地氟醚对内毒素致急性肺损伤大鼠肺泡毛细血管膜通透性的影响

目的 研究地氟醚对内毒素致急性肺损伤鼠肺泡毛细血管膜通透性和肺泡灌洗液(BAIF)内炎性细胞的影响。方法 48只雄Wistar大鼠随机分为4组,每组12只,C组:生理盐水对照组,股静脉注射生理盐水1.2 ml后机械通气4 h;L组:股静脉注射内毒素(LPS)5 mg/kg后机械通气4 h;D1L和D2L组:股静脉注射LPS 5 mg/kg后机械通气,分别吸人1.0 MAC和1.5 MAC地氟醚4 h。每组有6只大鼠不注射伊万斯蓝,用于病理学检查及肺泡灌洗。测定肺组织病理形态学积分、肺湿/干重比(W/D)、肺水含量、肺通透指数(LPI)、伊万斯蓝(EB)含量、BALF内炎性细胞总数及百分比、大鼠死亡率。结果 与C组比较,L组病理形态学积分、W/D、肺水含量、LPI和EB含量均升高(P<0.05或0.01),D1L组病理形态学积分和LPI升高(P<0.01)。与L组比较,D1L组W/D、肺含水量和EB含量升高(P<0.05)。与D1L组比较,D2L组病理形态学积分升高(P<0.05)。与C组比较,L组、D1L组、D2L组炎性细胞总数、中性粒细胞、巨噬细胞、淋巴细胞均升高(P<0.01)。与L组、D1L组比较,D2L组死亡率升高(P<0.01)。结论 吸入大剂量地氟醚加重内毒素致急性肺损伤。     

七氟醚对内毒素诱导大鼠肺组织氧化应激反应的影响

目的 探讨七氟醚对内毒素（LPS）诱导大鼠肺组织氧化应激反应的影响。方法Wistar大鼠48只，体重200-290g，随机分为4组（n=12）：对照组（C组）、LPS组（L组）、1．0MAC七氟醚组（S1L组）和1．5MAC七氟醚组（S2L组）。各组大鼠腹腔注射异戊巴比妥钠100mg／kg，麻醉后机械通气。维持呼气末二氧化碳分压在35～45mmHg。L组股静脉注射LPS5mg／kg，C组给予生理盐水1．2ml，S1L组、S2L组注射LPS后分别吸入1．0MAC、1．5MAC七氟醚4h。吸入七氟醚后4h处死大鼠，测定肺组织超氧化物超歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）、总一氧化氮合酶（tNOS）水平、诱导型一氧化氮合酶（iNOS）活性及iNOS mRNA、蛋白表达。结果 与C组比较，L组肺组织SOD活性下降，MDA、NO、tNOS水平、iNOS活性及iNOS mRNA及蛋白表达均升高（P〈0．01）；与L组比较，S1L组、S2L组肺组织SOD活性升高，MDA、NO、tNOS水平及iNOS mRNA及蛋白表达降低（P〈0．05）；S1L组与S2L组上述各项指标比较差异无统计学意义（P〉0．05）。结论 吸入1．0MAC和1．5MAC七氟醚4h可减轻LPS诱导肺组织氧化应激反应。     

地氟醚对内毒素诱导大鼠肺组织氧化应激反应的影响

目的探讨地氟醚对内毒素（LPS）诱导大鼠肺组织氧化应激反应的影响。方法雄性Wistar大鼠48只,体重200～290 g,随机分为4组（n=12）,对照组（C组）股静脉注射生理盐水1.2ml后机械通气4 h;LPS组（L组）股静脉注射LPS 5mg/kg后机械通气4 h;地氟醚1.0MAC组（D1）和地氟醚1.5 MAC组（D2）组：股静脉注射LPS 5 mg/kg后机械通气,分别吸入地氟醚1.0 MAC和1.5 MAC 4 h,机械通气4 h后处死大鼠,测定肺组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量、一氧化氮（NO）含量、总一氧化氮合酶（tNOS）活性、诱导型一氧化氮合酶（iNOS）活性、iNOS mRNA和iNOS表达水平。结果与C组比较,L组SOD活性下降,MDA含量、NO含量、tNOS活性、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.01）;与L组比较,D1组上述各项指标差异无统计学意义（P〉0.05）,D2组SOD活性下降,MDA含量、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.05）;与D1组比较,D2组SOD活性下降,MDA含量、iNOS活性、iNOS mRNA和iNOS表达升高（P〈0.05）。结论吸入地氟醚1.5 MAC 4 h可加重LPS诱导大鼠肺组织氧化应激反应,吸入地氟醚1.0 MAC对其无影响。     

