脑胶质瘤术后瘤间质内放射治疗,取得良好近期效果。     

人工股骨头置换和PFN术治疗老年股骨粗隆间骨折的对比分析

目的:分析及评价应用人工双动股骨头置换和PFN术治疗高龄老年人不稳定股骨粗隆间骨折的方法及疗效.方法:应用人工双动股骨头置换和PFN术治疗股骨粗隆间骨折62例,男28例,女34例,年龄68～94岁,平均76岁.骨折按Evans分类,Ⅱ型14例、ⅢA型22例、ⅢB型16例、Ⅳ型7例、Ⅴ型5例.结果:人工假体置换手术和PFN都是治疗高龄股骨粗隆间骨折有效方法.结论:人工假体置换手术近期疗效满意.     

高渗氯化钠琥珀酰明胶溶液对出血性休克犬氧代谢的影响

出血性休克是以心输出量降低，氧输送（ＤＯ２）减少为特征，组织灌注和氧合不充足的临床综合征。氧输送和氧消耗（ＶＯ２）能正确反映组织灌注和氧代谢状态。我们用高渗氯化钠复合琥珀酰明胶溶液（ＨＳＧ）复苏犬出血性休克，观察其对氧代谢的影响。一、材料与方法１．选...     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

马尾肿瘤的MRI诊断

目的分析马尾肿瘤MRI的诊断特点。方法选择我院15例马尾肿瘤患者全部行MRI检查，其中男9例，女6例，14例经手术治疗。结果病理诊断15例马尾肿瘤中，神经纤维瘤8例，皮样囊肿和表皮样囊肿3例，脂肪瘤2例，室管膜瘤1例，转移瘤1例。术前MRI诊断与术后病理诊断基本相符。结论MRI对马尾肿瘤的诊断可靠，为，临床的手术治疗提供了正确的病变分析。     

乳化异氟醚预处理对大鼠心肌缺血再灌注时NF-κB活性的影响

目的 探讨乳化异氟醚预处理对大鼠心肌缺血再灌注时NF-κB活性的影响.方法 健康雄性SD大鼠48只,体重230～280 g,随机分为4组(n=12):假手术组(S组)仅穿线不结扎;缺血再灌注组(IR组)结扎左冠状动脉前降支30 min,恢复灌注120 min制备心肌缺血再灌注损伤模型;脂肪乳剂组(L组)经股静脉输注30%脂肪乳剂4 ml·kg-1·h-1 30 min后制备模型;乳化异氟醚组(EI组)经股静脉输注乳化异氟醚4 ml·kg-1·h-130 min,洗脱15 min后制备模型.于再灌注120 min时采集股动脉血样,采用ELISA法测定血清心肌肌钙蛋白Ⅰ(cTnI)、IL-6浓度及磷酸肌酸激酶同工酶(CK-MB)活性,随后处死大鼠取心脏,采用Western blot法测定心肌细胞NF-κB活性,电镜下观察心肌细胞的超微结构.结果 与S组比较,IR组、EI组和L组心肌细胞NF-κB活性升高,血清IL-6、cTnI浓度及CK-MB活性升高(P＜0.05或0.01);与IR组比较,ET组心肌细胞NF-κB活性降低,血清IL-6、cTnI浓度及CK-MB活性降低(P＜0.05);电镜结果显示:EI组心肌细胞损伤程度较IR组和L组减轻.结论 乳化异氟醚预处理可通过降低NF-κB活性抑制炎性反应,从而减轻大鼠心肌缺血再灌注损伤.     

