目的 探讨急诊快速诱导麻醉气管插管对重型颅脑损伤治疗的诱导方案及临床有效性和安全性.方法 28例重型颅脑损伤患者在急诊快速麻醉诱导下快速气管插管,以静脉推注咪唑安定0.1 mg/kg,异丙酚1～2 mg/kg,芬太尼0.002 μg/kg,维库溴铵0.1 mg/kg快速麻醉诱导,微量泵静脉注入异丙酚0.3～0.4 mg/(kg·h),维库溴铵间断静脉注射,控制呼吸,维持循环呼吸功能稳定.结果 28例患者诱导期均平稳,无呕吐、烦躁、严重低血压等症状首次置管成功率高,气管插管接呼吸机控制呼吸后患者脉搏血氧饱和度(SpO2)为95%～100%,携监护仪呼吸机行急诊头颅CT检查,并直接转送手术室,转运期手术期患者无死亡;急诊手术后患者均带气管导管入ICU,术后9例患者即行气管切开,16例无临床症状的神经系统后遗症出院,4例死于脑部并发症及多器官功能衰竭,8例遗留神经系统后遗症出院.结论 重型颅脑损伤患者急诊选择合适的快速诱导麻醉方案有效控制气道,加强麻醉监测和控制颅内高压,减轻脑水肿,尽早完成影像学检查,专科及时急诊手术,是降低急诊重型颅脑损伤早期病死率的重要措施.

Objective To explore the effects of case introduced method in teaching emergency.Methods 65 students in 2005 Clinical Medicine Major,the Second Clinical Institute of Wuhan University was test group and 57 students in 2004 Clinical Medicine Major as the control group.The case introduced method teaching and the traditional teaching method were used in emergency in the two groups,respectively.The effects of the case introduced method were investigated.Results The emergency examination score of the students in the test group was significantly higher than that in the control group.In the questionnaire,most of the experimental group students think that case introduced method is better than the traditional teaching method.Conclusions Using the case introduced method to teach emergency may improve the quality of teaching.

Objective: To investigate the factors associated with failure of noninvasive positive pressure ventilation(NPPV) in patients presenting with acute exacerbation of COPD(AECOPD) in emergency department.Methods: Forty-five patients admitted to the emergency department with AECOPD for NPPV treatment were retrospectively analyzed.The mode of ventilation is PSV plus PEEP.The patients were divided into NPPV success group and NPPV failure group.The changes of the arterial blood gas,respiratory rate,dyspnea scores(DS),and oxygenation indexes(PaO2/FiO2) were compared before and after 1-hour NPPV between the two groups.Results: Respiratory rate and DS were higher in NPPV failure group,but pH was higher in NPPV success group.Factors associated with failure of NPPV were respiratory rate 20 beats/min(OR=4.55,95%CI=1.22-16.97),DS≥5(OR=9.36,95%CI=2.1-42.8),and pH7.35(OR=10.7,95%CI=1.25-91.6) after one hour NPPV.Conclusion: Patients with RR20 beats/min,DS≥5,and pH7.35 had an increased risk of endotracheal intubation after one hour of NPPV.

目前我国存在多种院前急救模式~([1]).为了能够更好地完成院前急救的急、救、转三方面的任务,即以最快的速度到达患者身边,并进行针对性的救治,然后再迅速转运到医疗机构,武汉大学中南医院于2007年10月借鉴法国院前急救模式,组建了依托于综合医院急救科,专业化的,用于医院间陆路急救转运急危重患者228例,取得良好效果,现报道如下。

目的 观察姜黄素对大鼠溃疡性结肠炎的抗炎疗效,探讨其可能机制.方法 雄性健康sD大鼠60只,随机分4组(每组15只):A组,正常对照组;B组,模型组;C组,姜黄素治疗组;D组,地塞米松治疗组.造模治疗后,行大体损伤评分,HE染色后组织损伤评分,用免疫组化S-P法检测组织标本中PPAγ、NF-κB、TNF-α表达并评分.结果 大鼠结肠组织大体损伤形态、HE染色评分均显示C、D组分别与B组比较差异有极显著性(P<0.01),C、D组比较差异有显著性(P<0.05).NF-κB、TNF-α在B组表达明显强于C、D组(P<0.01),且D组表达强于C组.PPARγ在c、D组间表达强于B组,且C组表达强于D组.NF-κB与TNF-α表达呈显著正相关,与PPARγ表达成负相关.结论姜黄素对溃疡性结肠炎大鼠模型有明显疗效,且优于地塞米松.姜黄素可能通过激活PPARγ的表达,抑制NF-κB、TNF-α的表达获得抗炎的效果.

