低浓度七氟醚与异氟醚吸入麻醉对小儿血流动力学的影响

目的 研究低流量七氟醚与异氟醚吸入麻醉对小儿血流动力学的影响.方法 40例1～5岁小儿随机分为七氟醚组(S组)和异氟醚组(I组),每组20例.分别测量呼气末麻醉药浓度为0MAC(T0)、0.5MAC(T1)、1.0MAC(T2)和1.5MAC(T3)稳定5 min后的每搏指数(SI)、心脏指数(CI)、外周血管阻力(SVR)、HR及MAP.结果 与T0时比较,T1时两组MAP和SVR均有降低(P<0.05),其他指标均无明显变化.T2时,SVR和MAP进一步降低,HR略增快和SI略升高,但两组间差异无统计学意义,S组Cl值显著高于Ⅰ组(P<0.05).T3时,S组的HR显著快于Ⅰ组,而SI下降与T0近似;SVR和MAP两组无进一步降低.结论 低浓度七氟醚和异氟醚麻醉对小儿心肌无明显抑制,仅降低MAP和SVR,七氟醚增快HR作用大于异氟醚.     

异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响

目的 探讨异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响。方法 选择SD雄性大鼠20只,随机分为两组,制备提睾肌微循环模型。吸入异氟醚、七氟醚麻醉后,分别记录吸入异氟醚、七氟醚1．5MAC3h内微循环、小动脉A1的直径和血流速度,微循环毛细血管后微静脉的白细胞滚动和粘附数量。结果 吸入异氟醚、七氟醚1．5MAC3h内HR,MAP,CVP和A1的直径和血流速度无明显改变（P＞0．05）。微循环毛细血管后微静脉的白细胞流动和粘附数量显著增加（P＜0．01）。结论 长时间吸入异氟醚、七氟醚后,可引起大鼠骨骼肌微循环毛细血管后微静脉的白细胞滚动和粘附数量显著增加。     

静吸复合麻醉下七氟醚与异氟醚对颅内压的影响

目的:在颅内顺应性正常神经外科病人,观察1.0 MAC七氟醚与异氟醚对颅内压的影响。方法:垂体瘤或颅咽管瘤手术病人16例,随机分为两组:A组为咪唑安定 芬太尼 1.0 MAC异氟醚;B组为咪唑安定 芬太尼 1.0 MAC七氟醚。选择L_(3～4)行蛛网膜下腔穿刺。麻醉诱导采用芬太尼-咪唑安定-阿曲库铵。插管后维持稳定30分开始吸入七氟醚(或异氟醚)。分别于麻醉前、吸入麻醉药前、达预定呼气末浓度30分内观察监测指标。结果:1.0 MAC七氟醚和异氟醚均可显著降低脑灌注压,异氟醚作用较强。吸入1.0 MAC七氟醚后颅内压首先呈显著性下降,15分后回复至基础水平。吸入1.0 MAC异氟醚后颅内压无显著性变化。结论:在颅内顺应性正常患者,1.0 MAC七氟醚和异氟醚均可安全用于神经外科麻醉。     

地氟醚与异氟醚麻醉对小儿循环功能的影响

目的：比较地氟醚和异氟醚麻醉对小儿血液动力学的影响。方法：28例1－5岁小儿，ASAI－Ⅱ级，快速诱导气管插管后随机分为地氟醚（D）帮异氟醚（I）两组，每组14例。分别测量呼气末麻醉药浓度为0、0．5、1．0和1．5MAC稳定5分钟后的SI、CI、SVR、HR及MAP。结果：与0MAC比较，0．5MAC时两组MAP和SVR均略有降低（P＜0．05），其他指标均无明显变化（P＞0．05）。1．0MAC时，SVR和MAP进一步降低，其幅度两组间无显著差异；HR和SI均略有升高，但无显著差异；CI值D组显著高于I组。达1．5MAC时，D组的HR显著高于I组，而SI下降与0MAC近似；SVR和MAP两组无进一步降低。结论：地氟醚和异氟醚麻醉对小儿心肌收缩功能均有一定抑制作用,但地氟醚使小儿HR增快的作用大于异氟醚。     

