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11.
目的 研究喷他佐辛对靶控输注(TCI)咪哒唑仑患者镇静程度的影响.方法 选择ASAI~II级的择期手术患者60例,随机分为P1组、P2组和P0组.以咪哒唑仑血浆药物浓度作为靶目标进行靶控输注(TCI),咪哒唑仑血浆靶控浓度维持在80 ng/mL.静脉微泵注入15 min后,按分组给药,P1组(n=20):喷他佐辛0.5 mg/kg,生理盐水稀释至10 mL静脉注射(30 s);P2组(n=20):P2组喷他佐辛1 mg/kg,方法 同P1组;P0组(n=20):生理盐水10 mL,方法 同P1组.记录咪哒唑仑TCI启动前(T0),咪哒唑仑TCI启动后5 min(T1)、10 min(T2)、15 min(T3),分组给药后5 min(T4)、10 min(T5)、15 min(T6)各时点的RE、SE、MAP、HR、SpO2及OAA/S评分.结果 3组患者在靶控咪哒唑仑80 ng/mL后10~15 min,RE、SE及OAA/S评分均显著下降,T2-3与T0比较,差异具有统计学意义(P<0.05或P<0.01);P0和P1组注药后5~15 min,RE、SE和OAA/S未见有显著改变(P>0.05);P2组静注喷他佐辛1 mg/kg后RE、SE及OAA/S评分继续下降,T6与T3比较差异具有统计学意义(P<0.05).P2组静脉注射喷他佐辛后T5-6与T3时点比较MAP和HR轻度升高(P<0.05).P1、P2组在静注喷他佐辛后SpO2明显降低(P<0.05).结论 喷他佐辛与咪哒唑仑联合用药具有协同作用,静脉注射喷他佐辛1 mg/kg可加深血浆浓度80 ng/mL咪哒唑仑靶控的镇静程度,患者由清醒镇静状态进入睡眠状态,可降低RE和SE值. 相似文献
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舒芬太尼复合丙泊酚对小儿麻醉诱导期血流动力学及脑电双频指数的影响 总被引:1,自引:0,他引:1
目的 研究舒芬太尼复合丙泊酚对小儿全麻诱导期血流动力学及脑电双频指数(BIS)的影响.方法 45例择期全麻手术患儿随机均分为三组,每组15例.舒芬太尼剂量分别为0.1μg/kg(S1组)、0.2μg/kg(S2组)和0.3μg/kg(S3组).3 min后三组均静注丙泊酚2.5 mg/kg和维库溴铵0.1 mg/kg麻醉诱导.经口行气管插管.记录诱导前(T1)、静注舒芬太尼后(T2)、静注丙泊酚后(T3)、插管即刻(T4)、插管后2 min(T5)、5 min(T6)时的BP、HR和BIS.结果 S1、S2组在T4时SBP、DBP、MAP明显高于T1时(P<0.05);而S3组变化不明显,但与S1组同一时点比较,SBP、DBP、MAP明显低于S1组、HR慢于S1组(P<0.05).三组间各时点的BIS差异无统计学意义.结论 应用舒芬太尼0.3 μg/kg复合丙泊酚诱导能较好地抑制气管插管时的心血管应激反应. 相似文献
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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. 相似文献
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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. 相似文献
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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. 相似文献
19.
浅谈疼痛医学教育管理 总被引:2,自引:1,他引:1
当前,我国疼痛医学在临床诊断、治疗方面有较大的发展,但教育管理相对滞后,这将影响学科的进一步发展。当务之急是在医学教育中强调疼痛医学的重要性,建立和完善疼痛医学教学体系,加强医学生对疼痛医学的认识和兴趣培养,制定和落实疼痛科临床医生“三基”培训和继续医学教育制度,以确保疼痛医学的可持续发展。 相似文献
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药物反应的个体差异是临床用药中的常见现象,认识和阐明药物反应个体和群体间差异的产生机制可明显提高药物治疗效果,降低并发症。产生药物反应个体差异的原因虽然很多,但主要的因素还是药物代谢和处置的遗传差异和药物作用靶点的遗传多态性。随着人类基因组计划的完成,人类23条染色体上所有基因的序列都已测定,许多功能蛋白的结构以及编码它们的基因都已基本弄清,根据病人的遗传结构制定最佳的用药方案已成为近年来研究的热点之一,阿片类药物也不例外。药物代谢酶、转运蛋白、受体和药物作用靶点的基因多态性是引起阿片类药物效应和副作用个体差异的重要原因。 相似文献