七氟醚预处理对大鼠内毒素性急性肺损伤的影响

目的 探讨七氟醚预处理对大鼠内毒素性急性肺损伤的影响.方法 健康雄性SD大鼠24只,体重220～250 g,随机分为4组(n=6):对照组(c组)、内毒素组(LPS组)、七氟醚组(Sev组)和七氟醚预处理组(SP组).C组和LPS组机械通气30 min后分别静脉注射生理盐水和脂多糖(LPS)5 mg/kg;Sev组和SP组吸入七氟醚(呼气末浓度2.4%)30 min,洗脱5 min,然后分别静脉注射生理盐水和LPS 5 mg/kg.于给予LPS或生理盐水后6 h时,心脏放血处死大鼠,取肺组织,计算湿重/干重(W/D)比;采用弥漫性肺泡损伤(DAD)评分评价肺组织损伤程度;测定肺组织髓过氧化物酶(MPO)活性、细胞因子诱导中性粒细胞化学趋化因子-1(CINC-1)含量、CINC-1和CINC-1 mRNA的表达水平.结果 与C组比较,LPS组和SP组肺组织W/D比、DAD评分、MPO活性和CINC-1含量升高,CINC-1和CINC-1 mRNA的表达上调(P<0.01),Sev组上述指标差异无统计学意义(P>0.05);与LPS组比较,SP组肺组织W/D比、DAD评分、MPO活性和CINC-1含量降低,CINC-1和CINC-1 mRNA的表达下调(P<0.01).结论 七氟醚预处理可减轻大鼠内毒素性急性肺损伤,可能与其抑制肺组织炎性反应有关.     

七氟醚减轻大鼠呼吸机相关性肺损伤

目的 探讨七氟醚对大鼠呼吸机相关性肺损伤(VILI)的影响并探讨其可能机制。方法 健康SPF级雄性SD大鼠36只,6～8周龄,体重220～280 g。随机分为三组：对照组(C组)、VILI组(V组)和七氟醚组(S组),每组12只。大鼠给予1%戊巴比妥钠40 mg/kg麻醉后行气管切开插管术,C组自主呼吸4 h, V组和S组插管后机械通气4 h, S组机械通气期间吸入2%七氟醚4 h。通气参数：V_T 20 ml/kg, RR 80次/分,I∶E 1∶1,FiO₂ 21%,PEEP 0 cmH₂O。机械通气结束时采集股动脉血测定PaO₂。处死大鼠,取肺组织和支气管肺泡灌洗液(BALF),计算肺组织湿/干重比值(W/D),采用ELISA法检测BALF中白细胞介素(IL)-1β、IL-18浓度,二氯荧光黄双乙酸盐法检测BALF中肺泡巨噬细胞活性氧(ROS)水平,Western blot法及qRT-PCR法检测肺组织NF-E2相关因子2(Nrf2)、NLRP3、凋亡相关斑点样蛋白(ASC)、caspase-1...     

幼猪机械通气中异氟醚或七氟醚混合一氧化氮吸入的安全性

目的研究吸入异氟醚或七氟醚混合一氧化氮(NO)在幼猪机械通气中的安全性。方法36头幼猪随机分为6组:Ⅰ组(对照组):单纯机械通气;Ⅱ组(NO组):吸入20ppmNO;Ⅲ组(异氟醚组):吸入1.3MAC异氟醚;Ⅳ组(异氟醚 NO组):吸入1.3MAC异氟醚及20ppmNO;Ⅴ组(七氟醚组)吸入1.3MAC七氟醚;Ⅵ组(七氟醚 NO组)吸入1.3MAC七氟醚及20ppmNO。用麻醉机行间歇正压通气4h,测定各组机械通气前、机械通气1、2、3、4h(T0、T1、T2、T3、T4)的呼吸频率(RR)、呼吸系统总顺应性(Crs)、气道压力(Paw)、潮气量(VT)、分钟通气量(MV)以及呼末二氧化碳分压(PETCO2);测定T0、T2、T4时点动脉血高铁血红蛋白(MetHb)和亚硝酸根(NO2-/NO3-)水平;处死动物后比较各组肺组织湿/干重比、支气管肺泡灌洗液(BALF)中饱和磷脂/总磷脂(DSPC/TPL)及饱和磷脂,总蛋白(DSPC/TP)、肺表面张力和白细胞计数,并行肺组织损伤评分。结果Ⅲ、Ⅳ、Ⅴ、Ⅵ组BALF中DSPC/TP及肺表面张力较Ⅰ组下降(P<0.05),通气结束时Crs较通气前下降(P<0.05),而Ⅱ组无显著性变化(P>0.05);与通气前比较,各组通气结束时MetHb与:NO2-/NO3-水平无变化,各组BALF中白细胞计数、肺组织损伤评分、肺泡扩张度和湿/干重比之间比较差异无统计学意义。结论1.3MAC异氟醚或七氟醚混合20ppmNO吸入可以安全用     