Objective: To evaluate the effect of penehyclidine hydrochloride(PHC)resisting acute focal cerebral ischem/reperfusion(IR) injury in rats,and to explore the mechanism through apoptosis and signal transduction pathway.Methods: Healthy male SD rats were randomly divided into sham operation group(S group,n=32),ischemia/ reperfusion group(IR group,n=32) and PHC treated group(P group,n=32).Each group was divided equally into four subgroups according to the reperfusion time of 3,12,24 or 48 hours after 10 minutes of ischemia.The model of focal cerebral ischemia reperfusion injury was established by using Pulsinelli's method.Immunohistochemical SP method was performed to examine the expression of cytochrome C(CytC) and Caspase-3 at different time points after reperfusion.The pathological changes of nerve cells and mitochondria ultrastructure at hippocampus CA1 region were observed at 24 h after reperfusion by light microscope and electron microscope.Results:①The activation of CytC began to increase at 3 h after reperfusion,reached the peak at 12 h,and then gradually decreased.Caspase-3 began to increase at 3 h after reperfusion and reached the peak at 24 hours,and remained at highlevels till 48 h.②Compared with that in S group,the expression of CytC and Caspase-3 in IR and P group was increased significantly(P0.01).The pathological changes of nerve cells and mitochondria ultrastructure at hippocampus CA1 region were exacerbated at 24 h after reperfusion.③Compared with that in IR group,the expression of CytC and Caspase-3 in P group were decreased significantly(P0.05 or P0.01).The pathological changes of nerve cells and mitochondria ultrastructure at hippocampus CA1 region were improved at 24 hours after reperfusion.Conclusion: PHC shows protective effects on focal cerebral I/R injury partly through intervening in mitochondria mediated and Caspase-dependent apoptopic pathway.PHC reduces apoptosis,plays a role of protecting nerve by maintaining mitochondrial basical form,stabilizes mitochondrialmembrane and inhibits the release of cyt C and activation of Caspase-3.

目的:探讨老年低血糖症的临床特点及治疗原则。方法:对43例老年低血糖症患者的临床资料进行回顾性分析。结果:43例患者发生低血糖症诱因多样,临床表现复杂。结论:老年低血糖症应提高警惕,防重于治。

Objective: To observe the effect of postconditioning,preconditioning and pre-and post-conditioning on the expression of heat shock protein 70(HSP70) and ultrastructure of brain and injury of global cerebral ischemia reperfusion in rats,and to explore the mechanisms.Methods: The SD rats were randomly divided into five groups: group A(sham operation group),group B(global cerebral ischemia reperfusion group),group C(preconditioning group),group D(postconditioning group),and group E(pre-and post-conditioning group).The model of global ischemia and reperfusion was established in group B,C,D,and E by improved Pulsinelli's method.The rats were sacrificed at 6,8,or 24 hours after ischemia-reperfusion.The expression of HSP70 in brain tissue was examined by immunohistochemistry,and the ultrastructure of cortex was observed by electron microscope.Results: The expression of HSP70 in brain tissue of rats after cerebral ischemia-reperfusion injury increased reactively at the 6th hour,reached the peak at the 8th hour,and decreased at the 24th hour in group E,which was significant different from that in group B,C,and D,respectively.In group B,the ultrastructure image presented fragmental destruction of neuronal membrane,swelling mitochondria,aggregation of chromatin,or neuron apoptosis,while in other groups,especially in group E,the above ultrastructural damages were ameliorated markedly.Conclusion: The expression of HSP70 is induced in the brain of rats after cerebral ischemia-reperfusion,and through which,pre-and post-conditioning contributes to the protection of brain neurotrophic cells after ischemia-reperfusion.