地氟醚、七氟醚和异氟醚对犬血液动力学和氧供需平衡的影响

目的　采用连续温度稀释法观察不同浓度地氟醚对血液动力学和氧供需平衡的影响 ,并与七氟醚和异氟醚比较。方法　犬 18只 ,1.5 %硫喷妥钠 2 0 mg/ kg、阿曲库胺 0 .8mg/ kg麻醉诱导 ,气管插管后机械通气。左股静脉穿刺置入 7.5 F的六芯肺动脉漂浮导管 ,接 CCO/ SvO2 监测仪 ,连续测定并计算血液动力学及氧供需平衡各项指标。操作完成后平稳 1小时 ,取基础指标。然后随机依次吸入 0 .7、1.2和 1.7MAC的地氟醚、七氟醚或异氟醚 ,呼气末浓度达预定值后稳定 2 0分钟 ,记录各指标 ,再增加吸入浓度达下一个预定浓度。结果　 MAP、SVR和 CO在三组均呈剂量依赖性下降 ,地氟醚和异氟醚组 HR明显增快 ,七氟醚组 HR则明显减慢 ,异氟醚组 1.7MAC时 VO2 增加 ,DO2 和Sv O2 下降。结论　地氟醚对循环功能和氧供需平衡的影响与异氟醚相似 ,与七氟醚则有所不同     

七氟醚对神经外科手术患者颅内压的影响

目的 :观察静吸复合麻醉下 0 5、1 0MAC七氟醚对颅内压的影响。方法 :选颅内顺应性正常的择期行垂体瘤或颅咽管瘤手术患者 16例 ,随机分为两组 :A组用咪唑安定 +芬太尼 + 0 5MAC七氟醚 ;B组咪唑安定 +芬太尼+ 1 0MAC七氟醚。于L3～ 4穿刺至蛛网膜下腔以监测腰部脑脊液压 (ISP)。麻醉诱导采用芬太尼 咪唑安定 阿曲库铵。气管内插管后静脉泵入咪唑安定 0 1mg·kg-1·h-1、阿曲库铵 0 5mg·kg-1·h-1。插管后稳定 3 0分钟开始吸入七氟醚。分别于麻醉诱导前、吸入七氟醚前、达预定呼气末七氟醚浓度即刻、5、10、15、2 0、3 0分钟时观察并记录各监测指标。结果 :吸入 0 5MAC七氟醚后颅内压逐渐上升 ,达预定浓度后 3 0分钟上升 11 2 % ;吸入 1 0MAC七氟醚后颅内压首先呈显著性下降 ,15分钟后逐渐回复至基础水平。结论 :0 5、1 0MAC七氟醚可安全用于神经外科颅内顺应性正常的患者。     

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     

七氟醚麻醉对脑葡萄糖能量代谢的影响

目的研究吸人不同浓度七氟醚对健康志愿者脑内葡萄糖能量代谢（CMGlu）的影响,探讨七氟醚在人脑可能的作用部位。方法选择健康志愿者10名,每人分别做三次正电子发射计算机体层扫描：第一次在清醒状态下扫描作为对照;第二、三次分别吸人0．5MAC和1．0MAC七氟醚。结果（1）与清醒状态比较,镇静状态下脑电双频指数（BIS）明显降低（P〈0．05）,MAP、RR和HR等指标无显著改变;而意识消失状态下,MAP、BIS显著降低,呼吸抑制,PgrCO2升高（P〈0．05）。（2）清醒时全脑内CMGlu计数为2268．3±91．2,吸入0．5MAC七氟醚麻醉后CMGlu计数降低至1875．9±86．2（P〈0．05）,降低17％;吸入1．0MAC七氟醚后CMGlu计数降低至1556．3±80．4（P〈0．01）。与清醒时比较,吸入0．5MAC麻醉后脑内各区CMGlu计数均显著降低（P〈0．05）,以丘脑、楔叶、楔前叶和扣带回cMGlu计数降低更为显著（P〈0．01）,分别降低46％、41％、42％和40％;吸人1．0MAC麻醉后,全脑及脑内各区CMGlu计数均进一步降低8％～11％（P〈0．05）。结论七氟醚麻醉可明显降低全脑及脑内各区葡萄糖代谢,且程度与吸入七氟醚的浓度相关。丘脑、楔叶、楔前叶和扣带回对吸入七氟醚麻醉更为敏感,可能是七氟醚麻醉在脑内作用的主要靶区。     