不同血浆靶浓度舒芬太尼对腹腔镜气腹刺激时七氟醚MACBAR的影响

目的观察不同血浆靶浓度舒芬太尼对腹腔镜手术患者气腹刺激时抑制50%患者交感肾上腺素能反应的七氟醚最低肺泡有效浓度(MAC_(BAR))的影响。方法选择行腹腔镜胆囊切除术的患者125例,性别不限,年龄30～65岁,ASAⅠ或Ⅱ级,随机分为S_0、S_1、S_2、S_3、S_4共五组,舒芬太尼血浆靶浓度分别为0、0.1、0.3、0.5、0.7 ng/ml。吸入七氟醚麻醉诱导,意识消失后,静脉注射罗库溴铵0.6 mg/kg完成喉罩置入,调节呼气末七氟醚浓度,靶控舒芬太尼,待呼气末七氟醚浓度达预设值并稳定15 min以上,建立气腹。采用序贯法测定5组七氟醚MAC_(BAR)值,同时测定患者气腹前后肾上腺素、去甲肾上腺素浓度。结果当静脉靶控输注0、0.1、0.3、0.5及0.7 ng/ml的舒芬太尼时,S_0、S_1、S_2、S_3和S_4组七氟醚MAC_(BAR)值分别为(5.33±0.13)%、(4.53±0.08)%、(2.86±0.15)%、(2.23±0.10)%和(2.13±0.08)%。五组气腹刺激前后肾上腺素、去甲肾上腺素浓度差异无统计学意义。结论腹腔镜气腹刺激时七氟醚MAC_(BAR)随舒芬太尼血浆靶浓度的增加而降低,当舒芬太尼血浆靶浓度超过0.5 ng/ml时,七氟醚MAC_(BAR)值的下降出现封顶效应。当患者交感肾上腺素能反应被抑制时,血中肾上腺素、去甲肾上腺素浓度变化不受舒芬太尼血浆靶浓度的影响。     

吸入七氟醚、地氟醚对大鼠肺组织超微结构和肺表面活性物质的影响

目的观察不同吸入浓度七氟醚和地氟醚对大鼠肺组织超微结构及支气管肺泡灌洗液 (BALF)中肺表面活性物质相关蛋白-A(SP-A)、磷脂酰胆碱(PC)浓度的影响。方法雄性Wistar大鼠 50只,随机分为5组,每组10只,C组:单纯机械呼吸组;S1组和S2组:分别吸入1．0 MAC、1．5 MAC七氟醚4 b;D1组和D2组:分别吸入1．0MAC、1．5MAC地氟醚4 b。在相应时点处死大鼠,观察肺组织超微结构并测定BALF中SP-A和PC浓度。结果与C组比较,S1、S2、D1、D2组肺泡Ⅱ型上皮细胞微绒毛破坏程度较重,以D1、D2组改变更明显,板层体减少,并呈大量空泡化;BALF中SP-A、PC浓度下降 (P<0．01或0．05)。结论吸入1-0 MAC、1．5 MAC七氟醚或地氟醚4 h可降低肺泡Ⅱ型上皮细胞合成肺表面活性物质。     