乳化异氟烷对兔心肌缺血再灌注损伤的保护作用

背景比较乳化异氟烷和吸入异氟烷的心肌保护效应。方法给32只兔进行临时结扎左冠状动脉前降支30分钟以造成心肌缺血,然后再灌注3小时。在结扎左前降支前,随机将兔分为4组（每组8只）：c组,无缺血前预处理措施;IS组：吸入呼气末浓度为1．1％异氟烷;EI组：持续泵注8％乳化异氟烷以达到呼气末浓度为0．64％;IN组：持续泵注30％脂肪乳。在缺血前30分钟进行预处理,异氟烷组随后还有15分钟的洗脱时间。再灌注3小时后取标本测定心肌梗死面积、乳酸脱氢酶和肌酸激酶活性及线粒体超微结构。结果IS组和EI组在再灌注3小时后心肌梗死面积明显低于C组和Ⅲ组（20％±8％,18％±8％,39％±6％和34％±9％,P〈0．01）。IS组和EI组的心肌梗死面积无差异,C组和IN组的心肌梗死面积亦无差异。心肌再灌注3小时后IS组和EI组血浆乳酸脱氢酶（456±58U／L,451±54U／L）和肌酸激酶活性（1725±230U／L,1686±444U／L）明显低于C组（676±82U／L,2373±529U／L;P〈0．01）。IS组和EI组心肌线粒体超微结构改变比对照组减轻。结论静脉注射乳化异氟烷对兔心肌缺血再灌注有保护作用,其效应与吸入异氟烷相似。     

电刺激迷走神经对感染性休克大鼠心脏功能及超微结构的影响

目的:研究电刺激迷走神经对感染性休克心脏功能及超微结构的影响。方法:采用盲肠结扎穿孔法(CLP)复制感染性休克模型。取成年雄性SD大鼠20只,随机分为4组:假CLP组(Sham);CLP组(CLP);迷切组(VGX);电刺激组(STIM)。刺激方法是将左迷走神经远端连接刺激电极,于CLP术毕即刻持续电刺激(5 V、2ms和1 Hz)20 min。各组动物均行颈总动脉置管连续监测平均动脉压(MAP),分别在各组模型制备完毕或者电刺激后0,1,2,4 h检测血浆肿瘤坏死因子α(TNF-α)和4 h抽动脉血行肌酸激酶(CK)、肌酸激酶MB(CK-MB)、乳酸脱氢酶(LDH)水平检测,电镜观察心肌细胞超微结构变化。结果:CLP组和VGX组平均动脉血压进行性下降,血浆TNFα、CK、CK-MB、LDH水平显著升高,透射电镜观察可见脓毒血症大鼠心肌细胞线粒体排列紊乱,空泡变性,肌纤维水肿;与CLP组比较,STIM组动物平均动脉压下降幅度减轻,血浆CK、CK-MB、LDH水平显著降低(P<0.01),电镜心肌损伤减轻。结论:电刺激迷走神经能缓解CLP致感染性休克大鼠的进行性血压下降及炎性因子表达,降低血清CK、CK-MB、LDH水平,减轻心肌组织损害,对心脏功能有潜在的保护作用。     

乳化异氟醚预处理对兔心肌缺血再灌注损伤的影响

目的 探讨乳化异氟醚预处理对兔心肌缺血再灌注损伤的影响.方法 健康雄性新西兰大白兔32只,体重2.0～2.5 kg,阻断冠状动脉1 h,再灌注3 h建立心肌缺血再灌注损伤模型,随机分为4组(n=8),缺血再灌注组(IR组),异氟醚组(Ⅰ组)吸入异氟醚,维持呼气末浓度0.5 MAC 30min,洗脱15 min后缺血1h再灌注3 h;乳化异氟醚组(EI组)静脉注射(1 ml/s)8%乳化异氟醚4～6 ml至呼气末浓度0.5 MAC,以4～6 ml·kg-1·h-1静脉输注乳化异氟醚维持呼气末浓度0.5 MAC 30 min,洗脱15 min后缺血1 h再灌注3 h;脂肪乳组(L组)静脉输注(5 m1·kg-1·h-1)与乳化异氟醚等量的30%脂肪乳注射液30 min,停止静脉输注脂肪乳15 min后缺血1 h再灌注3 h.再灌注3 h后测定血清磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)活性和一氧化氮(NO)浓度,并计算梗死区心肌与左心室干重比值、梗死区心肌与缺血区心肌干重比值.结果 与IR组比较,Ⅰ组和EI组梗死区心肌与左心室干重比值、梗死区心肌与缺血区心肌干重比值均明显降低,血清CK和LDH活性降低,NO浓度增加(P＜0.05),L组上述指标差异无统计学意义(P＞0.05);Ⅰ组和EI组各指标差异无统计学意义(P＞0.05).结论 8%乳化异氟醚预处理可减轻兔心肌缺血再灌注损伤,其机制可能与NO生成量增加有关.