光导纤维支气管镜经口和经鼻气管插管患儿心血管反应的比较

目的比较小儿光导纤维支气管镜(FOB)经口和经鼻气管插管的心血管反应。方法选择美国麻醉医师协会(ASA)身体状态分级为Ⅰ级、在全身麻醉下施择期整形外科手术的患儿65例,随机分为经口组(n=36)和经鼻组(n=29)。在常规静脉麻醉诱导后实施FOB气管插管。测定麻醉诱导前(基础值)、后,气管插管时和气管插管后5 min内(测定间隔为1 min)血压(BP)和心率(HR),记录气管插管时间。结果经鼻组气管插管时间显著长于经口组(P<0.05)。FOB气管插管导致两组BP和HR均比麻醉诱导前基础值显著升高(P均<0.05)。与经口组相比,气管插管致BP增高和HR增快反应在经鼻组较轻,持续时间较短。经口组气管插管时BP和HR及观察过程中BP和HR最大值均显著高于经鼻组(P均<0.05)。结论FOB经口和经鼻气管插管均可引起小儿BP和HR显著升高,但FOB经鼻气管插管时心血管反应较FOB经口气管插管时轻。     

光导纤维支气管镜经口和经鼻气管插管对血液动力学影响的比较

光导纤维支气管镜（fiberoptic bronchoscope,FOB）引导气管插管具有经口和经鼻两种途径。既往许多研究曾经对FOB和直接喉镜经口气管插管时的血液动力学变化进行了比较性研究,发现两者之间差异无显著意义。另有一些研究则对局部麻醉和镇静处理下FOB引导经鼻气管插管的心血管反应进行了研究。但是,有关静脉全身麻醉诱导后FOB引导经口和经鼻气管插管对血液动力学的影响尚无报道。     

不同浓度硝酸甘油对大鼠离体心脏缺血再灌注损伤的影响

目的 探讨不同浓度硝酸甘油对大鼠离体心脏缺血再灌注损伤的影响.方法 健康成年雌性SD大鼠,体重220～330 g,周龄7周,建立Langendorff离体心脏灌注模型,取模型制备成功的心脏30个,随机分为3组(n=10):缺血再灌注组(IR组)K-H液灌注15 min,停灌20 min,再灌注60 min;低浓度硝酸甘油组(LN组)采用含有2.5 μg/L硝酸甘油的K-H液灌注15 min,停灌20 min,再灌注60 min;高浓度硝酸甘油组(HN组)采用含有25μg/L硝酸甘油的K-H液灌注15 min,停灌20 min,再灌注60 min.于再灌注10、20、30、40、50、60 min时记录心率(HR)、冠状动脉流量(CF)、左心室舒张末压(LVEDP)、左心室发展压(LVDP)、左心室内压最大上升速率(+dp/dtmax)和左心室内压最大下降速率(-dp/dt_(max)).于平衡灌注末、再灌注5、30和60 min时收集冠状动脉流出液1.5 ml,测定乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性;于再灌注60 min时取心脏,测定心肌梗死面积,计数心肌凋亡细胞.结果 与IR组比较,LN组HR、CF、LVDP,+dp/dt_(max)和-dp/dt_(max)升高,LVEDP、CK活性、LDH活性、心肌梗死面积和细胞凋亡率降低(P<0.05),HN组HR、CF、LVDP、+dp/dt_(max)和-dp/dt_(max)降低,LVEDP、CK活性、LDH活性、心肌梗死面积和细胞凋亡率升高(P<0.05).与LN组比较,HN组HR、CF、LVDP、+dp/dt_(max)和-dp/dt_(max)降低,LVEDP、CK活性、LDH活性、心肌梗死面积和细胞凋亡率升高(P<0.05).结论 低浓度硝酸甘油(2.5μg/L)可减轻大鼠离体心脏缺血再灌注损伤,而高浓度硝酸甘油(25 μg/L)则可加重心脏缺血再灌注损伤.     