异氟醚麻醉对内毒素诱导的大鼠急性肺损伤的预处理效应

目的：探讨异氟醚醉对内毒素诱导的大鼠急性肺损伤的预处理效应，方法：内毒素经股静脉注射Wistar大鼠复制急性肺损伤模型。动物分为：对照组（C组）、单纯异氟醚预处理组（SIso组）内毒素（LSP组）2小时，4小时、8小时组异氟醚预处理＋内毒素（Iso＋LPS组）2小时、4小时、8小时组，观察大体标本，组织病理、肺泡灌洗液中性粒细胞比，蛋白含量，肺湿／干重比，肺血管通透性。结果：LPS组、Iso＋LPS组肺泡灌洗液中中性粒细胞比，蛋白含量均较Ｃ组和SIso组显著增加（P＜0．01）Iso＋LPS组肺泡灌洗液中中性粒细胞比，蛋白含量与LPS组比没有显著差异（P＞0．05）。LPS组和Iso＋LPS组肺湿／干重比、肺血管通透性显著高于C组和SIso组（P＜0．01），而LPS组和Iso＋LPS组两组间无显著差异（P＞0．05）。结论：内毒素可引起严重的急性肺损伤，而异氟醚麻醉对内毒素诱导的急性肺损伤的预处理效应不明显。     

盐酸戊乙奎醚预先给药对大鼠内毒素性急性肺损伤的影响

目的研究盐酸戊乙奎醚预先给药对内毒素诱导大鼠急性肺损伤(ALI)的影响及其机制。方法40只雄性SD大鼠随机分为5组(n=8),对照组(C组):腹腔和尾静脉均注射生理盐水1 ml/kg;模型组(L组):腹腔注射生理盐水1 ml/kg,30 min后经尾静脉注射脂多糖(LPS)5mg/kg;盐酸戊乙奎醚低剂量组(DL组)、中剂量组(DM组)和高剂量组(DH组)分别腹腔注射盐酸戊乙奎醚0.03 mg/kg、0.1 mg/kg、0.3 mg/kg,30 min后经尾静脉注射LPS 5 mg/kg。LPS注射后4 h放血处死动物。检测肺组织湿/干重比(W/D)、肺通透性指数(LPI)、髓过氧化物酶(MPO)活性、丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性;检测支气管肺泡灌洗液蛋白浓度、乳酸脱氢酶(LDH)活性和中性粒细胞数;测定血清MDA水平和SOD活性;光镜观察肺组织形态学改变;电镜观察肺组织超微结构。结果与C组比较, L组、DL组、DM组和DH组肺W/D、肺含水量、LPI、支气管肺泡灌洗液LDH活性增加,支气管肺泡灌洗液中性粒细胞数和肺组织MPO活性、肺组织和血清MDA水平升高,SOD活性降低(P<0.05);与L组相比,DL组、DM组和DH组肺W/D、肺含水量、LPI、支气管肺泡灌洗液LDH活性降低,支气管肺泡灌洗液中性粒细胞数和肺组织MPO活性以及肺组织和血清MDA水平降低,SOD活性升高(P<0.05); DL组、DM组和DH组各指标组间差异无统计学意义(P>0.05)。光镜、电镜观察:盐酸戊乙奎醚预先给药各组肺组织病理学变化较L组减轻。结论盐酸戊乙奎醚预先给药可减轻内毒素诱导的大鼠急性肺损伤。     

Temperatures in soda lime during degradation of desflurane, isoflurane, and sevoflurane by desiccated soda lime

Rarely, fire and patient injury result from the degradation of sevoflurane by desiccated Baralyme. The present investigation sought to determine whether high temperatures also arose with sevoflurane use in the presence of desiccated soda lime. We desiccated soda lime by directing a 10 L/min flow of oxygen through fresh absorbent. Using 1140 +/- 30 g (mean +/- sd) of this desiccated absorbent, we filled a single standard absorber canister placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 minimum alveolar concentration (MAC) desflurane or sevoflurane, or 3.0 MAC desflurane, isoflurane, or sevoflurane (with and without concurrent delivery of 200 mL/min carbon dioxide). In an additional test, 2 canisters (rather than a single canister) containing desiccated absorbent were used and 3.0 MAC sevoflurane was applied. A 3-L reservoir bag served as a surrogate lung, and we ventilated this lung with a minute ventilation of 10 L/min. With desflurane at 1.5 MAC or 3.0 MAC or isoflurane at 3.0 MAC temperatures increased in 20 to 40 min to a peak of 30 degrees C to 45 degrees C and then declined. With 1.5 or 3.0 MAC sevoflurane, temperatures increased to approximately 90 degrees C, after which temperatures declined. Concurrent delivery of carbon dioxide and sevoflurane did not increase the peak temperatures reached. The use of 2 canisters increased the duration but not the peak of increased temperature reached with 3.0 MAC sevoflurane. No fires resulted from degradation of any anesthetic.     

