Effect of halothane on the peripheral cutaneous vasoconstriction and shivering induced by internal body cooling in rabbits]

Although suppression of thermoregulatory mechanisms by anesthetics is generally assumed, the extent to which thermoregulatory responses are active during general anesthesia is not known. To evaluate the effect of anesthetics on thermoregulation, we investigated the threshold body core temperatures to induce peripheral cutaneous vasoconstriction and shivering in spontaneously breathing rabbits. Rabbits are anesthetized with halothane at 0.05, 0.2 and 0.4 MAC (minimum alveolar concentration). Internal whole body cooling was performed by perfusing the cool water through an intestinal U-shaped thermode placed in the colon. Core (esophagus) and peripheral (ear) temperatures were measured with thermistors. The esophageal temperatures at the beginning of peripheral cutaneous vasoconstriction and shivering induced by internal whole body cooling were determined. Peripheral cutaneous vasoconstriction was not significantly affected by halothane. However, the incidence of shivering was significantly decreased by halothane dose-dependently. Threshold of shivering (37.3 +/- 0.8 degrees C) was significantly lower than that of peripheral cutaneous vasoconstriction (38.9 +/- 1.1 degrees C). We conclude that the halothane can exert an influence on shivering.     

Tracheal dilatation by halothane and enflurane in man

The effect of halothane and enflurane on tracheal tone were studied in 21 patients during the induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia, maintained by nitrous oxide 70% in oxygen, was supplimented with succinylcholine drip infusion to immobilize the patient. Ventilation was controlled by a Volume-preset ventilator. In the halothane group, the initial cuff pressure was 14.8 ± 1.3 (mean ± SE) cmH₂O but 10min after 0.15mg/kg of pancuronium injection, it increased to 21.7 ± 2.3cmH₂O (control). Ten min after inhalation of 0.75% of halothane, cuff pressure decreased to 14.7 ± 2.3cmH₂O (34 ± 11% decrease from the control value). In the enflurane group, the initial cuff pressure was 17.6 ± 1.8cmH₂O and it increased to 21.0 ± 1.7cmH₂O (control) 10min after pancuronium injection. Ten min after 1.7% of enflurane inhalation, cuff pressure decreased to 17.1 ± 2.3cmH₂O (23.9 ± 6% decrease from the control value). Halothane and enflurane produced similar tracheal dilatation in healthy individuals.(Yasuda I, Irimada M, Hirano T et al.: Tracheal dilatation by halothane and enflurane in man. J Anesth 2: 46–49, 1988)     

Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs

We investigated the relative effects of 0.5, 1.0, 1.5, 2.0 MAC halothane and enflurane, and concurrent noxious stimulus on hepatic blood flow and oxygen consumption in 14 mongrel dogs randomly divided into groups of seven each. Hepatic arterial and portal venous blood flow (HABF and PVBF, respectively) were measured continuously using ultrasonic transit time flow meter. Mean arterial blood pressure (MAP), cardiac index (CI), hepatic oxygen supply, and hepatic oxygen consumption (H _{O 2}) were measured. Halothane significantly deceased HABF, but not PVBF in a dose dependent manner. Enflurane did not affect HABF and PVBF significantly. MAP and CI decreased in both groups, with halothane producing more marked decreases than enflurane. H _{O 2} did not change with enflurane, but did with halothane, producing significant differences, with halothane being greater at 1.5, 2.0 MAC. A noxious stimulus only caused minor change in blood flow. The results suggest that liver blood flow and oxygen consumption are affected differently by halothane and enflurane and that halothane has a stronger tendency to cause an imbalance between liver oxygen supply and consumption than dose enflurane.(Masaki E, Yasuda N, Tanifuji Y et al.: Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs. J Anesth 3: 118–122, 1989)     

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.     

