A comparison of sympathetic adrenal nerve responses to intravenous high-dose morphine and fentanyl administration in rats

We compared the effects of intravenous morphine (5 mg·kg⁻¹) and fentanyl, (50μg·kg⁻¹) on systolic blood pressure (SBP), heart rate (HR), and efferent sympathetic adrenal nerve action potentials (SANA) in rats. We also determined the extent of the reflex responses of these parameters of 9% carbon dioxide (CO₂) challenge during the above narcotic anesthesia. In the morphine group, SBP was elevated and the elevated levels were maintained, while changes in SBP in the fentanyl group were not significant. In the morphine group, SANA showed initial stimulation and subsequent depression, while in the fentanyl group, SANA showed sustained depression. CO₂ challenge induced only very small changes in SBP and HR, suggesting that during high-dose narcotic anesthesia the hypercapnic stimulus may not be reflected in circulatory parameters. In both groups, hypercapnia increased SANA to 30% of the baseline values from the pre-challenge level. However, these values were only 91% and 56% of the baseline value in the morphine and the fentanyl, groups, respectively.     

Circulatory and catecholamine responses to tracheal intubation and skin incision during sevoflurane, isoflurane, or halothane anesthesia

The anesthetic suppression of responses to noxious stimuli might reflect a summation of the suppression of the basal functions and the response capability. We investigated the basal suppression and response capability in hemodynamics and plasma catecholamine levels with different anesthetics at the same minimum alveolar concentration (MAC) level. Fifty-four patients were allocated to one of 6 groups to receive sevoflurane, isoflurane, or halothane at 1.25 or 2.0 MAC. Anesthesia was induced with the test agent in oxygen and the end-tidal concentration of the agent was maintained for at least 15 min at 1.25 or 2.0 MAC. The trachea was intubated under muscle relaxation with 0.1 mg·kg⁻¹ vecuronium. Skin incisions were made after maintaining the end-tidal concentration of the agent for at least 15 min after tracheal intubation. The mean arterial pressure, heart rate, rate-pressure product, and plasma levels of noradrenaline and adrenaline at the prestimuli period showed no difference between agents at each MAC. The rises in these variables by tracheal intubation and skin incision were greatest in the sevoflurane group, least in the halothane group, and intermediate in the isoflurane group. Although basal hemodynamic suppression is similar at the same MAC, the suppressive action of sevoflurane on the circulatory response capability to noxious stimuli is weaker than that of isoflurane and halothane. This study was presented in part at the 42nd annual congress of the Japan Society of Anesthesiology, April 20, 1995     

快速和慢速导入异氟醚和氟烷气体对冠状小动脉直径的影响

目的　应用微血管口径测量技术 ,异氟醚和氟烷以两种不同的导入方式 ,观察猪冠状动脉细小分支血管直径的变化。方法　分离 2 3只猪心脏的冠状动脉小分支 ,平均内径为 ( 167± 4 5 )μm。每根血管均接受两种方式的异氟醚和氟烷的导入 :快速导入 (即灌流液已预先用 2 %麻醉气体进行了完全的平衡 )和慢速导入 (灌流液中的麻醉气体浓度从 0 %开始每次增加 0 .5 % ,直至 2 % )。结果　在挥发罐设定浓度 >0 .5 %时 ,异氟醚和氟烷均显著增加冠脉小血管的直径。在相同浓度下 ,快速导入比慢速导入的扩血管作用大 ,异氟醚的作用比氟烷大。结论　异氟醚和氟烷是猪冠脉循环小动脉血管的扩张剂 ,这种作用呈浓度依赖性 ,快速导入比慢速导入增加血管直径的作用更大     

Effects of isoflurane and halothane on the calcium ion-tension curve in rat myocardium