Role of polymorphonuclear leukocytes in experimental lung injury--chemotaxis and active oxygen metabolite production

To clarify the role of polymorphonuclear leucocytes (PMNs) in acute lung injury, acute experimental lung injury was produced by intravenous injection of endotoxin to male Hartley guinea pigs. White blood cell (WBC) counts in the peripheral blood, total nucleated cell counts and PMNs' population in the lung lavage fluid, chemotaxis and chemiluminescence of the PMNs in the blood and in the lung lavage fluid were studied. Results were as following 1. WBC counts in the blood decreased after injection of endotoxin. In the lung lavage fluid, total nucleated cell counts and the differential counts of PMNs increased with time. 2. The chemotaxis of PMNs in the blood decreased significantly (647 +/- 118 cells/5 high-power-fields (5HPF) in no treatment group (NT group), vs 256 +/- 120 cells/5HPF in 6 hours after endotoxin injection group (6h group), p less than 0.01), but that in the lung lavage fluid increased significantly (93 +/- 63 cells/5HPF in NT group, vs 334 +/- 24 cells/5HPF in 6h group p less than 0.01). 3. The chemiluminescence of the PMNs in the blood increased (3.64 +/- 2.41 counts/cell in NT group, vs 51.2 +/- 32.9 counts/cell in 6h group, p less than 0.01), and that in the lung lavage fluid increased (1.89 +/- 0.94 counts/cell NT group, vs 59.2 +/- 49.1 counts/cell in 6h group, p less than 0.01). We concluded that increased chemotaxis of PMNs contributed to the influx of PMNs into the alveolar spaces after endotoxin injection. As the pMNs in the alveolar spaces had increased ability to produce active oxygen metabolite, they might be involved in the progression of endotoxin-induced acute lung injury.     

The in-vitro effects of sevoflurane and desflurane on the contractility of pregnant human uterine muscle

The effect of desflurane and sevoflurane on the contractility of the uterus was examined in vitro on strips of human myometrium obtained at the time of elective cesarean section. Small strips (1 mm x 2 mm x 10 mm) of muscle were prepared and suspended in an organ bath containing oxygenated physiological saline. Force of contraction was recorded continuously using an isometric tension transducer. Following the onset of regular spontaneous contractions, baseline measurements were obtained and the strips were exposed to varying concentrations of sevoflurane or desflurane corresponding to 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC). Sevoflurane depressed contractility to 72 +/- 18% of control at 0.5 MAC, 37 +/- 15% at 1.0 MAC and 27 +/- 16% at 1.5 MAC compared with 65 +/- 14 of control at 0.5 MAC, 43 +/- 18% at 1.0 MAC and 22 +/- 11% at 1.5 MAC for desflurane. The degree of depression of uterine muscle contractility produced by both these agents was significantly different from control at all concentrations. In conclusion, both sevoflurane and desflurane depress the contractility of isolated pregnant human myometrium at concentrations of 0.5, 1.0 and 1.5 MAC. These agents produce a similar degree of depression of uterine muscle contractility.     

Does epidural anesthesia have general anesthetic effects? A prospective, randomized, double-blind, placebo-controlled trial

BACKGROUND: Clinically, patients require surprisingly low end-tidal concentrations of volatile agents during combined epidural-general anesthesia. Neuraxial anesthesia exhibits sedative properties that may reduce requirements for general anesthesia. The authors tested whether epidural lidocaine reduces volatile anesthetic requirements as measured by the minimum alveolar concentration (MAC) of sevoflurane for noxious testing cephalad to the sensory block. METHODS: In a prospective, randomized, double-blind, placebo-controlled trial, 44 patients received 300 mg epidural lidocaine (group E), epidural saline control (group C), or epidural saline-intravenous lidocaine infusion (group I) after premedication with 0.02 mg/kg midazolam and 1 microg/kg fentanyl. Tracheal intubation followed standard induction with 4 mg/kg thiopental and succinylcholine 1 mg/kg. After 10 min or more of stable end-tidal sevoflurane, 10 s of 50 Hz, 60 mA tetanic electrical stimulation were applied to the fifth cervical dermatome. Predetermined end-tidal sevoflurane concentrations and the MAC for each group were determined by the up-and-down method and probit analysis based on patient movement. RESULTS: MAC of sevoflurane for group E, 0.52+/-0.18% (+/- 95% confidence interval [CI]), differed significantly from group C, 1.18+/-0.18% (P < 0.0005), and from group I, 1.04+/-0.18% (P < 0.001). The plasma lidocaine levels in groups E and I were comparable (2.3+/-1.0 vs. 3.0+/-1.2 microg/ml +/- SD). CONCLUSIONS: Lidocaine epidural anesthesia reduced the MAC of sevoflurane by approximately 50%. This MAC sparing is most likely caused by indirect central effects of spinal deafferentation and not to systemic effects of lidocaine or direct neural blockade. Thus, lower concentrations of volatile agents than those based on standard MAC values may be adequate during combined epidural-general anesthesia.     