七氟醚对小儿食管下段括约肌功能的影响

目的　观察七氟醚麻醉对小儿食管下段括约肌 (LES)功能的影响。方法　 15例行择期手术小儿 ,年龄 3～ 7岁 ,ASAⅠ～Ⅱ级 ,术前无胃食管反流症状 ,亦未用术前药。静脉注射γ 羟基丁酸钠和阿曲库铵诱导插管后 ,吸入七氟醚维持麻醉。吸入前及吸入浓度分别达 0 5、1 0和1 5MAC时 ,用PaPolygrafHR胃肠动力监测系统进行测压。用专业软件处理、储存下列数据 :LES压力 (LESP)、胃压 (GP)、屏障压 (BrP)、长度 (SL)、压力向量容积 (PVV)。结果　随七氟醚MAC的升高 ,LESP、BrP和PVV均有所下降 ,与基础值相比 ,0 5MAC和 1 0MAC时差异无显著意义 (P >0 0 5 ) ;1 5MAC时差异有显著性意义 (P <0 0 5 )。而SL和GP无明显变化。结论　七氟醚对小儿LES功能的影响较小 ,有利于维持其功能稳定。但有高度反流危险的小儿 ,应避免使用高浓度七氟醚     

腹部手术患者吸入七氟醚与异氟醚麻醉恢复的比较

目的比较腹部手术患者吸入七氟醚与异氟醚麻醉恢复的情况。方法全麻下行开腹手术患者40例,随机分为2组（n=20）：七氟醚组（S组）及异氟醚组（Ⅰ组）。麻醉诱导后行气管插管,机械通气。诱导后吸入纯氧,氧流量2 L/min,30min后调整为1 L/min。手术开始前,调整吸入麻醉药的呼气末浓度为1.0 MAC。麻醉维持：吸入七氟醚或异氟醚,间断静脉注射罗库溴铵和芬太尼,维持血压和心率波动幅度不超过基础值30%。缝皮结束时,停止吸入七氟醚或异氟醚,纯氧流量调整为5 L/min。记录睁眼时间（停止吸入麻醉药到睁眼的时间）、拔除气管导管时间（停止吸入麻醉药到拔除气管导管的时间）、Aldrete评分达到9分时间（从停止吸入麻醉药计时）及麻醉后恢复室（PACU）停留时间。记录吸入麻醉药用量。结果与Ⅰ组比较,S组睁眼时间、拔除气管导管时间、Aldrete评分达到9分时间及PACU停留时间缩短（P〈0.05）,吸入麻醉药的总用量和单位时间用量差异无统计学意义（P〉0.05）。结论与异氟醚比较,吸入七氟醚患者麻醉恢复较快,且麻醉恢复质量较好。     

地氟醚对内皮素、前列腺素和血栓素的影响

目的：观察地氟醚对上腹手术患者血浆中内皮素（ET）、6酮－前列腺素1a(6-keto-PGF1a）和血栓素B2（TXB2）的影响。方法:随机选取ASAI－II级择期上腹部手术患者10例,全麻诱导气管插管后吸入1MAC的地氟醚维持麻醉。于麻醉前、诱导后、吸入地氟醚10分钟、吸入地氟醚50分钟及手术结束时抽取静脉血,采用放免法测定血浆中ET、6-keto-PGF1a和TXB2的含量。结论：术中ET虽有升高,但无统计学意义。6-keto-PGF1a在诱导后显著降低（P＜0.01）,吸入地氟醚后开始升高（P＜0.01）直至术毕。TXB2在诱导后显著降低（P＜0.01）,吸和地氟醚后逐渐恢复,但仍显著低于术前水平（P＜0.05）。6-keto-PGF1a与TXB2的比值在诱导后及吸入地氟醚后显著增大（P＜0.05及P＜0.01）。结论：吸入1MAC地氟醚时,血浆前列腺素水平增加,血栓素降低,二者比值增加有助于保护心血管功能。     

Cerebral blood flow at 0.5 and 1.0 minimal alveolar concentrations of desflurane or sevoflurane compared with isoflurane in normoventilated pigs