In order to clarify the interaction of volatile anesthetics and extracellular calcium ion on the myocardial contraction, effects of both isoflurane (1.0%) and halothane (0.5%) on the extracellular calcium ion concentration ([Ca²⁺]_O)-tension curve were studied. Increasing [Ca²⁺]_O enhanced the myocardial contraction response, and the maximal response was obtained at [Ca²⁺]_O of 3.0mM. Halothane depressed the maximal value of the tension development in response to increasing [Ca²⁺]_O, while isoflurane did not (P 0.01). The probit response of the developed tension to the changes in [Ca²⁺]_O indicated that isoflurane increased the median effective concentration (EC₅₀) of [Ca²⁺]_O significantly from 0.484 ± 0.051 (mean ± SEM) to 0.870 ± 0.056mM (P = 0.001), but halothane did not (P = 0.018). Therefore, 1.0% isoflurane was concluded to move the [Ca²⁺]_O-tension curve to the right, while a downwards shift occurred with 0.5% halothane.(Saeki S, Hirakawa M, Shimosato S: Effects of Isoflurane and Halothane on the Calcium Ion-tension Curve in Rat Myocardium. J Anesth 6: 172–175, 1992)     

吸入麻醉药对兔肾交感神经活动的影响

目的比较吸入麻醉药对交感神经活动和血液动力学的影响。方法18只兔被随机分为三组:安氟醚组、异氟醚组和地氟醚组。兔麻醉、肌松和人工通气后,暴露肾交感神经并记录其电生理活动。分别吸入呼气末浓度为0.8%、1.6%、2.4%、3.2%安氟醚,0.6%、1.2%、1.8%、2.4%异氟醚,或3.0%、6.0%、9.0%、12.0%地氟醚。结果交感神经活动在兔吸入2.4%安氟醚、0.6%异氟醚和6.0%地氟醚时分别增加到44%、36%和32%,当进一步增加吸入麻醉药的浓度则抑制肾交感神经活动。血压随着吸入麻醉药浓度的增加不断下降而心率除了2.4%异氟醚诱发心率减慢外无明显变化。结论安氟醚、异氟醚和地氟醚具有双向作用,低浓度兴奋交感神经,高浓度抑制交感神经活动和降低血压。     

Comparison of the epinephrine-induced arrhythmogenic effect of sevoflurane with isoflurane and halothane

The effect of sevoflurane on cardiac arrhythmias induced by the infusion of epinephrine into dogs was compared with those of isoflurane and halothane. The arrhythmogenic doses of epinephrine determined in this comparative study were expressed by both infusion rates of epinephrine and the corresponding plasma levels obtained by a series of three-minute epinephrine infusions during sevolurane, isoflurane, and halothane anesthesia at 1.25 MAC. The mean values of the arrythmogenic infusion rates of epinephrine and the corresponding plasma levels were 17.3µg/kg/min and 275.7ng/ml for sevoflurane, 6.7µg/kg/min and 149.2ng/ml for isoflurane and 1.9µg/kg/min and 39.1ng/ml for halothane, respectively. These results indicate that the arrythmogenic doses of epinephrine during sevoflurane and isoflurane anesthesia were significantly higher than those during halothane anesthesia.(Imamura S et al.: Comparison of the epinephrine-induced arrhythmogenic effect of sevoflurane with isoflurane and halothane. J Anesth 1: 62–68, 1987)     

Postanesthetic respiratory depression in humans: A comparison of sevoflurane,isoflurane and halothane

The postanesthetic respiratory depression with sevoflurane, isoflurane and halothane was studied in twenty-one patients. They were divided into three groups of seven patients each. One group underwent sevoflurane anesthesia, another group isoflurane and the third group halothane. Following extubation, the decrease in blood concentration of the anesthetic agent was most rapid with sevoflurane and slowest with halothane. Twenty minutes following extubation, resting ventilation and ventilatory response to carbon dioxide returned to the preanesthetic state with sevoflurane and isoflurane anesthesia. With halothane anesthesia, however, the depressive respiratory effects of halothane remained; depressed ventilatory response to carbon dioxide, decreased tidal volume and increased respiratory frequency. Although halothane has been reported to have the least depressive respiratory effect of the three, its elimination was slowest. Thus the respiratory effects of halothane persisted up to and past the twenty minute mark, far longer than with sevoflurane or isoflurane.(Doi M, Ideda K: Postanesthetic respiratory depression in humans: A comparison of sevoflurane, isoflurane and halothane. J Anesth 1: 137–142, 1987)     

Effects of four volatile anesthesics on postanesthetic ventilation: a comparison of halothane,enflurane, isoflurane,and sevoflurane