The minimum alveolar concentration (MAC) and hemodynamic effects of halothane, isoflurane, and sevoflurane in newborn swine

To determine the minimum alveolar concentration (MAC) and hemodynamic responses to halothane, isoflurane, and sevoflurane in newborn swine, 36 fasting swine 4-10 days of age were anesthetized with one of the three volatile anesthetics in 100% oxygen. MAC was determined for each swine. Carotid artery and internal jugular catheters were inserted and each swine was allowed to recover for 48 h. After recovery, heart rate (HR), systemic systolic arterial pressure (SAP), and cardiac index (CI) were measured awake and then at 0.5, 1.0, and 1.5 MAC of the designated anesthetic in random sequence. The (mean +/- SD) MAC for halothane was 0.90 +/- 0.12%; the MAC for isoflurane was 1.48 +/- 0.21%; and the MAC for sevoflurane was 2.12 +/- 0.39%. Awake (mean +/- SD) measurements of HR, SAP, and CI did not differ significantly among the three groups. Compared to the awake HR, the mean HR decreased 35% at 1.5 MAC halothane (P less than 0.001), 19% at 1.5 MAC isoflurane (P less than 0.005), and 31% at 1.5 MAC sevoflurane (P less than 0.005). Compared to awake SAP, mean SAP measurements decreased 46% at 1.5 MAC halothane (P less than 0.001), 43% at 1.5 MAC isoflurane (P less than 0.001), and 36% at 1.5 MAC sevoflurane (P less than 0.005). Mean SAP at 1.0 and 1.5 MAC halothane and isoflurane were significantly less than those measured at equipotent concentrations of sevoflurane (P less than 0.005). Compared to awake CI, mean CI measurements decreased 53% at 1.5 MAC halothane (P less than 0.001) and 43% at 1.5 MAC isoflurane (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Naloxone does not increase the minimum alveolar anesthetic concentration of sevoflurane in mice

Several previous studies concluded that opioid receptors do not mediate the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation because administration of naloxone (a nonspecific opioid receptor antagonist) does not increase the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetic that produces immobility in 50% of subjects given a noxious stimulation. In contrast, a recent study found that 0.1 mg/kg naloxone given intraperitoneally increased sevoflurane MAC in mice by 18% (P < 0.01). We repeated the recent study with sevoflurane in the same strain of mice, administering nothing (control), 0.1 mg/kg, and 1.0 mg/kg of naloxone. Our study differed in that we also tested a parallel group given saline rather than naloxone. We were blinded to drug administration. MAC decreased 4.8% +/- 11.0% (mean+/- sd) and 2.4% +/- 12.5% with the first and second administrations of saline. Similarly, MAC decreased 4.7% +/- 7.1% and 5.5% +/- 10.0% with the administration of 0.1 mg/kg and 1.0 mg/kg of naloxone. We do not find that naloxone increases MAC. Opioid receptors do not underlie a portion of the capacity of inhaled anesthetics to produce immobility.     

Influence of propofol and volatile anaesthetics on the inflammatory response in the ventilated lung

