Effects of desflurane, sevoflurane and halothane on postinfarction spontaneous dysrhythmias in dogs

Background: Although desflurane (DES) and sevoflurane (SEV) have desirable features for use in patients with coronary artery disease, their effects on ventricular dysrhythmias following infarction are less known. We therefore examined the effects of DES and SEV upon spontaneous postinfarction ventricular dysrhythmias in dogs, and compared those effects to the well-established antidysrhythmic effects of halothane (HAL) in this model.
Methods : After institutional approval, the left anterior descending coronary artery was ligated in 16 adult mongrel dogs during isoflurane anesthesia. All dogs developed acute myocardial infarction and severe ventricular tachydysrhythmias. Twenty-two hours after infarction, dogs were anesthetized at 1.5 MAC with desflurane (10.8%) followed by sevoflurane (3.5%) in the treatment group (n=10), or halothane (1.3%) in the other group (n=6). Anesthetic gases were allowed to equilibrate for at least 20 min at each end-tidal concentration. At this time, the ECG was recorded for 9 min and evaluated for the number of ventricular ectopic and sinoatrial beats and summed duration of ventricular tachycardia.
Results: DES and SEV reduced the average rate of total ventricular ectopic beats by 40 ±4% and 42 ±4%, respectively. HAL decreased total ventricular ectopic rate by 59 ±6% and 62 ±5% after durations of anesthesia comparable to DES and SEV, respectively. Decreases in dysrhythmia in the presence of DES and SEV were significantly smaller than those produced by HAL after a comparable total duration of anesthesia.
Conclusions: DES and SEV inhibit spontaneous postinfarction ventricular dysrhythmias, although attenuation of dysrhythmias was smaller than the inhibition during comparable doses of HAL.     

Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart

A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts perfused at a constant flow (10 ml min-1, PO2 80 kPa) and paced at 350 beat min-1, we determined left ventricular developed pressure (LVDP) and release of creatine kinase (CKR) as indices of myocardial performance and cellular injury, respectively. Seven control hearts underwent 30 min of no-flow ischaemia and 1 h of reperfusion. In the treatment groups, halothane, enflurane, isoflurane, sevoflurane or desflurane (each group n = 6) was added to the perfusion medium for the first 30 min of reperfusion at a concentration corresponding to 1.5 MAC in the rat. In the control group, cellular injury occurred at early reperfusion (peak CKR 283 (SEM 57) iu litre-1 at 10 min of reperfusion). Peak CKR to the coronary venous effluent was attenuated by all anaesthetics (halothane group 156 (45), enflurane group 134 (20), sevoflurane group 132 (20), desflurane group 159 (25) iu litre-1; each P < 0.05). Isoflurane did not differ from controls (303 (53) iu litre-1; P = 0.5). In the sevoflurane group, there was a delayed peak CKR after discontinuation of the anaesthetic at 30 min of reperfusion (260 (34) iu litre-1). Functional recovery was improved by all anaesthetics, but was seen much earlier with desflurane (LVDP 28 (3)% of baseline at 5 min reperfusion compared with halothane (6 (1)%), enflurane (11 (3)%), isoflurane (9 (6)%), sevoflurane (10 (2)%) and controls (3 (1)% of baseline)). At 30 min of reperfusion, recovery of LVDP was improved to a similar extent by all anaesthetics (halothane 30 (9)%, enflurane 36 (9)%, isoflurane 33 (5)%, sevoflurane 30 (5)%, desflurane 36 (4)% of baseline values) compared with controls (13 (5)%; each P < 0.05). All inhalation anaesthetics protected against myocardial reperfusion injury, but showed differences in attenuation of cellular injury and functional recovery. These differences may suggest different protective mechanisms.      