To investigate the effects of four volatile anesthetics (halothane, enflurane, isoflurane, and sevoflurane) on postanesthetic ventilation and levels of consciousness, we enrolled 24 patients undergoing tympanoplasty in this study. Anesthesia was maintained with 67% nitrous oxide and one of four volatile anesthetics. We measured end-tidal carbon dioxide concentration (C_ETco₂), minute volume ( ) and respiratory rate (RR), and determined the volatile anesthetic concentration in whole arterial blood (C_BAnesth) and arterial carbon dioxide tension (Paco₂) at 20 min and 2h after tracheal extubation. We also observed the level of consciousness (awake, drowsy, and asleep) before the measurement. Ventilatory variables were similar among the four groups at 20 min, although the ratio of volatile anesthetic concentration in the alveoli to the minimum alveolar concentration (MAC) (C_AAnesth/MAC ratio) calculated from C_BAnesth in the halothane group was twice those in the other groups. In the halothane group, Paco₂ was significantly higher, and and RR were significantly lower compared with the isoflurane and sevoflurane groups at 2h. Halothane tended to prolong the recovery of levels of consciousness. We conclude that isoflurane and sevoflurane provide clinical advantages over halothane on postanesthetic ventilation and recovery of levels of consciousness.     

The comparative cardiovascular effects of sevoflurane with halothane and isoflurane

Using closed chest dogs, the cardiovascular effects of sevoflurane were compared with those of halothane and isoflurane in equipotent doses of 1.0, 1.5, 2.0, 2.5 and 3.0 MAC. They were evaluated by the changes of arterial blood pressure, central venous pressure, pulmonary artery pressure, maximum rate of left ventricular pressure rise (LV dp/dt), cardiac output and coronary sinus blood flow. The suppression of left cardiac function by sevoflurane was less than that of halothane, but was greater than that of isoflurane. Heart rate, systemic vascular resistance with sevoflurane were slightly lower than that of isoflurance. The coronary sinus blood flows with sevoflurane and isoflurane were significantly (P < 0.05 at 1.0 MAC, P < 0.005 at 2.0 MAC) higher than halothane. There was no significant difference on coronary sinus flow between sevoflurane and isoflurane. The depth of anesthesia could be quickly changed by adjustment of inspired sevoflurane concentration in comparison with the other two anesthetics.(Kazama T, Ikeda K: The comparative cardiovascular effects of sevoflurane with halothane and isoflurane. J Anesth 2: 63–68, 1988)     

Differential effects of isoflurane,halothane, and ketamine on the regional methionine-enkephalinlike immunoreactivity in the mouse brain

The widely used measurement index for anesthetic potency, minimum alveolar concentration (MAC), is hypothesized to be the sum of the effects on multiple neural systems whose contribution to anesthesia differs depending on the agents used. The present study, which compared the effects of halothane, isoflurane, and ketamine, at equipotent level of anesthesia, on the methionine-enkephalinergic neurons in 9 brain regions, showed a significant difference in the methionine-enkephalin-like immunoreactivity (Met-ENK-like IR) among the anesthetics in each region. The order of the Met-ENK-like IR was: halothane > ketamine > isoflurane in the caudatus putamen; halothane > isoflurane ≊ketamine in the nucleus accumbens and the ventral pallidum; halothane ≊isoflurane > ketamine in the globus pallidus, the nucleus dorsomedialis hypothalami, and the nucleus ventromedialis hypothalami; and halothane > isoflurane > ketamine in the arcuate nucleus, the periaqueductal gray, and the nucleus reticularis parvocellularis. These findings indicate that these three anesthetics affect the methionine-enkephalinergic neurons in the motor and pain controlling pathways in different fashions.     