Whether desflurane and sevoflurane have clinical advantages over isoflurane in neuroanesthesia is much debated. A porcine model was used for comparison of desflurane and sevoflurane with isoflurane with respect to their cerebrovascular effects. The minimal alveolar concentration (MAC) of each of the three agents was first determined in a standardized manner in six domestic juvenile pigs to enhance comparison reliability. Six other pigs were then anesthetized with isoflurane, desflurane, and sevoflurane, given in sequence to each pig in an even crosswise order with the first agent also used to maintain anesthesia during surgical preparation. Cerebral blood flow (CBF) was calculated from the clearance curve of intraarterially injected 133Xe. The mean arterial pressure (MAP) was invasively monitored. The estimated cerebrovascular resistance (CVRe) was calculated by dividing MAP with CBF, thereby approximating the cerebral perfusion pressure with MAP. For both MAC levels, the trend for CBF was desflurane > isoflurane > sevoflurane, and the trend for MAP and CVRe was sevoflurane > isoflurane > desflurane. Statistical comparison of desflurane and sevoflurane with isoflurane with respect to CBF and MAP revealed two statistically significant differences-namely, that CBF at 1.0 MAC desflurane was 17% higher than CBF at 1.0 MAC isoflurane (P =.0025) and that MAP at 1.0 MAC sevoflurane was 16% higher than MAP at 1.0 MAC isoflurane (P =.011). Consequently, in this study at normocapnia, these agents did not seem to differ much in their cerebral vasodilating effects at lower doses. At higher doses, however, desflurane, in contrast to sevoflurane, was found to induce more cerebral vasodilation than isoflurane.     

地氟烷和七氟烷在稳态条件下对脑氧饱和度的影响

我们研究了七氟烷和地氟烷对局部脑组织氧饱和度（rSO2）的影响。22例经腹行子宫切除术的患者在稳态条件下以随机交叉的方式间隔30分钟吸入七氟烷和地氟烷各15分钟，维持脑电双频指数（bispectral index，BIS）值为40～50。另一组接受同样手术和麻醉的22例患者维持BIS值为20—30。在每种麻醉药15分钟的维持期间，每3分钟记录一次稳态条件下的rSO2、BIS、麻醉药吸入浓度和呼气末浓度、呼气末二氧化碳、SpO2、舒张压和收缩压以及心率。当BIS值维持于40～50或20—30时，两种麻醉药的rSO2均无差异。维持BIS值为40～50和20—30所需地氟烷和七氟烷的MACBIS值分别为1．0和1．2（P=0．004）及1．6和1．8（P〈0．001）。吸入1．6MAC地氟烷的rSO，值（71±13）高于1MAC时的rSO2值（66±10，P〈0．001），吸入1．8MAC七氟烷的rSO2值（72±11）高于1．2MAC时的rSO2值（66±13，P〈0．001）。因此，BIS值等效浓度的地氟烷或七氟烷的rSO，值相似，而提高两种麻醉药的吸入浓度均可增加rSO2值。     

Effects of 0.5 and 1.0 MAC isoflurane,sevoflurane and desflurane on intracranial and cerebral perfusion pressures in children