Differential effects of halothane and enflurane on end-systolic pressure-diameter relationship in anesthetized,mechanically ventilated dogs

To clarify the difference of negative inotropic effects, we evaluated the effects of 0, 0.5, and 1 MAC halothane and enflurane on systolic performance in anesthetized, mechanically ventilated, vagotomized dogs. Left ventricular myocardial contractility was assessed by the slope of the end-systolic pressure-diameter relationship (Ees), which have been reported to be independent of alterations in preload and afterload but sensitive to changes in myocardial contractility. Both anesthetics decreased heart rate and dose-dependently decreased left ventricular systolic pressure. Enflurane decreased heart rate and left ventricular systolic pressure more than an equivalent MAC of halothane. Both anesthetics increased left ventricular end-diastolic diameter without any change in % shortening of the left ventricular internal diameter. TheEes was decreased to a similar extent at both 0.5 and 1 MAC halothane. TheEes was decreased with increasing concentrations of enflurane. TheEes was significantly larger (P<0.05) with 1 MAC of halothane than with 1 MAC enflurane. These results suggest that halothane preserves myocardial contractility better than enflurane in the presence of fentanyl.     

Comparison of the placental transfer of halothane,enflurane, sevoflurane,and isoflurane during cesarean section

The concentrations of placental transfer of halothane (H), enflurane (E), sevoflurane (S), and isoflurane (I) were measured in 46 patients during cesarean section. The mean inhalation times of H (0.5%), E (1%), S (0.8%), and I (0.6%) were 13 min 27 s, 13 min 49s, 13 min 20s, and 8 min 8s, respectively. The mean concentrations in the maternal artery (MA) were 5.2mg·dl⁻¹ in H, 12.3 mg·dl⁻¹ in E, 5.2mg·dl⁻¹ in S, and 2.4mg·dl⁻¹ in I. The concentration ratio between the MA and the fetal umbilical vein (UV) was 0.44 for H, 0.49 for E, and 0.38 for S, and these ratios were not significantly different for these anesthetics. Although the concentration ratio for I (0.27) was significantly lower than those of the other three anesthetics, the UV:MA ratio was calculated to be 0.4 for an inhalation time 13 min. Our result, therefore, suggests that if the inhalation times were equal, the ratios of placental transfer would not differ among these four inhalational anesthetics. The Apgar scores in these four groups were not different from that in the group given only 66% nitrous oxide in oxygen as anesthetic (N₂O group). The cardiovascular changes induced by skin incision were bigger in the N₂O group than in the other groups. The use of a low concentration of H, E, S, or I is, therefore, suggested to be a useful and acceptable anesthetic method for cesarean section.     

Retrospective study of post-anesthetic mild liver disorder associated with inhalation anesthetics,halothane and enflurane

The incidence of post-anesthetic mild liver disorder (PAMLD) was compared between 928 patients administered halothane and 1766 patients administered enflurane. They were selected from 19504 surgical patients administered general anesthesia at Kyushu University Hospital over the past 6 years and 4 months. They had had normal liver function before operation and had no history of blood transfusion. Alanine aminotransferase (ALT) levels exceeding 70IU·l ^–1 within 180 days after operation were found in 226 patients in the halothane group (24.4%), and in 250 patients in the enflurane group (14.2%) (P 0.01). Both maximum ALT levels and duration of ALT elevation were higher and longer in the halothane group (P 0.01). These results suggest that, not only in the development of fulminant hepatitis but also in PAMLD, enflurane is less hepatotoxic than halothane.(Sakaguchi Y, Inaba S, Umeki Y, et al.: Retrospective study of post-anesthetic mild liver disorder associated with inhalation anesthetics, halothane and enflurane. J Anesth 6: 183–191, 1992)     