Anticonvulsant effects of sevoflurane on amygdaloid kindling and bicuculline-induced seizures in cats: comparison with isoflurane and halothane

Purpose. We compared the anticonvulsant effects of sevoflurane with those of isoflurane and halothane in amygdaloid kindling and bicuculline-induced seizures in cats. Methods. In a crossover design, the effects of 70% nitrous oxide, and 0.3, 0.6, and 1.5 minimum alveolar concentration (MAC) of volatile anesthetics were studied in five cats in which the amygdala was electrically stimulated at the current used for establishing the kindled state. The effects of 0.6 and 1.5 MAC of volatile anesthetics were studied in another five cats, in which 0.2 mg·kg⁻¹ of bicuculline was administered IV. Results. In the amygdaloid kindling model, all four anesthetics decreased the duration of after-discharge (AD), the rise of multiunit activity in midbrain reticular formation (R-MUA), and the behavior scores compared with findings without anesthetics. Halothane, at 1.5 MAC, significantly decreased the number of cats showing AD (P < 0.05). In the bicuculline-induced seizure model, all five cats showed repetitive spikes during 1.5 MAC of sevoflurane, whereas only two and three cats, respectively, showed the repetitive spikes during 1.5 MAC of isoflurane and halothane. All three volatile anesthetics decreased the rise of R-MUA, the duration of the repetitive spikes, and the behavior scores. The suppression of the rise in R-MUA and the behavior scores with 1.5 MAC of sevoflurane was significantly less than that with 1.5 MAC of isoflurane. Conclusion. The anticonvulsant effects of sevoflurane were less potent than those of halothane in the amygdaloid kindling model and less potent than those of isoflurane in the bicuculline-induced seizure model. Received: January 11, 2001 / Accepted: May 9, 2001     

不同动脉血二氧化碳分压对数量化脑电图的影响

目的 观察不同动脉血二氧化碳分压对数量化脑电图参数的影响。方法 １５例ＡＳＡⅠ～Ⅱ级手术患者,术中吸入１ＭＡＣ异氟醚维持麻醉,非去极化肌松药维持肌松。通过调节分钟通气量随机使ＰａＣＯ２分别达到２６．５、３５．２及４５．７ｍｍＨｇ,并分别稳定１０ｍｉｎ后监测并记录数量化脑电图各参数变化。结果 随ＰａＣＯ２降低,各频率波动功率均显著上升,但δ比率无显著变化;ＳＥＦ及ＢＩＳ均显著升高。结论 ＰａＣＯ２的     

Frequency- and length-dependent tension development in rat heart muscles exposed to isoflurane and halothane

Using 22 isolated rat ventricular muscle preparations, we investigated whether or not the increase in preload and/or contraction frequency may counteract the negative inotropy of both isoflurane (2.0%) and halothane (1.0%). Increases in preload from 94% of Lmax (the length where muscles produce the maximal tension) to Lmax did not alter significantly the percent decrements in tension development caused by either isoflurane or halothane. The increases in contraction frequency from 0.1 to 0.6Hz augmented the depressant effect of isoflurane significantly (P < 0.001), while the depressant effect of halothane was not altered at these contraction frequencies. Small but significant counteraction occurred in the depressant effects of halothane at 0.8 and 1.6Hz (P = 0.002). These changes in intracellular mechanism(s), resulted from the increase in contraction frequency, interacted with the two anesthetics on tension development, while these may not be the case for the increase in preload.(Saeki S, Shimosato S, Kosaka F: Frequency and length-dependent tension development in rat heart muscles exposed to isoflurane and halothane. J Anesth 5: 338–343, 1991)     

Cerebrovascular responses to carbon dioxide in children anaesthetized with halothane and isoflurane