BACKGROUND: Isoflurane has been a commonly used agent for neuroanesthesia, but newer agents, sevoflurane and desflurane, have a quicker onset and shorter emergence from anesthesia and are increasingly preferred for general pediatric anesthesia. But their effects on intracranial pressure (ICP) and cerebral perfusion pressure (CPP), especially in pediatric patients with already increased ICP, have not been well documented. METHODS: We studied 36 children scheduled for elective implantation of an intraparenchymal pressure device for 24 h monitoring for suspected elevated ICP. After a standardized intravenous anesthesia, the patients were moderately hyperventilated with 60% nitrous oxide (N2O) in oxygen. The patients were then randomized to receive 0.5 and 1.0 MAC of isoflurane (Group I, n = 12), sevoflurane (Group S, n = 12) or desflurane (Group D, n = 12) in 60% N2O in oxygen. Respiratory and hemodynamic variables, ICP and CPP were recorded at baseline and after exposure to a target level of test drug for 10 min or until CPP fell below 30 mmHg (recommended lower ICP level is 25 mmHg in neonates, rising to 40 mmHg in toddlers). RESULTS: When comparing baseline values with values at 1.0 MAC, mean arterial pressure (MAP) decreased (P < 0.001) in all groups, with no differences between the groups. ICP increased (P < 0.001) with all agents, mean +2, +5, and +6 mmHg in Group I, S and D, respectively, with no differences between the groups. Regression analyzes found no relationship between baseline ICP and the increases in ICP from baseline to 1.0 MAC for isoflurane or sevoflurane. However, increased baseline ICP tended to cause a higher ICP increase with 1.0 MAC desflurane; regression coefficient +0.759 (P = 0.077). The difference between regression coefficients for Group I and Group D were not significant (P = 0.055). CPP (MAP-ICP) decreased (P < 0.001) in all groups, mean -18, -14 and -17 mmHg in Group I, S and D, respectively, with no significant difference between the groups. CONCLUSIONS: 0.5 and 1.0 MAC isoflurane, sevoflurane and desflurane in N2O all increased ICP and reduced MAP and CPP in a dose-dependent and clinically similar manner. There were no baseline dependent increases in ICP from 0 to 1.0 MAC with isoflurane or sevoflurane, but ICP increased somewhat more, although statistically insignificant, with higher baseline values in patients given desflurane. The effect of MAP on CPP is 3-4 times higher than the effect of the increases in ICP on CPP and this makes MAP the most important factor in preserving CPP. In children with known increased ICP, intravenous anesthesia may be safer. However, maintaining MAP remains the most important determinant of a safe CPP.     

Preservation of the Ratio of Cerebral Blood Flow/Metabolic Rate for Oxygen during Prolonged Anesthesia with Isoflurane, Sevoflurane, and Halothane in Humans

Background: In several animal studies, an increase in cerebral blood flow (CBF) produced by volatile anesthetics has been reported to resolve over time during prolonged anesthesia. It is important to investigate whether this time-dependent change of CBF takes place in humans, especially in clinical situations where surgery is ongoing under anesthesia. In this study, to evaluate the effect of prolonged exposure to volatile anesthetics (isoflurane, sevoflurane, and halothane), the CBF equivalent (CBF divided by cerebral metabolic rate for oxygen (CMRO2)) was determined every 20 min during anesthesia lasting more than 4 h in patients.

Methods: Twenty-four surgical patients were assigned to three groups at random to receive isoflurane, sevoflurane, or halothane (8 patients each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 MAC before surgery and then 1.5 MAC for the 3 h of surgical procedure. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 60 mmHg, using phenylephrine infusion, if necessary. CBF equivalent was calculated every 20 min as the reciprocal of arterial-jugular venous oxygen content difference.

Results: CBF equivalent at 0.5 MAC of isoflurane, halothane, and sevoflurane was 21+/-4, 20+/-3, and 21+/-5 ml blood/ml oxygen, respectively. All three examined volatile anesthetics significantly (P < 0.01) increased CBF equivalent in a dose-dependent manner (0.5, 1.0, 1.5 MAC). At 1.5 MAC, the increase of CBF equivalent with all anesthetics was maintained increased with minimal fluctuation for 3 h. The mean value of CBF equivalent at 1.5 MAC in the isoflurane group (45+/-8) was significantly (P < 0.01) greater than those in the halothane (32+/-8) and sevoflurane (31+/-8) groups. Electroencephalogram was found to be relatively unchanged during observation periods at 1.5 MAC.     

胸段硬膜外镇痛对开胸手术病人血糖、胰岛素和皮质醇水平的影响

目的　观察胸段硬膜外镇痛 (TEA)对开胸手术病人血糖、胰岛素和皮质醇水平的影响。方法　 2 0例在地氟醚麻醉下行开胸手术病人 ,随机分为TEA组和对照组。于麻醉前、术中 90分钟、术毕 6 0分钟和术后第 1、2、3天测定血糖、胰岛素及皮质醇浓度 ,计算胰岛素敏感性指数。结果　两组病人血糖均自术中 90分钟时明显升高 ,术毕 6 0分钟达峰值 ,术后第 1、2天仍居高不下 (P<0 0 5或P <0 0 1)。TEA组术中及术后胰岛素水平无明显改变 ;对照组术后第 1、2天胰岛素水平升高明显 (P <0 0 5或P <0 0 1)。TEA组病人皮质醇仅术毕 6 0分钟时明显升高 (P <0 0 5 ) ,而对照组于手术中 90分钟明显升高 ,并持续到术后第 1、2天 (P <0 0 5 )。两组胰岛素敏感性指数均明显下降 (P <0 0 5 ) ,于术后第 3天TEA组恢复接近麻醉前水平 (P >0 0 5 ) ;而对照组至术后第 3天仍低于麻醉前值 (P <0 0 5 )。结论　TEA可缓解开胸手术应激反应 ,减轻术后糖代谢紊乱。     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood Flow Velocity of Middle Cerebral Artery during Prolonged Anesthesia with Halothane, Isoflurane, and Sevoflurane in Humans