Effects of halothane on carotid occlusion in rabbits

Effects of halothane on the carotid sinus baroreflex control of circulation were stuied in chronically instrumented rabbits. The carotid sinus baroreflex was evaluated by the hemodynamic responses to bilateral carotid occlusion (BCO). Either 0.5 or 1.0 MAC of halothane inhalation did not alter mean arterial pressure (MAP) or total peripheral resistance (TPR), but significantly increased heart rate (HR). Carotid occlusion produced a significant increase in MAP and HR, and both responses were attenuated dose-dependently by halothane. Halothane depressed the reflex gain of arterial pressure from 3.5 ± 0.3 at conscious state to 1.3 ± 0.2 at 1.0 MAC halothane. Response of cardiac output (CO) to BCO was attenuated significantly only at 1.0 MAC compared with those responses at conscious state and at 0.5 MAC. Response of TPR was attenuated at both 0.5 and 1.0 MAC halothane as compared with at conscious state but no significant defference existed between the two concentrations of halothane. These data suggested that halothane could attenuate the carotid occlusion responses to various degrees in the involved effector componets. 0.5 MAC halothane attenuated MAP response to BCO predominantly by attenuating reflex peripheral vasoconstriction. The reduced CO response was mainly responsible for further attenuation of MAP response at 1.0 MAC halothane.(Sumida T, Ohsumi H, Yamazaki T, et al.: Effects of halothane on carotid occlusion in rabbits. J Anesth 7: 218–225, 1993)     

安氟醚和异氟醚对肝脏缺血/再灌注损害的影响

目的 研究安氟醚和异氟醚预处理对肝脏缺血／再灌注损害的影响。方法 １８只家兔随机分３组,对照组阻断肝劝脉和门静脉血流形成肝缺血４５ｍｉｎ,开放再灌注１２０ｍｉｎ;安氟醚和异氟醚预处理组,于缺血再灌注前分别吸入１．６８％安氟醚和１．１５％异氟醚２０ｍｉｎ和药物清除１０ｍｉｎ。结果 缺血前,三组血清谷丙转氨酶（ＡＬＴ）,谷草转氨酶（ＡＳＴ）、乳酸脱氢酶（ＬＤＨ）、碱性磷酸酶（ＡＬＰ）和谷氨酰酶（ＧＣＴ     

Interaction between diltiazem and halothane or enflurane in the canine blood-perfused papillary muscle and sinoatrial node preparations cross-circulated by chronically instrumented conscious donor dog

Interaction of cardiovascular effects of diltiazem with those of halothane or enflurane was estimated in the canine isolated papillary muscle and sinoatrial node preparations perfused by arterial blood of the chronically instrumented conscious and halothane- or enflurane-anesthetized donor dog, into which diltiazem was infused i.v. at a rate of 20µg/kg/min for 60min. One hour after diltiazem infusion, in the conscious donor dog, mean arterial pressure (MAP) and heart rate (DHR) were decreased to 84 ± 3 and 84 ± 2% and PQ interval (PQ) was prolonged to 148 ± 5%, while in the isolated preparations, developed tension (DT) of the papillary muscle and sinoatrial rate (SAR) were decreased to 68 ± 3 and 74 ± 3% and blood flow (BF) was increased to 155 ± 5% (n = 10). On the other hand, halothane (0.8%) anesthesia per se decreased MAP, DHR, DT and SAR to 89 ± 8, 84 ± 3, 79 ± 3 and 89 ± 5% (n = 7) of each basal value in conscious state 20min after the inhalation. During halothane anesthesia, the same dose of diltiazem infused decreased MAP to 74 ± 4 (n = 7), DHR to 66 ± 4 (n = 6), DT to 62 ± 7 (n = 7) and SAR to 69 ± 1% (n = 3) of each value suppressed by halothane itself. Meanwhile, enflurane (1.7%) anesthesia itself decreased MAP, DHR, DT and SAR to 81 ± 3, 85 ± 2, 81 ± 2 and 88 ± 2% (n = 10) of each basal value in conscious state 30min after enflurane inhalation. During enflurane anesthesia diltiazem decreased MAP to 74 ± 3 (n = 10), DHR to 67 ± 3 (n = 8), DT to 45 ± 5 (n = 10) and SAR to 74 ± 6% (n = 3) of each value under enflurane anesthesia alone. PQ interval of the donor dog heart was prolonged by halothane alone to 111 ± 5% (n = 7) and by enflurane alone to 110 ± 2% (n = 10) of the value before each anesthesia, and then diltiazem prolonged PQ interval to 160 ± 8% (n = 6) and 174 ± 10% (n = 8) of each value suppressed by the anesthetic itself during halothane- or enflurane-anesthesia, respectively. The second degree AV conduction block was induced in 1 of 7 halothane- and in 2 of 10 enflurane-anesthetized donor dogs, respectively. The sinus arrest was induced by diltiazem in 4 of 7 sinoatrial node preparations under halothane and in 7 of 10 ones during enflurane anesthesia. Moreover, plasma concentration of diltiazem 60min after the start of infusion was 556 ± 121ng/ml in conscious dogs and tended to increase to 752 ± 101ng/ml in enflurane anesthetized donor dogs (n = 4), but there was no significant difference between two values (0.05 < P < 0.1). These results indicate that effects of diltiazem could be potentiated during halothane or enflurane anesthesia by elimination of compensatory reflex noted in conscious state, and that the negative inotropic effect of diltiazem was enhanced by enflurane anesthesia due to unknown mechanisms which probably include a slight but insignificant increase in plasma concentration.(Manabe M, Motomura S, Hashimoto K: Interaction between diltiazem and halothane or enflurane in the canine blood-perfused papillary muscle and sinoatrial node preparations cross-circulated by chronically instrumented conscious donor dog. J Anesth 2: 50–62, 1988)     