To determine the effects of isoflurane and halothane on cerebrovascular reactivity to CO2, 30 children aged one to six years were anaesthetized with isoflurane or halothane in an air and oxygen mixture with an FIO2 of 0.3. The end-tidal concentrations (0.5 minimum alveolar concentration (MAC) or 1.0 MAC) of isoflurane or halothane were age-adjusted. After achieving a steady-state at both 0.5 MAC and 1.0 MAC isoflurane and halothane, the end-tidal carbon dioxide tension (PETCO2) was randomly adjusted to 20, 40, or 60 mmHg. Cerebral blood flow velocity (CBFV) and the cerebrovascular resistance index (RI+) in the middle cerebral artery (MCA) were measured by a transcranial Doppler monitor. Three measurements of CBFV and RI+ were obtained at each PETCO2 and isoflurane or halothane concentration. Any rise in the PETCO2 caused an increase in CBFV during both 0.5 MAC (r2 = 0.99 and 0.99) and 1.0 MAC (r2 = 0.96 and 0.95) isoflurane and halothane anaesthesia, respectively (P less than 0.05). The CBFV for isoflurane increased as PETCO2 increased from 20 to 60 mmHg for both 0.5 MAC and 1.0 MAC (P less than 0.05). The CBFV for halothane increased as PETCO2 increased from 20 to 40 mmHg for both 0.5 MAC and 1.0 MAC halothane (P less than 0.05), but did not change as PETCO2 increased from 40 to 60 mmHg for both 0.5 MAC and 1.0 MAC halothane. The RI+ showed an inverse relationship with CBFV at each PETCO2 for 0.5 MAC (r2 = 0.98 and 0.99) and 1.0 MAC (r2 = 0.76 and 0.53) isoflurane and halothane, respectively (P less than 0.05). The CBFV did not differ significantly between 0.5 and 1.0 MAC isoflurane and halothane at corresponding PETCO2 values. The cerebrovascular response to CO2 at 20 mmHg between 0.5 MAC and 1.0 MAC halothane was not significantly different. These data strongly suggest that isoflurane and halothane in doses up to 1.0 MAC do not affect the cerebrovascular reactivity of the MCA to CO2 in anaesthetized, healthy children.     

大鼠肾上腺交感神经离断对肾上腺髓质增生的治疗作用

目的观察大鼠肾上腺交感神经离断对于肾上腺髓质增生的治疗作用。方法雄性Wistar大鼠80只随机平均分为A、B、C、D四组。A组为单侧（左侧）肾上腺交感神经离断组，B组为假手术组，C组为肾上腺髓质增生组，D组为正常对照组。A、B组术后1周同C组给予相同剂量利血平6周。C组停药后1周测定激素水平并处死5只大鼠，测定肾上腺髓质百分数。剩下大鼠行双侧肾上腺交感神经离断，术后1个月处死并与1个月前比较。结果A、B组激素水平明显高于D组，A组手术侧（左侧）肾上腺髓质百分数明显低于未手术侧（右侧，P〈0．05），而与D组无明显差异。C组双侧肾上腺交感神经离断术的大鼠，术后激素水平较术前有所下降。结论大鼠肾上腺交感神经离断可抑制利血平诱导大鼠肾上腺髓质增生，同时降低髓质增生大鼠的激素水平。     

异氟醚对新生大鼠认知功能的影响

目的 观察异氟醚对新生大鼠认知功能的影响。方法 新生1周Wistar大鼠40只，雌雄不拘，随机分为5组（n=8）：对照组（A组）吸入空气，B、C组分别吸入1．8％和1．2％异氟醚6h，D、E组分别吸入1．8％、1．2％异氟醚3次，1次／日，2h／次。吸入异氟醚后3周进行认知功能测试，包括旷场实验和Morris水迷宫测试，认知功能测试完毕后立即处死大鼠，取海马组织，进行免疫组织化学染色，测定N-甲基-D-天冬氨酸受体-2（NMDAR2）及谷氨酸转运体（GLAST）的表达。结果 吸入异氟醚可导致大鼠认知功能降低，海马NMDAR2和GLAST表达增加，吸入高浓度异氟醚后海马NMDAR2和GLAST表达增加更明显，单次吸入和多次吸入异氟醚后海马NMDAR2和GLAST表达差异无统计学意义（P〉0．05）。结论 异氟醚可降低新生大鼠认知功能，与上调海马NMDAR2及GLAST表达有关。     