Pharmacokinetics of desflurane, sevoflurane, isoflurane, and halothane in pigs

We tested the prediction that the alveolar washin and washout, tissue time constants, and pulmonary recovery (volume of agent recovered during washout relative to the volume taken up during washin) of desflurane, sevoflurane, isoflurane, and halothane would be defined primarily by their respective solubilities in blood, by their solubilities in tissues, and by their metabolism. We concurrently administered approximately one-third the MAC of each of these anesthetics to five young female swine and determined (separately) their solubilities in pig blood and tissues. The blood/gas partition coefficient of desflurane (0.35 +/- 0.02) was significantly smaller (P less than 0.01) than that of sevoflurane (0.45 +/- 0.02), isoflurane (0.94 +/- 0.05), and halothane (2.54 +/- 0.21). Tissue/blood partition coefficients of desflurane and halothane were smaller than those for the other two anesthetics (P less than 0.05) for all tissue groups. As predicted from their blood solubilities, the order of washin and washout was desflurane, sevoflurane, isoflurane, and halothane (most to least rapid). As predicted from tissue solubilities, the tissue time constants for desflurane were smaller than those for sevoflurane, isoflurane, and halothane. Recovery (normalized to that of isoflurane) of the volume of anesthetic taken up was significantly greater (P less than 0.05) for desflurane (93% +/- 7% [mean +/- SD]) than for halothane (77% +/- 6%), was not different from that of isoflurane (100%), but was less than that for sevoflurane (111% +/- 17%). The lower value for halothane is consistent with its known metabolism, but the lower (than sevoflurane) value for desflurane is at variance with other presently available data for their respective biodegradations.     

Effect of temperature on the solubility of desflurane, sevoflurane, enflurane and halothane in blood

We have investigated the effect of temperature on the blood-gas solubility of desflurane, sevoflurane, enflurane and halothane. Blood was equilibrated with gas mixtures of known composition in open cuvette or closed flask tonometers over a temperature range of 29-39 degrees C, and the concentration of each anaesthetic in blood was measured at 37 degrees C by repeated headspace analysis using a gas chromatograph. Solubility increased by 5.4% of the solubility at 37 degrees C for each degree that equilibration temperature was reduced. This result was true for all anaesthetics in all blood samples, and is in keeping with results for other volatile anaesthetics.      

Effects of enflurane, isoflurane, sevoflurane and desflurane on reperfusion injury after regional myocardial ischaemia in the rabbit heart in vivo

It is known that volatile anaesthetics protect myocardial tissue against ischaemic and reperfusion injury in vitro. In this investigation, we have determined the effects of the inhalation anaesthetics, enflurane, isoflurane, sevoflurane and desflurane, administered only during early reperfusion, on myocardial reperfusion injury in vivo. Fifty chloralose-anaesthetized rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. Left ventricular pressure (LVP, tip-manometer), cardiac output (CO, ultrasonic flow probe) and infarct size (triphenyltetrazolium staining) were determined. During the first 15 min of reperfusion, five groups of 10 rabbits each received 1 MAC of enflurane (enflurane group), isoflurane (isoflurane group), sevoflurane (sevoflurane group) or desflurane (desflurane group), and 10 rabbits served as untreated controls (control group). Haemodynamic baseline values were similar between groups (mean LVP 106 (SEM 2) mm Hg; CO 281(7) ml min-1). During coronary occlusion, LVP and CO were reduced to the same extent in all groups (LVP 89% of baseline; CO 89%). Administration of inhalation anaesthetics during early reperfusion further reduced both variables, but they recovered after discontinuation of the anaesthetics to values not different from control animals. Infarct size was reduced from 49 (5)% of the area at risk in the control group to 32 (3)% in the desflurane group (P = 0.021), and to 36 (2)% in the sevoflurane group (P = 0.097). In the enflurane group, infarct size was 39 (5)% (P = 0.272). Isoflurane had no effect on infarct size (48 (5)%, P = 1.000). The results show that desflurane and sevoflurane markedly reduced infarct size and therefore can protect myocardium against reperfusion injury in vivo. Enflurane had only a marginal effect and isoflurane offered no protection against reperfusion injury in vivo. These different effects suggest different protective mechanisms at the cellular level.      