Objective: To investigate the protective effects and mechanism of Na+/H+ exchanger inhibitor on cultured neonatal rat cardiomyocytes during hypoxia/reoxygenation. Methods: Cultured neonatal rat myocardial cells were divided into control, EIPA-I, EIPA-R1 and EIPA-R2 group. The hypoxia/reoxygenation injury model using the cells was developed. The intracellular free calcium concentrations in single cells were measured with Fura-2/AM, and the cells' survival rate was observed simultaneously. Results: In comparison with control group, both EIPA-I and EIPA-R2 group showed a marked decrease in [Ca2+]i and a significant increase in the cells’ survival rate. However, there was no significant difference between EIPA-R1 and control group. Conclusion: Either a larger dose of EIPA used just before reoxygenation or a general dose added at the beginning of hypoxia can efficiently inhibit Na+/H+ exchange and attenuate intracellular Ca2+ overload,and reduce the degree of hypercontracture of cardiomyocytes and enhanced the survival rate of myocytes.

在美国和英国,对乙酰氨基酚使用不当已成为药源性急性肝衰竭的主要原因之一,甚至列为主要致死原因之一.近1月在我院急诊科连续遇到3例对乙酰氨基酚过量或中毒的患者,经及时处理未见严重不良反应(尤其急性肝衰竭)发生.现报道如下,并结合我科参照国内、外文献制定的急诊处理流程进行讨论,以探讨急性对乙酰氨基酚中毒的规范化急诊处理原则.

目的探讨毒鼠强中毒的早期诊断与治疗方法。方法对2001年1月～2005年8月收治的急性毒鼠强中毒18例进行分析。结果治愈14例,病人清醒后自动出院3例,死亡1例。结论毒鼠强中毒救治成功的关键是从病人接触史、临床表现、毒物鉴定入手,进行早期诊断,采取早期洗胃、吸氧、辅助呼吸、净化血液、及时抗惊厥和应用二巯基丙磺酸钠等综合治疗。

Objective: To observe whether arachidonic acid (AA) could induce apoptosis in human bladder carcinoma cells ECV304 and the potential mechanism involved. Methods: Cell viability was monitored by MTT assay. The release of lactate dehydrogenase (LDH) was determined by colorimetric assay. Lipid peroxidation in ECV304 cells was measured as malondialdehyde (MDA) content. Hoechst 33258 dying was used to observe AA-induced morphological changes. Agarose gel electrophoresis was used to detect DNA fragmentation. Results: Treatment of ECV304 cells with AA for 24 h, in the range of 40-160 μmol·L -1, caused a great decrease in cell viability, an increase in MDA contents and a release of LDH simultaneously(P < 0.01). Cells treated by 160 μmol·L-1 AA showed typical morphological changes of apoptosis. A "ladder" pattern representing DNA fragmentation was also observed after 24 h of AA treatment. Conclusion: Higher concentration of arachidonic acid (80-160 μmol · L-1), could induce apoptosis in ECV304 cells. Lipid peroxidation might play a role in AA-induced apoptosis of ECV304 cells.

目的探讨气胸致ECG变化的特点及可能的机制.方法将病例分为左侧气胸组和右侧气胸组,在气胸急性期用12导ECG自动分析仪描记ECG,并测量各导联QRS波群振幅.结果同右侧相比,左侧气胸组QRS波群振幅以V1最大,并从V2～V6逐渐减小,在V3～V6出现低电压.两组Rv5/Sv1比值(P＜0.001)及钟向转位(P＜0.05)有显著性差异.左侧气胸组中V1及Rv1的振幅与气胸量呈直线相关(r=0.356 P＜0.05;r=0.373P＜0.05),其余导联及右侧气胸各导联振幅与气胸量无相关性(P＞0.05).结论左侧气胸时,心脏和前胸壁之间的空气阻碍了左侧胸导联(V3～V6)的心电活动向体表的传导,其振幅减小程度与气胸量无关.而V1与Sv1振幅的大小与气胸量呈正相关.左侧气胸导致的心脏顺时钟转位,可能也参与了上述过程的形成.右侧气胸却无上述变化.

