地氟醚、异氟醚和七氟醚对脑血流速率的影响

目的　通过经颅多普勒超声 (TCD)监测大脑中动脉 (MCA)血流速率 ,观察地氟醚、异氟醚和七氟醚三种吸入麻醉药对平均血流速率 (Vm)的影响。方法　 42例 18～ 6 0岁、ASAⅠ～Ⅱ级、择期非颅脑手术病人 ,随机接受地氟醚、异氟醚或七氟醚吸入麻醉。机械通气维持PETCO2 在 40± 1mmHg。当呼气末吸入麻醉药浓度分别为 :1 0MAC平衡 15分钟后 ,快速 (2分钟内 )从 1 0MAC升高至 1 5MAC即时 ,1 5MAC平衡 15分钟后 ,以及稳定于 1 5MAC并且维持和 1 0MAC平衡下相似的MAP时 ,记录Vm、MAP和心率。结果　 (1)吸入浓度从 1 0MAC上升至 1 5MAC ,且MAP维持相同水平的情况下 ,地氟醚和异氟醚使Vm增加非常显著 (分别从 5 6cm/s上升至 6 1cm/s,从47cm/s上升至 5 2cm/s,P <0 0 1) ,而七氟醚无显著变化 (从 6 0cm/s至 6 0cm/s,P >0 0 5 )。 (2 )当吸入浓度快速从 1 0MAC上升至 1 5MAC时 ,地氟醚使血压升高、心率增快 ,同时 ,脑血流速率显著增加 (从 5 6cm/s上升至 6 1cm/s,P <0 0 1)。而异氟醚和七氟醚在MAP显著下降的同时使Vm无显著变化 (从 47cm/s升至 49cm/s,P >0 0 5 ) ,或显著下降 (从 6 0cm/s降至 5 6cm/s,P <0 0 1)。结论　 (1)吸入浓度从 1 0MAC增加到 1 5MCA时 ,地氟醚、异氟醚使脑血流速率显著增加 ,而七氟醚作     

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。     

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.     

七氟醚、异氟醚不同呼气末浓度对熵和脑电双频指数的影响

目的 观察不同呼气末浓度的七氟醚和异氟醚对熵、脑电双频指数(BIS)及血流动力学的影响.方法 40例ASA Ⅰ或Ⅱ级全麻手术患者随机均分为七氟醚组(Ⅰ组)和异氟醚组(Ⅱ组).麻醉诱导用丙泊酚1 mg/kg,1 min后吸入七氟醚或异氟醚;维持反应熵(RE)、状态熵(SE)、BIS45～55,6 min后置入喉罩.调节吸入浓度使两组患者呼气末浓度分别为0.4、0.6、0.8、1.0和1.3MAC时各维持10 min,记录RE、SE、BIS、HR和MAP.结果 两组患者不同呼气末浓度七氟醚和异氟醚RE、SE、BIS随浓度增加而逐渐下降(P<0.05),HR逐渐减慢、MAP逐渐降低(P<0.05).两组间各指标差异均无统计学意义.RE、SE、BIS间直线相关性随呼气末浓度增大相关系数有增加趋势.结论 熵和BIS均能有效监测七氟醚、异氟醚麻醉深度.     

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。     

患者低流量吸入地氟醚或异氟醚的药代动力学

目的比较腹部手术患者低流量吸入地氟醚或异氟醚的药代动力学。方法腹部手术患者40例,ASAⅠ级或Ⅱ级,年龄18～64岁,BMI＜35kg/m^2。随机分为2组（n=20）：地氟醚组（D组）和异氟醚组（Ⅰ组）。麻醉诱导后调节纯氧流量3L/min,术中调整挥发罐刻度,维持肺泡浓度（FA）0．8 MAC,稳定5min后纯氧流量改为1L/min。调节瑞芬太尼静脉输注速率,维持HR和BP波动幅度不超过基础值20%。手术结束时,停止吸入地氟醚或异氟醚,同时吸入纯氧3L/min。记录设定的吸入麻醉药浓度（FD）、吸入麻醉药浓度（FI）、FA/FI=1/2时间、FA/FAO=1/2时间（FAO为关闭挥发罐即时的肺泡浓度）,并计算各时点FA/FI、FA/FD。结果D组FA/FI=1/2时间及FA/FAO=1/2时间均较Ⅰ组缩短（P＜0．05）。低流量麻醉下,D组FD稳定,Ⅰ组FD波动较大。D组FA/FI、FA/FD上升速率较Ⅰ组快,且同一时点各比值D组均高于Ⅰ组。结论与异氟醚比较,腹部手术患者低流量吸入地氟醚时达到预定的肺泡浓度更迅速,可控性好,停止吸入时排泄较快。     