异氟醚麻醉对老龄大鼠海马突触体蛋白质组的影响

目的 评价异氟醚麻醉对老龄大鼠海马突触体蛋白质组的影响.方法 雌性SD大鼠27只,22月龄,体重480～550 g,采用随机数字表法,将其随机分为2组:对照组(C组,n=6)和异氟醚麻醉组(Ⅰ组,n=21).C组吸入含80％氧气的空氧混合气体2h,Ⅰ组吸入3％异氟醚麻醉诱导后,经口明视气管插管,吸入2％异氟醚+80％氧气维持麻醉2h.麻醉结束后24h时,进行Y型迷宫实验测试大鼠认知功能,记录训练次数.以训练次数＞ 75次为判断认知功能低下的标准,将Ⅰ组大鼠分为2组:认知功能低下组(IA组)和认知功能未低下组(IB组).Y型迷宫实验结束后,处死大鼠,取双侧海马组织,提取突触体,进行双向凝胶电泳和质谱分析.结果 Ⅰ组有6只大鼠发生认知功能低下,有13只大鼠未发生认知功能低下.与C组和IB组比较,IA组训练次数增多(P＜0.05);C组和IB组间比较训练次数差异无统计学意义(P＞0.05).IB组和IA组差异表达的蛋白质有21个,其中11个蛋白质表达上调,10个蛋白质表达下调.C组和IA组差异表达的蛋白质有19个,其中12个蛋白质表达上调,7个蛋白质表达下调.经质谱分析鉴定出31个蛋白质.结论 异氟醚麻醉导致老龄大鼠认知功能低下可能与突触部位能量代谢相关蛋白、突触部位的细胞骨架结构及调节蛋白的改变有关.     

Effects of halothane,isoflurane and sevoflurane on ischemiareperfusion injury in the perfused liver of fasted rats

Background : Although intraoperative ischemia-reperfusion of the liver generally occurs under general anesthesia, little is known about the direct effect of anesthetic agents on hepatic injury due to this phenomenon. The effect of volatile anesthetics on ischemia-reperfusion injury was studied using isolated liver perfusion. Methods : The liver was isolated from 24-h-fasted male Sprague-Dawley rats and perfused through the portal vein with a modified Krebs-Ringer bicarbonate solution in a recirculating perfusion-aeration system. Ischemia was induced by reducing the baseline perfusion pressure from 1.2 to 0.2 kPa followed by reperfusion to baseline level. The ischemia-reperfusion injury was assessed by LDH release from the perfused liver. We studied the effect of halothane, isoflurane and sevoflurane on the ischemia-reperfusion injury during 20 min of control conditions, exposure of the liver to 60 min of ischemia and reperfusion for 90 min. Results : Ischemia was evident by reduced portal vein flow and oxygen consumption, and caused an increase in lactate production. Reperfusion caused a transient reduction in lactate production and a significant increase in LDH release. All anesthetics reduced hepatic oxygen consumption and increased the net lactate production during control conditions. Volatile anesthetics also significantly attenuated LDH release during reperfusion. The suppression of LDH release was observed even when isoflurane was administered during the reperfusion period, but not when it was administered only during ischemia. Conclusion : These results indicate that volatile anesthetics may protect the fasted liver from early, neutrophil-independent, ischemia-reperfusion injury by acting during the reperfusion phase.     

异氟醚麻醉对大鼠血皮质醇及海马脑源性神经营养因子和神经生长因子的影响

目的 探讨异氟醚麻醉对大鼠血皮质醇及海马脑源性神经营养因子(BDNF)和神经生长因子(NGF)的影响.方法 成年SD雄性大鼠36只,10周龄,体重250～280 g,采用随机数字表法,将其随机分为6组:正常对照组(C组,n=6)、O2组(O组,n=6)和异氟醚组(I组,n=24).I组通入2％异氟醚2h,纯氧流量3 L/min,O组仅通入纯氧.O组于停止通入纯氧后进行水迷宫实验,Ⅰ组分别于停止给药后2h、1、7、14 d取6只大鼠、进行水迷宫实验,定位航行实验中记录逃避潜伏期和游泳总路程,空间探索实验中记录穿越平台次数和游泳总路程.每个时点水迷宫实验结束后,取眼眶血,测定血浆皮质醇浓度;取海马组织,测定BDNF和NGF的含量.结果 与C组比较,O组空间探索实验中穿越平台次数减少,游泳总路程缩短,血浆皮质醇浓度降低,Ⅰ组于停止给药后1d时定位航行实验中逃避潜伏期和游泳总路程均延长,空间探索实验中穿越平台次数减少,游泳总路程缩短、海马BDNF含量降低(p＜0.05或0.01).结论 异氟醚麻醉对大鼠认知功能短期内有一过性抑制作用,其机制与促进皮质醇释放与海马BDNF合成有关,而与海马NGF合成无关.