目的观察地塞米松对内毒素性急性肺损伤肺组织的影响,并探讨其机制.方法 30只SD大鼠随机分为3组,即正常对照组、损伤组和地塞米松组.用内毒素复制急性肺损伤模型,地塞米松组同时注射内毒素和地塞米松,注射后2 h处死动物.观察形态学变化并分别测定一氧化氮(NO)和丙二醛(MDA)的含量;用原位杂交方法检测各组大鼠肺组织中诱导型一氧化氮合酶mRNA(iNOS mRNA)的表达水平.结果损伤组肺组织MDA、NO含量和iNOS mRNA表达量较正常对照组显著增加(P<0.05);地塞米松组肺组织MDA、NO含量和iNOS mRNA表达量明显低于损伤组(P<0.05).结论内毒素性急性肺损伤时,肺组织iNOS mRNA大量表达,导致内源性NO爆发式产生,从而介导肺损伤.而地塞米松能显著减轻其损伤作用.

急性酒精中毒是临床急诊的常见病之一,是严重的社会问题,许多暴力及犯罪均与此有关.中毒后主要对中枢神经系统产生抑制作用进而使呼吸循环系统受影响,重度酒精中毒患者可诱发心血管系统疾病或因呼吸中枢麻痹而死亡[1].为了探讨纳络酮在治疗急性酒精中毒的作用及其机理,我科于2001年9月～2002年12月应用纳络酮治疗急性酒精中毒76例,并与同期收治的25例给予常规治疗进行了比较,现报告如下.

Objective:To compare the therapeutic effects of ginkgo biloba flavonal glyco and compound salvia miltiorrhiza tablets in treating patients with angina. Method:68 patients were divided randomly into study group(n=38, ginkgo biloba flavonal glyco, 2 tablets, tid, po) and control group(n=30, compound salvia miltiorrhiza, 3 tablets, tid, po). Before and 4 weeks after the treatment, the clinical symptoms, electrocardiograms, cardiac functions, hemorheology, dosage of nitroglycerin and the adverse effects were observed. Results:The study group had better therapeutic effects in improving clinical symptoms(P0.05), electrocardiograms, cardiac functions and hemorheology(P0.05); and needed a smaller dosage of nitroglycerin than the control group(P0.05). There were no obvious adverse effects in both groups. Conclusion:Ginkgo biloba flavonal glyco is safe and efficient in the therapy of patients with angina and it is superior to compound salvia miltiorrhiza.

毒鼠强是国家禁止生产、销售及使用的急性剧毒杀鼠剂,因其生产成本低廉,不法商贩为牟取暴利而导致毒鼠强在市场上销售屡禁不止,中毒事件时有发生.本院2001年1月至2002年8月共收治急性毒鼠强中毒患者16例,现报道如下.

22年前,美国首先报道了5例获得性免疫缺陷综合征(AIDS).现在,AIDS已传遍全球!联合国卫生组织宣布,全世界已有六千多万人感染了人免疫缺陷病毒(HIV),其中二千多万人被它夺去了生命.至2001年,中国发现HIV/AIDS患者三万多人,估计HIV感染人数已超过一百万.

本文通过对我科自2002.3-2003.3期间收治的27例戒酒硫样反应的临床特点进行分析,探讨了戒酒硫样反应和急性酒中毒的区别,并结合相关文献总结了戒酒硫样反应的诊治经验.

目的探讨丹参对内毒素肺损伤的保护作用.方法选用SD大鼠63只,随机分为对照组、肺损伤组、丹参防治组.3组动物根据注入内毒素时间不同分为1、2、4 h组.丹参防治组按10 g/kg体重经股静脉注入丹参,15 min后再按5 mg/kg体重注入大肠杆菌内毒素;肺损伤组用生理盐水代替丹参;对照组中丹参和内毒素均以生理盐水代替.放血处死大鼠检测血浆P-选择素和可溶性细胞间粘附分子 1(sICAM-1). 结果①肺损伤组及丹参防治组血浆P-选择素均较对照组增高(P<0.01),其中第2、4h丹参防治组血浆P-选择素较肺损伤组减低(P<0.01);②肺损伤组血浆sICAM-1较对照组增高(P<0.01),第2,4 h丹参防治组血浆sICAM-1较肺损伤组减低(P<0.01),其中第4 h丹参防治sICAM-1与对照组差别已无统计学意义(P>0.05).结论丹参可能通过抑制P-选择素、ICAM-1介导的炎性细胞肺部浸润而减轻内毒素所致的肺损伤.