Comparison of enflurane and halothane in hypotensive eye surgery

Thirty patients undergoing elective eye surgery had anaesthesia induced with sodium thiopentone, suxamethonium and d-tubocurarine chloride. Patients were ventilated with nitrous oxide, oxygen and either halothane or enflurane. The volatile agents were used to decrease the systolic blood pressure to 80 mmHg. The volatile agent concentration in the blood was measured at 30 min intervals. Both agents were effective in producing hypotension, but enflurane was the more potent hypotensive agent in terms of MAC equivalents. There was no significant differences between the agents with respect to speed of recovery.     

MORBIDITY AFTER DAY-CASE GYNAECOLOGICAL SURGERY: Comparison of enflurane with halothane

In 105 patients undergoing day-case surgery recovery of consciousnesswas significantly faster after enflurane compared with halothaneanaesthesia. There was no difference in postoperative morbiditybetween the two anaesthetic groups.     

Comparison of enflurane, halothane, and isoflurane for diagnostic and therapeutic procedures in children with malignancies

The authors performed a randomized, prospective trial comparing enflurane, halothane, and isoflurane (each administered with nitrous oxide) to establish which inhaled anesthetic produced the fewest complications and the most rapid induction of anesthesia for children undergoing general anesthesia for diagnostic procedures as oncology outpatients. Sixty-six children, ranging from 8 months to 18 years, underwent a total of 124 anesthetics. Induction of anesthesia (time from placement of facemask to beginning of skin preparation) was faster with halothane (2.7 +/- 1.0 min, mean +/- SD, n = 46) than with enflurane (3.2 +/- 0.8 min, n = 43) or isoflurane (3.3 +/- 1.2 min, n = 35). Emergence from anesthesia (time from completion of the procedure to spontaneous eye opening) was more rapid with enflurane (4.7 +/- 4.4 min) than with halothane (6.2 +/- 4.5 min) or isoflurane (6.2 +/- 3.9 min). Total time from the start of procedure until discharge was longer with isoflurane (25.1 +/- 6.8 min) than with enflurane (21.5 +/- 8.6 min) or halothane (22.3 +/- 7.6 min). During induction, the incidence of laryngospasm was greatest with isoflurane (23%) and the incidence of excitement least with halothane (13%). During the maintenance of, emergence from, and recovery from anesthesia, coughing occurred most frequently with isoflurane. During the recovery period, headache occurred most frequently with halothane (9%); there were no significant differences in the incidence of nausea, vomiting, hunger, or depressed effect. The authors conclude that the rapid induction and minimal airway-related complications associated with halothane anesthesia make it an excellent anesthetic agent for pediatric patients undergoing short diagnostic procedures.     

GENERAL ANAESTHESIA FOR CAESAREAN SECTION IN SEVERE PRE-ECLAMPSIA: Comparison of the renal and hepatic effects of enflurane and halothane

In a randomized study of patients undergoing Caesarean section,either enflurane (mean 0.24 MAC-h) or halothane (mean 0.23 MAC-h)and 50% nitrous oxide in oxygen were administered to women (n= 12) with severe pre-eclampsia-eclampsia and to 16 healthypregnant patients with normal renal and hepatic function. Noevidence of nephrotoxicity was found in any pre-eclamptic ornormal patient. Metabolism of enflurane resulted in plasma inorganicfluoride concentrations (max 15 µmol litre^–1) whichwere well below the toxic value. Postoperative liver functiontests showed no important changes from preoperative values,although reductive metabolites of halothane were not measured.In patients with severe pre-eclampsia there appears no contraindicationto enflurane or, probably, halothane as volatile supplementsduring general anaesthesia. * Present address: Department of Anaesthetics, Queen VictoriaHospital, Rose Park, Adelaide, Australia     

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)     

Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats

Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.     

In vivo effects of halothane, enflurane, and isoflurane on hepatic sinusoidal microcirculation

Background: It has been proposed that halogenated anaesthetics interfere with the endothelium-dependent circulatory control by attenuating the effects of endothelium-derived relaxing factor (EDRF/NO). This study was designed to determine whether or not volatile anaesthetics in vivo influence the microvascular tone in hepatic sinusoids. Methods: Using epifluorescence videomicroscopy, we compared the effects of the volatile anaesthetics halothane, enflurane, and isoflurane on hepatic microcirculation in ventilated Lewis rats. Animals were initially anaesthetized with pentobarbitone (50 mg-kg^-1 i.p.) to allow instrumentation and laparotomy and were randomly allocated to one of 4 groups (n=5–6 each) to receive either a supplementary dose of i.v. pentobarbitone (25 mg kg^-1; control group) or 0.75 MAC halothane, enflurane or isoflurane (1.5 MAC h). Results: Halothane decreased significantly the volumetric blood flow as compared with isoflurane (P < 0.05) or pentobarbitone controls (P < 0.05). The decrease in sinusoidal blood flow caused by halothane was largely attributable to a decrease in sinusoidal diameter (P < 0.05), while red blood cell velocity remained unchanged. Isoflurane led to a significant decrease in sinusoidal width compared with controls (P < 0.05) but an increase in red cell velocity offset the effect of sinusoidal narrowing on volumetric blood flow, while enflurane had no significant effect on any of the measured parameters. Conclusion: This study provides the first direct evidence that the volatile anaesthetics halothane and isoflurane in vivo shift the hepatic microvascular tone toward a more constricted state; however, flow velocity is enhanced with isoflurane, offsetting this effect. As a result the volumetric flow is at least affected by isoflurane, then enflurane and most significantly by halothane. Furthermore, our data are consistent with the concept that volatile anaesthetics in clinically relevant concentrations may influence the balance between endothelium-derived vasoactive factors which control microvascular tone.     