Background: It is not clear whether the increase of cerebral blood flow (CBF) produced by volatile anesthetics is maintained during prolonged anesthesia. In a previous study, the authors found that CBF equivalent, an index of flow-metabolism relationship, was stable over 3 h, suggesting no decay over time in CBF for 3 h during volatile anesthesia in humans. However, it may be possible that CBF changes in a parallel fashion to functional metabolic changes. In this study, to estimate the response of CBF to three volatile anesthetics, the authors used transcranial Doppler (TCD) ultrasonography to measure time-averaged mean velocity in the middle cerebral artery (Vmca).

Methods: Twenty-four surgical patients were randomly assigned to three groups to receive halothane, isoflurane, or sevoflurane (eight patients, each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5, 1.0, and 1.5 MAC before surgery and then at 1.5 MAC during surgery, which lasted more than 3 h. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 70 mmHg, using phenylephrine infusion, if necessary. TCD recordings of the Vmca were performed continuously.

Results: Vmca at 0.5 MAC of halothane, isoflurane, and sevoflurane was 49 +/- 19, 57 +/- 8, and 48 +/- 13 cm/s, respectively. Halothane significantly (P < 0.01) increased Vmca in a dose-dependent manner (0.5, 1.0, 1.5 MAC), whereas isoflurane and sevoflurane produced no significant dose-related changes. At 1.5 MAC for 3 h, Vmca changed significantly (P < 0.05) for the time trends, but it did not exhibit decay over time with all drugs. During burst suppression, observed electroencephalographically (EEG) on patients during isoflurane and sevoflurane anesthesia, the onset of a burst increased Vmca (approximately 5-30 cm/s), which was maintained for the duration of the burst.     

Desflurane reduces the effective therapeutic infusion rate (ETI) of cisatracurium more than isoflurane, sevoflurane, or propofol

PURPOSE: The present study investigated the interaction between the cumulative dose requirements of cisatracurium and anesthesia with isoflurane, sevoflurane, desflurane or propofol using closed-loop feedback control. METHODS: Fifty-six patients (18-85 yr, vitrectomies of more than one hour) were studied. In the volatile anesthetics groups, anesthesia was maintained by 1.3 MAC of isoflurane, sevoflurane or desflurane; in the propofol group, anesthesia was maintained by a continuous infusion of 6-8 mg.kg(-1).hr(-1) propofol. After bolus application of 0.1 mg.kg(-1) cisatracurium, a T1%-level of 10% of control level (train-of-four stimulation every 20 sec) was maintained using closed-loop feedback controlled infusion of cisatracurium. The effective therapeutic infusion rate (ETI) was estimated from the asymptotic steady-state infusion rate Iss. The Iss was derived from fitting an asymptotic line to the measured cumulative dose requirement curve. The ETI of the different groups was compared using Kruskal-Wallis- test, followed by rank sum test, corrected for the number of comparisons, P <0.05 was regarded as showing significant difference. RESULTS: ETI in the isoflurane group was 35.6 +/- 8.6 microg.m(-2).min(-1), in the sevoflurane group 36.4+/- 11.9 microg m(-2).min(-1), in the desflurane group 23.8 +/- 6.3 microg.m(-2).min(-1). The ETI of the volatile anesthetic groups were all significantly lower than the ETI in the propofol group at 61.7 +/- 25.3 microg.m(-2).min(-1) (P <0.002). The ETI in the desflurane group was significantly lower than in all other groups (P <0.02). CONCLUSION: In comparison to propofol, isoflurane, sevoflurane and desflurane reduce the cumulative dose requirements of cisatracurium to maintain a 90% neuromuscular blockade by 42%, 41% and 60%, respectively.