麻醉学专业学生临床实践能力培养的探索

为了探索麻醉学专业临床实践能力培养的教学方法，结合我校的实际情况，在麻醉学专业临床教学中，我们在制定临床教学目标和教学计划、制定临床麻醉操作常规、培养学生的分析问题能力、培养学生的临床应变能力、开展模拟操作训练提高实践操作能力等方面进行了探索与实践。实践证明，以上措施对培养麻醉学专业学生临床实践能力和提高临床实习教学质量具有较好效果。     

异丙酚—七氟醚静吸复合麻醉用于普胸手术的体会

异丙酚－七氟醚静吸复合麻醉用于普胸手术的体会赵雾红＊黄焕森＊钟钒＊异丙酚、七氟醚均具有诱导迅速、可控性好和苏醒快的优点。近年来我们在部分普胸手术中联合应用异丙酚－七氟醚，效果满意，现报告如下。资料与方法一般资料２０例胸科择期手术，男１５例，女５例，年...     

别嘌呤醇通过调节自噬及恢复Nrf2通路减轻糖尿病心肌病

目的:探讨抗氧化药物别嘌呤醇(ALP)对糖尿病心肌病的保护作用及机制。方法:用高浓度的葡萄糖培养H9C2细胞建立糖尿病心肌病模型,实验分组为正常糖浓度培养组(NG),高糖组(HG)及高糖加ALP处理组(HG+ALP),检测细胞分泌乳酸脱氢酶活性,观察细胞形态,用Western Blot和实时定量PCR分别检测Nrf2及LC3蛋白表达量和mRNA表达量。结果:HG组较NG组LDH释放量增多及细胞表面积增大(P<0. 05),ALP处理后可以改善上述指标(P<0. 05,HG+ALP vs HG);与此同时,HG组Nrf2的蛋白量相比NG组下降,而LC3Ⅱ/Ⅰ比值升高(P<0. 05),在给予ALP处理后,Nrf2及LC3Ⅱ/Ⅰ比值均恢复至正常水平(P<0. 05,HG+ALP vs HG),而Nrf2 mRNA在3组间均无统计学差异。结论:ALP通过调控自噬修复Nrf2保护通路发挥糖尿病心肌病的保护作用。     

高张盐水在局灶性脑缺血再灌注损伤中的作用及其机制

Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.     

高张盐水在局灶性脑缺血再灌注损伤中的作用及其机制

Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.     

乌拉地尔预防颅脑手术麻醉拔管期高血压

目的：观察乌拉地尔用于预防颅脑手术麻醉拔管期高血压应激反应的效应。方法：４０例择期颅脑手术患者,随机分为治疗组与对照组,各２０例。在麻醉清醒期分别静注乌拉地尔０．４ｍｇ／ｋｇ或生理盐水０．０８ｍｇ／ｋｇ。记录注药前,注射后１ｍｉｎ,吸痰时、拔管后１,５ｍｉｎ以及回监护室（ＮＩＣＵ）后的血压和心率的变化。结果 治疗组注药后各时期的血压维持均较平稳,与注药前比较变化无显著差异（Ｐ〉０．０５）;对照组的     

用万汶行急性高容量血液稀释对兔血流动力学及凝血功能的影响

目的 探讨使用万汶行急性高容量血液稀释(AHH)后对家兔血流动力学及凝血功能的影响.方法 健康家兔8只,麻醉后行颈内静脉、颈总动脉穿刺并接生理监测仪即时监测心率(HR)、平均动脉压(MAP)、中心静脉压(CVP),由颈内静脉输入万汶(15 ml/kg),速度为20 ml/min,分别于稀释前、稀释后30 min、稀释后60 min、稀释后120 min采血作血气分析、血常规及凝血四项检查.结果 与稀释前相比,稀释后家兔HR明显升高(P＜0.05),其他血流动力学指标变化不明显(P＞0.05).稀释后家兔血细胞压积(Hct)明显下降(P＜0.05).血红蛋白(Hb)、血小板计数(Plt)均明显减少(P＜0.05).活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)及凝血酶时间(TT)均有所延长,纤维蛋白原(FIB)有所减少,但与稀释前比较差异无显著性(P＞0.05).以上虽显示凝血功能有所降低,但与稀释前相比,差异无显著性.结论 用万汶行急性高容量血液稀释后家兔血流动力学稳定,对凝血功能影响较小.     

深圳市罗湖区1984～1991年病毒性肝炎流行病学调查

深圳市罗湖区１９８４～１９９１年病毒性肝炎流行病学调查黄焕森１９８４年以来，深圳市罗湖区病毒性肝炎的发病率逐年上升，为探讨其流行规律，更好地制定防制对策，现将罗湖区１９８４～１９９１年病毒性肝炎的疫情资料分析如下。１流行概况我区１９８４～１９９１年的...     

脑缺血/再灌注损伤保护性药物的研究进展

临床中多采用药物对脑缺血,再灌注损伤进行预防与处理,以达到脑保护效果.现就药物的抗氧化作用、抗凋亡作用、减少血脑屏障的损伤及抑制钙离子超载等方面对近年来神经保护性药物的研究现状作一综述,为临床防治脑缺血/再灌注损伤提供理论依据.     

高张盐水在局灶性脑缺血再灌注损伤中的作用及其机制

Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.