Haemodynamic changes during halothane, sevoflurane and desflurane anaesthesia in dogs before and after the induction of severe heart failure

BACKGROUND AND OBJECTIVE: The effects of desflurane and sevoflurane on the failing myocardium are still uncertain. We investigated the effects of different concentrations of sevoflurane, desflurane and halothane in dogs with pacing induced chronic heart failure. METHODS: Global (left ventricular pressure, left ventricular dP/dt, Konigsbergtransducer) and regional myocardial function (systolic segment length shortening, ultrasonic crystals) were measured in chronically instrumented dogs with tachycardia induced severe congestive heart failure. Measurements were performed in healthy dogs and after induction of heart failure in the awake state and during anaesthesia with 0.75, 1.0, 1.25 and 1.75 minimum alveolar concentration (MAC) of halothane, sevoflurane or desflurane. RESULTS: The anaesthetics reduced dP/dtmax in a dose-dependent manner in healthy dogs (dP/dtmax decreased to 43-53% of awake values at 1.75 MAC). Chronic rapid left ventricular pacing increased heart rate and left ventricular end-diastolic pressure and decreased mean arterial pressure, left ventricular systolic pressure and dP/dtmax. The reduction in contractility was similar in the failing myocardium (to 41-50% of awake values at 1.75 MAC). Segmental shortening was reduced during anaesthesia by 50-62% after pacing compared with 22-44% in normal hearts. While there were similar effects of the different anaesthetics on diastolic function in healthy dogs, after induction of heart failure a more pronounced increase of the time constant of isovolumic relaxation and a greater decrease of dP/dtmin was observed with sevoflurane than with desflurane, indicating a stronger depression of diastolic function. CONCLUSIONS: While the negative inotropic effects of sevoflurane and desflurane were similar in normal and in the failing myocardium in vivo, desflurane led to a better preservation of diastolic function in the failing myocardium.     

Pharmacological preconditioning: comparison of desflurane,sevoflurane, isoflurane and halothane in rabbit myocardium

Background. Recent investigations showed that isoflurane caninduce pharmacological preconditioning. The present study aimedto compare the potency of four different halogenated anaestheticsto induce preconditioning. Methods. Anaesthetized open-chest rabbits underwent 30 min ofcoronary artery occlusion followed by 3 h of reperfusion. Beforethis, rabbits were randomized into one of five groups and underwenta treatment period consisting of either no intervention for45 min (control; n=10), or 30 min of 1 MAC halogenated anaestheticinhalation followed by 15 min of washout. End-tidal concentrationsof halogenated agents were 3.7% for sevoflurane (n=11), 1.4%for halothane (n=9), 2.0% for isoflurane (n=11), and 8.9% fordesflurane (n=11). Area at risk and infarct size were assessedby blue dye injection and tetrazolium chloride staining. Results. Mean (SD) infarct size was 54 (18)% of the risk areain untreated controls and 40 (18)% in the sevoflurane group(P>0.05, ns). In contrast, mean infarct size was significantlysmaller in the halothane, isoflurane, and desflurane groups:26 (18)%, 32 (18)% and 16 (17)%, respectively (P<0.05 vscontrol). Conclusions. Halothane, isoflurane and desflurane induced pharmacologicalpreconditioning, whereas sevoflurane had no significant effect.In this preparation, desflurane was the most effective agentat preconditioning the myocardium against ischaemia. Br J Anaesth 2002; 89: 486–91     

Solubility of desflurane (I-653), sevoflurane, isoflurane, and halothane in human blood

The blood/gas partition coefficients for the new volatile anesthetic agent desflurane (I-653), sevoflurane, isoflurane, and halothane were determined, simultaneously, in 8 human volunteers to compare the solubilities of these agents in blood. The blood/gas partition coefficient for desflurane [0.49 +/- 0.03 (mean +/- SD)] was smallest, followed by sevoflurane (0.62 +/- 0.04), isoflurane (1.27 +/- 0.06), and halothane (2.46 +/- 0.09). Differences among the anesthetic agents were significant (P less than 0.001). The results of this study confirm that among these agents the solubility of desflurane in human blood is the smallest. The results suggest that the washin and washout of desflurane will be more rapid than that of sevoflurane, isoflurane, and halothane, and the washin and washout of sevoflurane will be more rapid than that of isoflurane and halothane.     