Effect of parecoxib on remifentanil induced postoperative shivering

Remifentanil based anesthesia was found to be associated with high incidence of postoperative shivering. This study was designed to evaluate the effect of preoperative administration of IV parecoxib sodium (a selective COX 2 inhibitor) on remifentanil induced shivering during the first 2 h following surgery.MethodIn a randomized, placebo-controlled, double blind study, sixty-seven patients with ASA physical status I, aged 20–60 years underwent elective lumber discectomy, were randomly allocated to receive either parecoxib sodium 40 mg IV (group P, n = 33) or saline IV (group S, n = 34) 30 min before induction of anesthesia which was induced with remifentanil 0.5 ug/kg/min, propofol, and cisatracurium and was maintained with remifentanil 0.1–0.3 ug/kg/min, sevoflurane, O₂/N₂O and cisatracurium. The incidence and grades of postoperative shivering were evaluated for 2 h.ResultsThe incidence of postoperative shivering was 36% in parecoxib group which was significantly less than that of saline group 64% (p < 0.05). Number of patients who developed grade 3 shivering, number of patients received meperidine to treat shivering and postoperative morphine requirement were significantly less in group P than that of group S (p < 0.05).ConclusionAdministration of parecoxib sodium 40 mg IV 30 min before induction of general anesthesia significantly reduced the incidence and severity of remifentanil induced shivering compared to placebo in patients underwent elective lumber discectomy under general anesthesia.     

Suppressive action of enflurane on dorsal horn neurons in rabbits

The neurophysiologic mechanism of the suppressive action of enflurane on spinal nociceptive transmission was examined in rabbits with intact and with transected spinal cords. Enflurane suppressed nociceptive responses in both intact and transected spinal cord groups. The suppressive effects of enflurane were significantly greater in the intact group than in the transected group. The suppressive effects of enflurane were not reversed by the addition of 0.2 mg·kg⁻¹ of naloxone. These results suggest that enflurane suppresses nociceptive responses by activating descending inhibitory systems and directly suppressing activity at the spinal level. This suppressive action of enflurane does not interact with the opioid receptor.     