癫(癎)外科手术麻醉进展

根据我国流行病学调查资料显示,癫(癎)年发病率为35～37/10万,现有癫(癎)患者约为4.89×106例,初发年龄＜20岁的患者为70%～74%,其中＜10岁者占37.00%～51.80%;有70%～80%的患者在神经内科医师的监督和指导下接受规范化药物治疗,其发作可以得到完全控制或显著减少,但也有20%～30%患者虽经多种药物治疗仍不能完全控制癫(癎)发作,成为难治性癫(癎)[1].其中,部分难治性癫(癎)患者可通过不同类型的神经外科手术治疗发作完全消除或症状显著改善,得以恢复工作或学习.随着神经外科手术技术逐年进步与发展,与之相关的麻醉方法亦不断更新.笔者在总结近年有关癫(癎)外科手术治疗相关文献的基础上,简要回顾有关癫(癎)诊断及手术相关麻醉方面的新进展.     

小儿光导纤维支气管镜引导三步气管插管技术的临床评估

目的 评价小儿光导纤维支气管镜(FOB)引导三步气管插管技术的可操作性和临床应用价值.方法 收治美国麻醉医师协会(ASA)Ⅰ级,年龄4～13岁,拟施择期外科手术患儿10例.常规静脉麻醉诱导,通过ID为5.5 mm的成人型FOB引导将ID为7.0 mm的较粗气管导管顶在声门口,小心退出FOB(第1步);在人工通气证实气管导管是位于喉口后,经较粗气管导管向气管内插入一根合适的可通气性气管导管交换芯(VETC),沿VETC退出较粗的气管导管(第2步).然后沿VETC将润滑良好且直径合适的细气管导管插人气管内(第3步).记录整个气管插管操作所需的时间和操作中遇到的困难及其采取的辅助措施,手术后随访有无呼吸道并发症发生.结果 本组患儿10例FOB引导三步气管插管成功100%.在沿VETC推送气管导管时,虽然2例小儿因润滑不满意和VETC外径不合适出现了沿VETC推送气管导管困难的情况,经过相应的处理措施均被有效解决.完成气管插管所需的时间为(124.1±15.2)s.所有患者手术后随访未发现呼吸道并发症.结论 在小儿,FOB引导三步气管插管技术具有操作简单、成功率高的优点,该方法可有效解决无法将成人型粗直径FOB应用于小儿困难呼吸道处理的临床难题.     

小剂量芬太尼、瑞芬太尼和舒芬太尼预防儿童经口气管插管心血管反应的比较

目的比较小剂量芬太尼、瑞芬太尼和舒芬太尼对患儿直接喉镜经口气管插管心血管反应的影响。方法选择120例施择期整形外科手术的患儿。随机平均分成对照组、芬太尼组、瑞芬太尼和舒芬太尼组,气管插管前采用盲法分别应用9g/L盐水0.2mL/kg、芬太尼2μg/kg、瑞芬太尼组1μg/kg和舒芬太尼0.2μg/kg。静脉麻醉诱导后采用直接喉镜实施经口气管插管。监测麻醉诱导前、后,气管插管时和气管插管后5min内血压(BP)和心率(HR)及观察期收缩压(SBP)和HR的变化率,并记录观察期SBP和HR达最大值时间及其气管插管后恢复至麻醉诱导后值时间。结果BP和HR基础值及气管插管时间在4组间均无显著性差异。气管插管致BP和HR较基础值显著升高,且是以对照组最为明显,芬太尼组次之,瑞芬太尼和舒芬太尼组最轻。对照组气管插管时BP和HR及其观察期最大值均显著高于芬太尼组、瑞芬太尼和舒芬太尼组;瑞芬太尼组和舒芬太尼组气管插管时的血压和HR及其观察期最大值均显著低于芬太尼组(Pa<0.05)。瑞芬太尼组观察期出现SBP和HR最大值时间显著长于对照组、芬太尼组和舒芬太尼组(Pa<0.05);舒芬太尼和瑞芬太尼组气管插管后SBP和HR恢复至麻醉诱导后值时间显著短于对照和芬太尼组(P<0.05)。瑞芬太尼和舒芬太尼组观察期SBP和HR增加大于基础值30%发生率较芬太尼组显著降低。结论与小剂量芬太尼比较,小剂量舒芬太尼和瑞芬太尼能更有效预防患儿经口气管插管的心血管反应。     