Background: The immunomodulatory effects of volatile anaesthetics in vitro and the protective effect of propofol in lung injury spurred us to study the effects of volatile anaesthetics and propofol on lung tissue in vivo. Methods: Twenty‐seven pigs were randomized to 4‐h general anaesthesia with propofol (8 mg/kg/h, group P, n=9), sevoflurane [minimum alveolar concentration (MAC)=1.0, group S, n=9) or desflurane (MAC=1.0, group D, n=9). Four healthy animals served as the no‐ventilation group. Bronchoalveolar lavage fluid (BALF) was obtained to measure the cell counts, platelet‐activating factor acetylhydrolase (PAF‐AcH), phospholipase A₂ (PLA₂) and superoxide dismutase (SOD) activity. Lung tissues were evaluated histologically and for caspase‐3 expression. Results: Volatile anaesthetics reduced PAF‐AcH levels without affecting PLA₂ activity and resulted in decreased alveolar macrophage and increased lymphocyte counts in BALF (sevoflurane: 29 ± 23%; desflurane: 26 ± 6%, both P<0.05 compared with 4 ± 2% in the no‐ventilation group). These findings were accompanied by atelectasis and inflammatory cells' infiltration in the inhalational anaesthetics groups. Also, sevoflurane reduced SOD activity and both sevoflurane and desflurane induced significant caspase‐3 expression. In contrast, propofol resulted in a minor degree of inflammation and preserved BALF cells' composition without triggering apoptosis. Conclusion: Halogenated anaesthetics seem to trigger an immune lymphocytic response in the lung, inducing significant apoptosis and impairment of PAF‐AcH. In contrast, propofol preserves anti‐inflammatory and anti‐oxidant defences during mechanical ventilation, thus preventing the emergence of apoptosis.     

Does Epidural Anesthesia Have General Anesthetic Effects?: A Prospective, Randomized, Double-blind, Placebo-controlled Trial

Background: Clinically, patients require surprisingly low end-tidal concentrations of volatile agents during combined epidural-general anesthesia. Neuraxial anesthesia exhibits sedative properties that may reduce requirements for general anesthesia. The authors tested whether epidural lidocaine reduces volatile anesthetic requirements as measured by the minimum alveolar concentration (MAC) of sevoflurane for noxious testing cephalad to the sensory block.

Methods: In a prospective, randomized, double-blind, placebo-controlled trial, 44 patients received 300 mg epidural lidocaine (group E), epidural saline control (group C), or epidural saline-intravenous lidocaine infusion (group I) after premedication with 0.02 mg/kg midazolam and 1 [mu]g/kg fentanyl. Tracheal intubation followed standard induction with 4 mg/kg thiopental and succinylcholine 1 mg/kg. After 10 min or more of stable end-tidal sevoflurane, 10 s of 50 Hz, 60 mA tetanic electrical stimulation were applied to the fifth cervical dermatome. Predetermined end-tidal sevoflurane concentrations and the MAC for each group were determined by the up-and-down method and probit analysis based on patient movement.

Results: MAC of sevoflurane for group E, 0.52 +/- 0.18% (+/- 95% confidence interval [CI]), differed significantly from group C, 1.18 +/- 0.18% (P< 0.0005), and from group I, 1.04 +/- 0.18% (P< 0.001). The plasma lidocaine levels in groups E and I were comparable (2.3 +/- 1.0 vs. 3.0 +/- 1.2 [mu]g/ml +/- SD).     

Cerebral autoregulation during sevoflurane or isoflurane anesthesia: evaluation with transient hyperemic response]

We investigated dynamic cerebral autoregulation during N2O-O2/fentanyl anesthesia (baseline) plus 1.0 and 2.0 minimum alveolar anesthetic concentrations (MAC) of sevoflurane or isoflurane anesthesia in 14 patients undergoing non-neurosurgical operation. Cerebral blood flow velocity in the right middle cerebral artery (Vmca) was measured continuously using transcranial Doppler ultrasonography. At normocapnia, dynamic cerebral autoregulation was tested by transient hyperemic response (a response of Vmca after a brief compression of the ipsilateral common carotid artery). For quantitative comparisons, ratio of systolic Vmca before, to immediately after compression (THRR) was calculated. Values of THRR were 1.14 +/- 0.03 (mean +/- SD), 1.15 +/- 0.04, and 1.12 +/- 0.03 during baseline, 1.0, and 2.0 MAC sevoflurane anesthesia, respectively. THRR was not significantly different among the 3 conditions. In contrast, THRR values were 1.17 +/- 0.03, 1.07 +/- 0.02, and 1.01 +/- 0.01 during baseline, 1.0, and 2.0 MAC isoflurane anesthesia, respectively. THRR was significantly attenuated in a dose dependent manner during isoflurane anesthesia. These results indicate that dynamic cerebral autoregulation is preserved during 2.0 MAC sevoflurane anesthesia, but not during 1.0 MAC isoflurane anesthesia.