Hepatic energy charge and adenine nucleotide status in rats anesthetized with halothane, isoflurane or enflurane

Background: Volatile anesthetics are known to have varying effects on hepatic oxygen supply in vivo and have been shown to depress hepatic mitochondrial respiration and so energy charge in vitro. However, the effect of halothane, isoflurane and enflurane on hepatic adenine nucleotide status in viuo has not been evaluated.
Methods: Ninety male rats were exposed to 40% oxygen (n=22) or 40% oxygen in equipotent (1 MAC) concentrations of halothane (1%) (n=23), isoflurane (1.4%) (n=22) or enflurane (2%) (n=23) for 2 hours. All animals were then administered intraperitoneal pentobarbital and anesthesia continued and laparotomy was performed. A liver biopsy was taken for determination of hepatocellular adenosine-5-triphosphate (ATP), adenosine-5-diphosphate (ADP) and adenosine-5-monophosphate (AMP) and computation of energy charge (EC) from ((ATP+1/2 ADP)+(ATP+ADP+AMP)) and total ade nine nucleotides (TAN) from (ATP+ADP+AMP). After the biopsy the aorta was cannulated for blood sampling.
Results: Rats in each group were similar in weight, as well as acid base and blood gas status just after liver biopsy. Hepatic energy charge, ATP, ADP, AMP, and TAN levels were not different in animals receiving either halothane, isoflurane or enflurane when compared with those receiving only oxygen.
Conclusions: One MAC of anesthesia for a period of 2 hours with the described volatile anesthetic agents did not affect adenine nucleotide status in viuo in rats.     

Ventilatory effects of halothane and enflurane in dogs

The ventilatory effects of halothane and enflurane were studied in permanently tracheostomized dogs at the same anesthetic depth of 1 MAC. Inspiratory and expiratory durations were longer and tidal volume greater during enflurane than during halothane anesthesia. Mean inspiratory flow rate and minute ventilation during enflurane anesthesia were less than those during halothane anesthesia. As a result, end-expiratory carbon-dioxide concentration was higher during enflurane than during halothane anesthesia. When end-expiratory carbon-dioxide concentration was held at 7.5%, tidal volume was not different between the two anesthetics, while the difference of other parameters still remained. In addition, the magnitude of Hering-Breuer reflex determined by end-expiratory airway occlusion was essentially identical between halothane and enflurane anesthesia. The present results indicate that 1) depressant effect of enflurane on respiratory drive is greater than that of halothane and 2) the two anesthetics act on the respiratory timing mechanism differently.     

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)     

Ventilatory response during halothane and enflurane anaesthesia

In six children with body weights between 11.4-18.7 kg, minute ventilation, tidal volume, respiratory rate, end-tidal CO2 concentration and CO2 elimination were measured during both CO2 free breathing and CO2 breathing due to low fresh gas flows (maximal inspired CO2 about 2%) or the addition of CO2 from Rotameters (mean inspired CO2 about 1.5%) during both halothane and enflurane anaesthesia. All patients were undergoing hypospadias repair, received caudal analgesia prior to surgery and were intubated and allowed to breathe halothane/enflurane in O2/N2O (FIO2 0.5) spontaneously through a modified T-piece system (Mapleson F). End-tidal CO2 concentrations were similar with both agents during CO2-free breathing and did not increase during CO2 breathing because of increased minute ventilation, of the same magnitude with both agents, which was achieved by larger tidal volumes. Respiratory rates were unchanged. No differences were found between halothane and enflurane at the light levels of general anaesthesia made possible by combination with caudal block.     

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     

Effect of sho-saiko-to (xiao-chai-hu-tang) on hepatic injury induced by halothane in rats]

The etiology of halothane induced hepatitis is unknown. This study investigated effect of oral administration of Sho-saiko-to on hepatic injury induced by exposure to 1.1% halothane under hypoxic condition (FIO2 = 0.12) for 2 hr in rats. Serum transaminase, histological score and area of necrosis were examined in rats treated with Sho-saiko-to (900 mg.kg-1) before and after halothane exposure. Twenty-four hours following halothane exposure, serum transaminase levels were significantly depressed; the level of sGOT was significantly lower in rats with treatment of Sho-saiko-to (211 +/- 34 IU.l-1) than in rats without treatment (264 +/- 42 IU.l-1) (P less than 0.05), and the level of sGPT was significantly lower in rats with treatment of Sho-saiko-to (144 +/- 20 IU.l-1) than in rats without treatment (215 +/- 46 IU.l-1) (P less than 0.01). Histological score in rats treated with Sho-saiko-to was significantly lower (3.8 +/- 0.6) than in rats without treatment (4.5 +/- 0.7) (P less than 0.05). The area of centrilobular necrosis was significantly lower in rats with treatment of Sho-saiko-to (21.2 +/- 8.7%) than in rats without treatment (34.5 +/- 12.7%) (P less than 0.05), too. These results indicate that Sho-saiko-to inhibits the hepatic necrosis and functional disorder following exposure to halothane.