活性氧在芬太尼后处理和肢体远隔缺血后处理减轻大鼠心肌缺血再灌注损伤中的作用

目的 探讨活性氧在芬太尼后处理和肢体远隔缺血后处理减轻大鼠心肌缺血再灌注损伤中的作用.方法 成年雄性SD大鼠63只,8周龄,体重250 ～ 350 g,采用随机数字表法,将其随机分为7组(n=9):假手术组(S组)、心肌缺血再灌注组(I/R组)、芬太尼后处理组(F组)、肢体远隔缺血后处理组(R组)、活性氧清除剂N-(2-巯基丙酰基)-甘氨酸(MPG)组(M组)、MPG+芬太尼后处理组(MF组)和MPG+肢体远隔缺血后处理组(MR组).除S组外,其余6组采用结扎左冠状动脉前降支30 min再灌注180 min的方法制备心肌缺血再灌注损伤模型.在缺血前5 min至再灌注15 min M组、MF组和MR组静脉输注MPG 5 mg/kg,其他4组给予等容量生理盐水,心肌缺血15 min时,F组和MF组静脉注射芬太尼30 μg/kg;R组和MR组结扎大鼠双后肢造成缺血10 min.心肌再灌注180 min时,采集动脉血样,测定血清心肌肌钙蛋白Ⅰ(cTnI)浓度,然后处死大鼠,取心肌组织,采用TTC染色法测定心肌梗死体积.结果 与S组比较,其余6组血清cTnI浓度和心肌梗死体积均升高(P＜0.05);与I/R组比较,M组血清cTnI浓度和心肌梗死体积差异无统计学意义(P＞0.05),F组和R组血清cTnI浓度和心肌梗死体积降低(P＜ 0.05);MF组和F组血清cTnI浓度和心肌梗死体积差异无统计学意义(P ＞0.05); MR组血清cTnI浓度和心肌梗死体积高于R组(P＞0.05).结论 活性氧参与了肢体远隔缺血后处理减轻大鼠心肌缺血再灌注损伤的效应,而未参与芬太尼后处理的心肌保护作用.     