地氟醚、七氟醚和异氟醚预处理对缺氧-复氧心肌细胞内游离Ca2+的影响

目的 观察地氟醚，七氟醚和异氟醚预处理对缺氧-复氧心肌细胞内Ca^2 的影响。方法 将原代培养乳鼠心肌细胞随机分为对照，缺氧-复氧及1.5MAC地氧醚，七氟醚和异氟醚预处理后缺氧-复氧五组，用Fra-2标记细胞内Ca^2 ，荧光光度计进行测定。结果 与对照组比，复氧20分钟时，其余四组细胞内Ca^2 均显著升高；而地氟醚，七氟醚和异氟醚预处理组的升高幅度明显低于缺氧-复氧组；三个吸入麻醉药组间无差异，复氧60分钟，缺氧-复氧组虽有明显下降，但仍显著高于对照组，地氟醚，七氟醚烽异氟醚预处理组则降至对照组水平。结论 地氟醚，七氟醚和异氟醚预处理，可明显减轻缺氧-复氧心肌引起的细胞内游离Ca^2 升高。     

七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位的影响

目的 比较七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位(MEPs)的影响.方法 择期行神经外科手术患者60例,年龄18～64岁,ASA分级Ⅰ或Ⅱ级.随机分为3组(n=20):七氟醚组、异氟醚组和地氟醚组.监测BIS值和经颅电刺激MEPs.调节七氟醚、异氟醚和地氟醚吸入浓度,使其呼气末浓度分别达到0.50、0.75、1.00和1.30 MAC,每一浓度均维持15 min,视为稳态呼气末浓度.于给予吸入麻醉药前(基础状态)和达到各稳态呼气末浓度(T1-4)时,记录MEPs的波幅和潜伏期以及BIS值.记录MEPs波形记录失败情况.结果 与七氟醚组和异氟醚组比较,地氟醚组T1.2时波幅和BIS值降低,T1-4时潜伏期延长(P＜0.05);七氟醚组和异氟醚组各指标比较差异无统计学意义(P＞0.05).七氟醚组、异氟醚和地氟醚组基础状态、T1、T2时的记录失败率均为0;T3时记录失败率分别为0、5%和20%,三组比较差异无统计学意义(P＞0.05);T4时记录失败率分别为5%、20%和45%,与七氟醚组和异氟醚组比较,地氟醚组记录失败率升高(P＜0.05);七氟醚组和异氟醚组比较差异无统计学意义(P＞0.05).结论 地氟醚对神经外科手术患者经颅电刺激MEPs的抑制作用强于七氟醚和异氟醚.术中行MEPs监测时,七氟醚和异氟醚适宜的呼气末浓度为1.00 MAC,地氟醚为0.75～1.00 MAC.     

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。     

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。     

比较硬膜外阻滞复合安氟醚或异氟醚对肝血流及氧代谢的影响

目的 探讨硬膜外阻滞与安氟醚或异氟醚吸入复合麻醉对血流动力学,肝血流及代谢的影响。方法 选用健康杂种犬２０只行胸段硬膜外阻滞后分为两缚,分别吸入,０．５和１．０ＭＡＣ安氟醚或异氟醚,监测麻醉前后体循环,肝动脉,门静脉血流动力及肝脏氧供,氧耗。结果 硬膜外阻滞后血压,门静脉血流和氧供下降,加吸安氟醚０．５ＭＡＣ使心排血量也下降,１．０ＭＡＣ后肝动脉血流及氧供也减少,加吸异氟醚０．５ＭＡＣ心排血量稳定     

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.     

Fires from the interaction of anesthetics with desiccated absorbent

Rarely, fire and patient injury have resulted from the degradation of sevoflurane by desiccated carbon dioxide absorbent. Desiccated absorbent also can degrade desflurane and isoflurane, and in the present investigation we sought to determine whether a danger of fire also arose with their use in the presence of desiccated absorbent. Baralyme was desiccated by heating and directing a 10 L/min flow of oxygen through the absorbent. Approximately 1200 g of this desiccated absorbent was used to fill a standard absorber placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 or 3.0 MAC desflurane, isoflurane, or sevoflurane. 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 or isoflurane, at both 1.5 MAC and 3.0 MAC, temperatures increased in 30 to 70 min to a peak of approximately 100 degrees C and then decreased. With 1.5 MAC sevoflurane (3.0 MAC was not studied), temperatures increased to over 200 degrees C, and in 2 of 5 studies, flames appeared in the anesthetic circuit. In a separate study, we found that concurrent delivery of carbon dioxide and desflurane did not increase peak temperatures. We conclude that the interaction of desflurane or isoflurane with desiccated absorbent is not likely to produce the conflagrations possible with sevoflurane.     