恩氟烷及异氟烷对食管癌切除术围术期病人外周血T淋巴细胞免疫功能的影响

目的 探讨恩氟烷及异氟烷对病人外周血中Ｔ淋巴细胞免疫功能的影响。方法 选择６０例食管癌病人,随机分成３组,Ⅰ组：恩氟烷组,Ⅱ组：异氟烷组,Ⅲ组：异丙酚组,每组２０例。Ⅰ、Ⅱ组术中吸入浓度分别维持１．５％～２％。Ⅲ组按４～６ｍｇ．ｋｇ＾－１．ｈ＾－１微量泵输入并辅助芬太尼６～８ｕｇ．ｋｇ＾－１ 。于麻醉前、吸入麻醉药后９０ｍｉｎ、术毕、术后２４ｈ、７２ｈ,抽取桡静脉血１经ｍｌ,采用流式细胞仪测定Ｔ３、Ｔ４、Ｔ８淋巴细胞的水平。结果 Ⅱ和０２８３组与术前相比,Ｔ３、Ｔ４、Ｔ８水平均无明显变化（Ｐ〈０．０５）。结论 异氟烷对肿瘤病人的免疫功能无明显影响。恩氟烷只对Ｔ３淋巴细胞显著抑制（Ｐ〈０．０５）。结论 异氟烷对肿瘤病人的免疫功能无明显影响。恩氟烷只对Ｔ３及Ｔ８细胞有程度很低的、一过性的抑制作用。因此两种吸入药物均     

安氟醚和异氟醚对泮库溴铵药代动力学的影响

研究观察安氟醚和异氟醚对泮库溴铵药代动力学的影响。１８例ＡＳＡⅠ级施择期整形外科 手术的患者，随机平均分成对照组、安氟醚组和异氟醚组。静注泮溴铵１００μｇ／ｋｇ后，用荧光法测定血 药浓度，并用３Ｐ８７药代动力学程序进行计算。泮库溴铵的体内过程能用二室开放模型完整描述。结果证 实，与对照组相比，安氟醚和异氟醚组的 Ｔ和ＭＲＴ明显延长而安氟醚组的ＣＩ和 Ｋ１０明显低于对 照组。Ｔ和ＡＵＣ在三组间明显差别。     

氟烷和七氟醚对兔肝细胞DNA及RNA的影响

实验选用健康家兔４２只，随机分为三组：对照组、氟烷组及七氟醚组。两实验组在应用氟烷和七氟醚后取其肝组织用流式细胞仪测定肝细胞ＤＮＡ、ＲＮＡ含量及细胞周期的变化情况。结果氟烷组用药后肝细胞ＤＮＡ含量与对照组相比无统计学差异，而该组的肝细胞增殖周期及ＲＮＡ含量均发生明显变化。七氟醚组此三项指标均未出现有统计学意义的变化。由此说明氟烷和七氟醚不会影响肝细胞ＤＮＡ的合成。氟烷组的变化主要反映肝细胞损伤后修复的过程。     

低温麻醉下安氟醚及异氟醚对心内传导系统的影响

目的　研究低温 3 0℃下安氟醚、异氟醚对心内传导系统的影响。方法　健康家兔 4 8只 ,离体 L angendorff灌注 ,随机分为六组 ( n=8) :常温 0 .65 MAC Enf组 ,常温 1.3 MAC Enf组 ,常温1.3 MAC Iso组 ,低温 0 .65 MAC Enf组 ,低温 1.3 MAC Enf组 ,低温 1.3 MAC Iso组。不同组别 K- H液平衡灌注 15分钟后测定 HR、SACT、CSNRT、SNRTI、AVERP、2∶ 1B、QTc、P- R间期、QRS时间。结果　常温 0 .65 MAC Enf对心内传导系统无影响。 1.3 MAC Enf使 SACT、CSNRT、P- R间期显著延长 ( P<0 .0 5 ) ,常温 1.3 MAC Iso使 CSNRT显著延长 ( P<0 .0 5 )。低温 0 .65 MAC Enf,1.3 MACEnf及 1.3 MAC Iso的心电生理参数值 ( SNRTI除外 )分别较常温相应麻醉强度时有显著 ( P<0 .0 5 )或非常显著 ( P<0 .0 1)的差异。结论　常温下安氟醚对窦房结自律性及房室传导功能有浓度依赖性抑制作用 ;低温显著加重安氟醚、异氟醚对心内传导系统的抑制。低温麻醉宜选用异氟醚     