联合应用缺血后处理、远隔缺血后处理和纳洛酮后处理对大鼠脑缺血-再灌注损伤的影响

Objective To assess the effects of ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats.Methods A total of 110 adult SD rats were randomly divided into 5 groups (n =22 each). The focal cerebral ischemia-reperfusion injury was induced by a 90-minute occlusion of right middle cerebral artery (MCA) and a 24-hour reperfusion sequentially. Group 1 was of ischemia-reperfusion control; Group 2 ischemic postconditioning induced by three 30-second cycles of MCA occlusion followed by a 30-second reperfusion; Group 3 remote ischemic postconditioning performed via a transient occlusion of right femoralartery at 5 min before the initiatlon of reperfusion:Group 4 naloxone posteonditioning with naloxone 10 mg/kg intraperitoneaUy injected at the initiation of reperfusion;Group 5 combined ischemic,remote ischernic & naloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2,3 & 4.The neumlogie deftcit scores(NDS)were obtained at 2 h & 24 h post-reperfusion.At 24 h post-reperfusion.the anesthetized rat was sacrificed by decapitation and the brain rapidly extracted to asseSS the size ofcerebral infaret(n=10),detect the cerebral expression of microtubule-associated protein2(MAP2)(n=6),measure the plasma volume of cerebral tissues and quantify the diameter and segment artery at 5 min before the initiation of reperfusion; Group 4 naloxone postconditioning with naloxone 10 mg/kg intraperitoneally injected at the initiation of reperfusion; Group 5 combined ischemic, remote ischemic & naloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2, 3 & 4. The neurologic deficit scores ( NDS) were obtained at 2 h & 24 h post-reperfusion. At 24 h post-reperfusion, the anesthetized rat was sacrificed by decapitation and the brain rapidly extracted to assess the size of cerebral infarct (n = 10), detect the cerebral expression of microtubule-associated protein2 ( MAP2) (n =6) , measure the plasma volume of cerebral tissues and quantify the diameter and segment length of cerebral microvessel (n = 6 ). Results There were no significant differences in the heart rate (HR) and mean arterial pressure (MAP) among the above five groups at all observed time points (P ＞ 0. 05). At 24 h post-reperfusion, the percentage of ischemic cerebral infarct size was 43% ±6% , 31% ±4% , 32% ±5% , 28% ±6% & 21% ±7% in ipsilateral hemisphere area (i. e. , cerebral infarct severity)in Groups 1-5 respectively. Compared with Group 1, the levels of NDS and cerebral infarct severity significantly decreased at ischemic side in Groups 2-5 ( P ＜ 0. 05 ). And the cerebral expression of MAP2,plasma volume of cerebral tissues, diameter and segment length of cerebral microvessel significantly increased at the ischemic side (all P＜0. 05). However, there were no significant differences in the abovementioned parameters at ischemic side among Groups 2, 3 and 4 (all P ＞0. 05). The parameters of NDS,cerebral infarct severity, cerebral expression of MAP2 and plasma volume of cerebral tissues in the ischemic side significantly increased in Group 5 compared with Groups 1,2,3 and 4 (all P ＜ 0. 05). The diameter and segment length of cerebral microvessel at ischemic side were not different among Groups 2,3,4 and 5 (all P＞0. 05). Conclusion In focal cerebral ischemia-reperfusion rats, ischemic, remote ischemic and naloxone postconditioning may produce significant neuroprotective effects of reduced cerebral infarct severity and improved neurologic dysfunctions. A combination of three postconditioning approaches enhances the above neuroprotective effects.     