Direct coronary vasomotor effects of sevoflurane and desflurane in in situ canine hearts

BACKGROUND: An extracorporeal system was used to investigate the direct coronary vasomotor effects of sevoflurane and desflurane in vivo. The role of the adenosine triphosphate-sensitive potassium channels (KATP channels) in these effects was evaluated. METHODS: Twenty-one open-chest, anesthetized (fentanyl-midazolam) dogs were studied. The left anterior descending coronary artery was perfused at controlled pressure (80 mmHg) with normal arterial blood or arterial blood equilibrated with either sevoflurane or desflurane. Series 1 (n = 16) was divided into two groups of equal size on the basis of whether sevoflurane (1.2, 2.4, and 4.8%) or desflurane (3.6, 7.2, and 14.4%) was studied. The concentrations for the anesthetics corresponded to 0.5, 1.0, and 2.0 minimum alveolar concentration (MAC), respectively. Coronary blood flow (CBF) was measured with an ultrasonic, transit-time transducer. Local coronary venous samples were obtained and used to evaluate changes in myocardial oxygen extraction (EO2). In series 2 (n = 5), changes in CBF by 1 MAC sevoflurane and desflurane were assessed before and during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 microg/min). RESULTS: Intracoronary sevoflurane and desflurane caused concentration-dependent increases in CBF (and decreases in EO2) that were comparable. Glibenclamide blunted significantly the anesthetic-induced increases in CBF. CONCLUSIONS: Sevoflurane and desflurane have comparable coronary vasodilative effects in in situ canine hearts. The KATP channels play a prominent role in these effects. When compared with data obtained previously in the same model, the coronary vasodilative effects of sevoflurane and desflurane are similar to those of enflurane and halothane but considerably smaller than that of isoflurane.     

Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog

The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. Systemic and coronary hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.25 and 1.75 MAC desflurane, isoflurane, halothane, and enflurane. Desflurane (+79 +/- 12% change from control) produced greater increases in heart rate than did halothane (+44 +/- 12% change from control) or enflurane (+44 +/- 9% change from control) at 1.75 MAC. Desflurane preserved mean arterial pressure to a greater degree than did equianesthetic concentrations of isoflurane. This result was attributed to a smaller effect on peripheral vascular resistance as compared to isoflurane and greater preservation of myocardial contractility as evaluated by peak positive left ventricular dP/dt and the rate of increase of ventricular pressure at 50 mmHg (dP/dt50) compared to other volatile anesthetics. Increases in diastolic coronary blood flow velocity (+19 +/- 6 and +35 +/- 12% change from control at 1.75 MAC, respectively) and concomitant decreases in diastolic coronary vascular resistance (-41 +/- 12 and -58 +/- 6% change from control at 1.75 MAC, respectively) were produced by desflurane and isoflurane. In the presence of autonomic nervous system blockade, the actions of desflurane and isoflurane were nearly identical with the exception of coronary vasodilation. After autonomic nervous system blockade, isoflurane increased coronary blood flow velocity, but desflurane did not. Furthermore, both desflurane and isoflurane continued to produce less depression of myocardial contractility than did halothane and enflurane. In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.     

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)     

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.     

Cardiovascular actions of common anesthetic adjuvants during desflurane (I-653) and isoflurane anesthesia in swine

To determine the cardiovascular actions of drugs commonly combined with inhalation anesthetics, we administered one drug from each of several classes of adjuvants to seven swine already anesthetized with equipotent concentrations (1.2 MAC) of desflurane, formerly I-653, a new inhaled anesthetic, or isoflurane. Succinylcholine (1 and 2 mg/kg), atracurium (0.6 mg/kg), and atropine (5 micrograms/kg) plus edrophonium (5 mg/kg) had no cardiovascular effects. Fentanyl was given in amounts that decreased MAC for the inhaled anesthetics by 25%-35%. A dose of 50 micrograms/kg IV had no cardiovascular effects during either anesthetic, whereas 100 micrograms/kg IV modestly increased systemic vascular resistance without changing other variables. Naloxone (100 micrograms/kg IV) during infusion of fentanyl decreased systemic vascular resistance and increased cardiac output during both desflurane and isoflurane anesthesia, increased heart rate during only isoflurane anesthesia, and did not affect mean arterial blood pressure during either anesthetic. Thiopental (2.5 and 5.0 mg/kg IV) decreased mean aortic blood pressure, cardiac output, stroke volume, and systemic vascular resistance during both anesthetics without altering heart rate or left- or right-sided cardiac filling pressures. The addition of 60% nitrous oxide caused no cardiovascular changes during desflurane anesthesia, but increased systemic vascular resistance and decreased cardiac output and stroke volume during isoflurane without altering heart rate or cardiac preload. We conclude that the usual clinical doses of adjuvants commonly administered during anesthesia have no untoward cardiovascular actions during 1.2 MAC desflurane or isoflurane anesthesia in swine.     

Pulmonary mechanics during isoflurane,sevoflurane and desflurane anaesthesia

This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n = 22), sevoflurane (n = 23), or desflurane (n = 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.