地氟醚与安氟醚对小儿食管下段括约肌功能的影响

目的观察地氟醚与安氟醚麻醉对小儿食管下段括约肌(LES)功能的影响.方法26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.静脉注射羟丁酸钠和阿曲库铵诱导插管后,随机分为地氟醚(D组)和安氟醚(E组)两组.在吸入地氟醚与安氟醚前以及当其吸入浓度分别达到0.5MAC、1.0MAC、1.5MAC时,用PaPolygraf HR胃肠动力监测系统测定下列数据LES压力(LESP)、胃压(GP)、屏障压(BrP)、长度(SL)、压力向量容积(PVV)和向量容积的三维立体图象.结果随地氟醚或安氟醚MAC的升高,D组各项指标与吸入前相比无明显变化(P＞0.05);而E组的LESP、BrP和PVV则呈进行性下降,与其基础值相比差异显著(＜0.01),并且也低于相同MAC的D组相应各值(＜0.01).结论地氟醚对小儿LES功能无明显影响而安氟醚对其影响较大,故有高度反流危险的小儿,以选用地氟醚维持麻醉更为安全.     

右美托咪定对剖宫产围术期体温及并发寒颤的影响

目的探讨右美托咪定对于蛛网膜下腔阻滞后剖宫产术围术期体温变化和寒颤的影响。方法选取2017年8—12月急诊或择期行剖宫产手术的足月单胎妊娠孕妇80例,年龄23～45岁,妊娠38～40周,ASAⅠ或Ⅱ级,随机分为右美托咪定组(D组)和对照组(C组),每组40例。胎儿娩出断脐后,D组给予右美托咪定0.5μg·kg~(-1)·h~(-1)至缝皮结束,C组则给予生理盐水0.125 ml·kg~(-1)·h~(-1)作为对照。记录产妇麻醉前(T_1)、断脐后(T_2)、术毕(T_3)及返回病房(T_4)时的膀胱温,并于以上时点采用Wrench寒颤分级法评估寒颤强度分级。术后采用状态焦虑量表对产妇进行焦虑评分。结果与T_1时比较,T_2—T_4时两组膀胱温明显降低(P0.05)。两组不同时点膀胱温差异无统计学意义。T_3、T_4时D组寒颤强度分级明显低于C组(P0.05)。D组术后焦虑评分明显低于C组[(41.1±10.6)分vs (51.6±13.1)分,P0.05]。结论右美托咪定对预防蛛网膜下腔阻滞后剖宫产患者围术期寒颤和焦虑具有显著效果,但并不能改变患者围术期的低体温率。     

常温及低温麻醉下安氟醚及异氟醚对心肌酶、氧自由基代谢及电解质的影响

目的 研究常温（37.5℃）及低温（30℃）麻醉下安氟醚及异氟醚对心肌酶、氧自由基代谢及电解质的影响。方法 健康家兔32只，离体Langendorff灌注，随机分为四组，每组8只。A组，常温1.3MAC安氟醚的K－H液灌液；B组，常温1.3MAC异氟醚的K－H液灌注；C组，低温1.3MAC安氟醚的K－H液灌注；D组，低温1.3MAC异氟醚的K－H液灌注。按不同组别要求测定冠状动脉流出液LDH、CK活性，心肌组织SOD、MDA及K^ 、Na^ 、Ca^2 、Mg^2 、Zn^2 含量。结果 A、B两组灌注前后LDH、CK无显著差异（P＞0.05），Zn^2 含量显著降低（P＜0.01），MDA明显降低（P＜0.05），Zn^2＋含量显著增高（P＜0.01）。四组心肌Ca^2 含量明显降低（P＜0.05或P＜0.01）。结论 临床常用麻醉强度的安氟醚及异氟醚对心肌细胞无直接损伤作用，但心肌Ca^2 、Zn^2 含量降低明显且安氟醚抑制心肌Ca^2 内流甚于异氟醚。低温下吸入安氟醚及异氟醚后能提高心肌抗氧化损伤能力，氧自由基产生减少。