联合应用缺血后处理、远隔缺血后处理和纳洛酮后处理对大鼠脑缺血-再灌注损伤的影响

Objective To assess the effects of ischemic postconditioning, remote ischemic postconditioning and naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rats.Methods A total of 110 adult SD rats were randomly divided into 5 groups (n =22 each). The focal cerebral ischemia-reperfusion injury was induced by a 90-minute occlusion of right middle cerebral artery (MCA) and a 24-hour reperfusion sequentially. Group 1 was of ischemia-reperfusion control; Group 2 ischemic postconditioning induced by three 30-second cycles of MCA occlusion followed by a 30-second reperfusion; Group 3 remote ischemic postconditioning performed via a transient occlusion of right femoralartery at 5 min before the initiatlon of reperfusion:Group 4 naloxone posteonditioning with naloxone 10 mg/kg intraperitoneaUy injected at the initiation of reperfusion;Group 5 combined ischemic,remote ischernic & naloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2,3 & 4.The neumlogie deftcit scores(NDS)were obtained at 2 h & 24 h post-reperfusion.At 24 h post-reperfusion.the anesthetized rat was sacrificed by decapitation and the brain rapidly extracted to asseSS the size ofcerebral infaret(n=10),detect the cerebral expression of microtubule-associated protein2(MAP2)(n=6),measure the plasma volume of cerebral tissues and quantify the diameter and segment artery at 5 min before the initiation of reperfusion; Group 4 naloxone postconditioning with naloxone 10 mg/kg intraperitoneally injected at the initiation of reperfusion; Group 5 combined ischemic, remote ischemic & naloxone postconditioning performed simultaneously in accordance with the methods used in Groups 2, 3 & 4. The neurologic deficit scores ( NDS) were obtained at 2 h & 24 h post-reperfusion. At 24 h post-reperfusion, the anesthetized rat was sacrificed by decapitation and the brain rapidly extracted to assess the size of cerebral infarct (n = 10), detect the cerebral expression of microtubule-associated protein2 ( MAP2) (n =6) , measure the plasma volume of cerebral tissues and quantify the diameter and segment length of cerebral microvessel (n = 6 ). Results There were no significant differences in the heart rate (HR) and mean arterial pressure (MAP) among the above five groups at all observed time points (P ＞ 0. 05). At 24 h post-reperfusion, the percentage of ischemic cerebral infarct size was 43% ±6% , 31% ±4% , 32% ±5% , 28% ±6% & 21% ±7% in ipsilateral hemisphere area (i. e. , cerebral infarct severity)in Groups 1-5 respectively. Compared with Group 1, the levels of NDS and cerebral infarct severity significantly decreased at ischemic side in Groups 2-5 ( P ＜ 0. 05 ). And the cerebral expression of MAP2,plasma volume of cerebral tissues, diameter and segment length of cerebral microvessel significantly increased at the ischemic side (all P＜0. 05). However, there were no significant differences in the abovementioned parameters at ischemic side among Groups 2, 3 and 4 (all P ＞0. 05). The parameters of NDS,cerebral infarct severity, cerebral expression of MAP2 and plasma volume of cerebral tissues in the ischemic side significantly increased in Group 5 compared with Groups 1,2,3 and 4 (all P ＜ 0. 05). The diameter and segment length of cerebral microvessel at ischemic side were not different among Groups 2,3,4 and 5 (all P＞0. 05). Conclusion In focal cerebral ischemia-reperfusion rats, ischemic, remote ischemic and naloxone postconditioning may produce significant neuroprotective effects of reduced cerebral infarct severity and improved neurologic dysfunctions. A combination of three postconditioning approaches enhances the above neuroprotective effects.     

食管引流型与标准型喉罩通气道用于正压通气的自身对照研究

目的采用随机自身对照设计方法比较食管引流型喉罩通气道(PLMA)和标准型喉罩通气道(SLMA)用于间歇正压通气的有效性。方法选择50例经美国麻醉医师协会(ASA)身体状态分级标准分为1~2级、拟在全身麻醉下实施择期整形外科手术患者。在常规麻醉诱导后,顺序插入PLMA和SLMA,将通气罩内压充气至60cmH2O(1cm H2O=0.098kPa),评价两种喉罩通气道充气前后的肺通气满意度和气道密封压,同时进行光导纤维支气管镜(FOB)评分,确定通气罩的解剖位置。然后将潮气量设定为10ml/kg实施间歇正压通气,记录间歇正压通气后连续5次呼吸的平均呼潮气量和平均吸气峰压。结果在通气罩未充气情况下,插入PLMA后有46例(92%)患者获得了良好和尚可的肺通气效果,而插入SLMA后仅有22例(44%)患者获得了良好和尚可的肺通气效果;PLMA的气道密封压显著高于SLMA(P<0.05)。将通气罩内压充气至60cmH2O,采用PLMA的50例患者均获得良好的肺通气效果,但采用SLMA时仅有28例获得良好的肺通气效果;PLMA所需的充气量和充气后获得的气道密封压均显著高于SLMA(P均<0.05)。采用PLMA时所有患者的气道密封压均高于或等于采用SLMA时;采用PLMA时除2例患者外,其他患者所需的充气量也均高于采用SLMA时。PLMA通气罩位置的FOB评分显著低于SLMA(P<0.05)。采用PLMA维持气道的29例患者和采用SLMA维持气道的21例患者的平均呼潮气量、吸气峰压及维持气道时间差异均无显著性(P均>0.05)。结论与SLMA相比,PLMA可为正压通气提供更好的气道密封压,而且对声门和食管上端具有潜在的隔离作用,用于正压通气时PLMA比SLMA更有效、更安全。