下腹部手术麻醉中不同靶浓度瑞芬太尼与异丙酚的作用研究

目的研究下腹部手术麻醉患者应用不同靶浓度瑞芬太尼和异丙酚的作用效果。方法将我院收治的下腹部手术麻醉患者为研究对象,并按随机分组法分为3组,均固定瑞芬太尼靶浓度,A组为6ng/ml,B组为8ng/ml,C组为10ng/ml,同时改变异丙酚靶浓度,范围为2~4μg/ml,观察比较各组的麻醉效果。结果 T1时刻A组的收缩压(SBR)高于B组,心率(HR)高于C组,差异有统计学意义(P0.05);而T2、T3时刻比较,A组的SBR以及HR均较B、C组高(P0.05)。随时间推移,去甲肾上腺素(NE)各时点比较,T1时刻A组的NE高于C组,而血清皮质醇(COR)低于B、C组;T2、T3时刻A组的NE均显著高于B、C组,但3组COR变化无显著差异性(P0.05)。C组自主呼吸恢复时间、拔除气管导管时间、指令反应时间和离室时间均较长,而其睁眼时间较短(P0.05)。结论将瑞芬太尼靶浓度调节为8ng/ml,可取得较为明显的麻醉镇痛效果。     

瑞芬太尼在全髋关节置换术中的麻醉效果观察

目的探讨瑞芬太尼在全髋关节置换术中的麻醉效果。方法将80例全髋关节置换术患者随机分为观察组和对照组各40例,观察组采用咪达唑仑、依托咪酯、舒芬太尼、罗库溴铵行全麻诱导,以丙泊酚、瑞芬太尼和阿曲库铵行麻醉维持;对照组采用咪达唑仑、依托咪酯、舒芬太尼、罗库溴铵行全麻诱导,以丙泊酚、芬太尼和阿曲库铵行麻醉维持。观察两组患者T0~T3各时点MAP和HR的变化情况以及手术时间、苏醒时间和语言恢复时间。结果观察组苏醒时间和语言恢复时间明显短于对照组,差异有统计学意义(P0.05)。结论瑞芬太尼用于全髋关节置换术中患者苏醒时间快,且手术过程血压、心率相对平稳,具有临床应用价值。     

镇痛指数在全麻手术中评估镇痛程度的临床价值

目的：探讨脑电镇痛指数（PRi）评估全身麻醉手术中镇痛程度的临床价值,为临床应用提供理论依据。方法：ASAI-Ⅱ级,拟于全身麻醉下行经腹手术的病人20例。患者入手术室后持续有创监测收缩压（SBP）、舒张压（DBP）、心率（HR）,实时监测脑电双频指数（BIS）和镇痛指数（PRi）。于麻醉诱导后气管插管前,气管插管后1 min、切皮前、切皮后2 min、追加芬太尼前,追加芬太尼5 min后记录BIS、PRi、SBP、DBP、HR的变化。结果：气管插管和切皮均引起SBP、DBP、HR的显著升高（P<0.05）;追加芬太尼后SBP、DBP、HR均降低（P<0.05）。气管插管和切皮均未引起BIS的显著变化（P>0.05）;追加芬太尼后BIS有所下降（P<0.05）。气管插管和切皮均引起PRi的显著升高（P<0.05）;追加芬太尼后PRi降低（P<0.05）。气管插管和切皮均引起SBP、DBP、HR、PRi的显著升高（P<0.05）,但均未引起BIS的显著变化（P>0.05）;追加芬太尼后SBP、DBP、HR、BIS和PRi均明显降低（P<0.05）。结论：在丙泊酚联合瑞芬太尼全身麻醉手术中,PRi能够反映伤害性刺激的变化,与伤害性刺激过程一致,对全身麻醉中镇痛程度的评估有指导意义。     

七氟醚-瑞芬太尼静吸复合麻醉对妇科腹腔镜子宫肌瘤摘除术患者术后认知功能的影响

目的:分析七氟醚-瑞芬太尼静吸复合麻醉对妇科腹腔镜子宫肌瘤摘除术患者术后认知功能的影响。方法:选取我院妇科收治行腹腔镜子宫肌瘤摘除术患者148例,采取数字随机法分成观察组和对照组,观察组采取七氟醚-瑞芬太尼静吸复合麻醉,对照组采取丙泊酚-瑞芬太尼静脉复合麻醉,比较两组麻醉方式对术后认知功能的影响。结果:对照组患者术后1天认知功能评分低于术前1天,差异有统计学意义(P0.05)。观察组患者术后1天认知功能评分高于对照组,差异有统计学意义(P0.05)。对照组患者术后1天TMT完成时间慢于术前1天,差异有统计学意义(P0.05)。观察组患者术后1天TMT完成时间快于对照组,差异有统计学意义(P0.05)。观察组患者术后呼吸抑制、恶心呕吐、躁动、嗜睡、头晕发生率均低于对照组,差异有统计学意义(P0.05)。结论:七氟醚-瑞芬太尼静吸复合麻醉对妇科腹腔镜子宫肌瘤摘除术患者术后认知功能的影响较小,并且比较安全,是较为适宜的麻醉方法。     

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Ischaemia/reperfusion (I/R)‐induced hepatic injury is regarded as a main reason of hepatic failure after transplantation or lobectomy. The current study aimed to investigate how the opioid analgesic remifentanil treatment affects I/R‐induced hepatic injury and explore the possible mechanisms related to HIF1α. Initially, an I/R‐induced hepatic injury animal model was established in C57BL/6 mice, and an in vitro hypoxia‐reoxygenation model was constructed in NCTC‐1469 cells, followed by remifentanil treatment and HIF1α silencing treatment. The levels of blood glucose, lipids, alanine transaminase (ALT) and aspartate transaminase (AST) in mouse serum were measured using automatic chemistry analyser, while the viability and apoptosis of cells were detected using CCK8 assay and flow cytometry. Our results revealed that mice with I/R‐induced hepatic injury showed higher serum levels of blood glucose, lipids, ALT and AST and leukaemia inhibitory factor (LIF) expression, and lower HIF1α and ZEB1 expression (P < .05), which were reversed after remifentanil treatment (P < .05). Besides, HIF1α silencing increased the serum levels of blood glucose, lipids, ALT and AST (P < .05). Furthermore, hypoxia‐induced NCTC‐1469 cells exhibited decreased HIF1α and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05). Moreover, HIF1α silencing down‐regulated ZEB1 expression, decreased cell viability, and increased cell apoptosis (P < .05). ZEB1 was identified to bind to the promoter region of LIF and inhibit its expression. In summary, remifentanil protects against hepatic I/R injury through HIF1α and downstream effectors.