Arterial to inspired partial pressure ratio of halothane, isoflurane, sevoflurane and desflurane in rats

The inspired partial pressure of an anaesthetic is often used as an index of arterial partial pressure in small animal experiments. We have investigated the influence of anaesthetic solubility on the ratio of arterial to inspired partial pressure in 24 rats, allocated randomly to receive halothane, isoflurane or desflurane at four different inspired concentrations. The arterial partial pressure of the volatile agent was measured by two-stage headspace analysis using a gas chromatograph calibrated with the same gas used to calibrate the Datex Capnomac that measured the inspired concentration. Mean values of arterial to inspired ratio at the lowest concentrations were 0.60 (95% confidence intervals 0.50, 0.71) for 0.8% halothane, 0.54 (0.38, 0.69) for 0.8% isoflurane, 0.72 (0.59, 0.86) for 1.5% sevoflurane and 0.71 (0.54, 0.87) for 4% desflurane. Analysis of variance showed a significant effect of anaesthetic agent (P = 0.008) on the arterial to inspired ratio. Thus volatile anaesthetic agents do not demonstrate a fixed arterial to inspired ratio in rats.      

In vitro effects of desflurane, sevoflurane, isoflurane, and halothane in isolated human right atria

BACKGROUND: Direct myocardial effects of volatile anesthetics have been studied in various animal species in vitro. This study evaluated the effects of equianesthetic concentrations of desflurane, sevoflurane, isoflurane, and halothane on contractile parameters of isolated human atria in vitro. METHODS: Human right atrial trabeculae, obtained from patients undergoing coronary bypass surgery, were studied in an oxygenated (95% O2-5% CO2) Tyrode's modified solution ([Ca2+]o = 2.0 mM, 30 degrees C, stimulation frequency 0.5 Hz). The effects of equianesthetic concentrations (0.5, 1, 1.5, 2, and 2.5 minimum alveolar concentration [MAC]) of desflurane, sevoflurane, isoflurane, and halothane on inotropic and lusitropic parameters of isometric twitches were measured. RESULTS: Isoflurane, sevoflurane, and desflurane induced a moderate concentration-dependent decrease in active isometric force, which was significantly lower than that induced by halothane. In the presence of adrenoceptor blockade, the desflurane-induced decrease in peak of the positive force derivative and time to peak force became comparable to those induced by isoflurane. Halothane induced a concentration-dependent decrease in time to half-relaxation and a contraction-relaxation coupling parameter significantly greater than those induced by isoflurane, sevoflurane and desflurane. CONCLUSIONS: In isolated human atrial myocardium, desflurane, sevoflurane, and isoflurane induced a moderate concentration-dependent negative inotropic effect. The effect of desflurane on time to peak force and peak of the positive force derivative could be related to intramyocardial catecholamine release. At clinically relevant concentrations, desflurane, sevoflurane, and isoflurane did not modify isometric relaxation.     

Effects of sevoflurane, isoflurane, and halothane on regional myocardial blood flow in the ischemic canine heart

The effects of sevoflurane (Sev), isoflurane (Iso), and halothane (Hal) on coronary circulation were studied in 30 dogs with acute coronary arterial stenosis. Regional myocardial blood flow (rMBF) was measured by hydrogen clearance method. There was no significant difference between each anesthetic agent in heart rate, mean arterial pressure, and cardiac output under any anesthesia level. As the inspired concentration of each anesthetic is increased, rMBF decreased significantly and rMBF/rate-pressure-product (RPP) ratio increased in normal area. In Sev and Iso groups, rMBF/RPP ratios were higher than that in Hal group, suggesting luxury perfusion caused by Sev and Iso. In the ischemic area, rMBF was reduced depending on the inspired concentration of each anesthetic agent and transmural maldistribution of blood flow was not observed with any anesthetic agent. Nevertheless the ratio of rMBF in ischemic area to that of normal area was decreased in Sev and Iso groups, but not in Hal group. In this study, neither Sev nor Iso worsened regional myocardial ischemia. However, Sev-induced coronary vasodilation may cause regional myocardial ischemia by redistribution of flow under steal prone condition.     

Effects of sevoflurane and halothane anesthesia on liver circulation and oxygen metabolism in the dog during hepatolobectomy

Purpose Effects of sevoflurane and halothane anesthesia on liver circulation and oxygen metabolism during hepatolobectomy were investigated in the dog, with the aim of choosing a better anesthetic for hepatic resection. Methods Sixteen mongrel dogs were randomly divided into two groups with eight in each. Electromagnetic flowmeters were used to measure hepatic arterial and portal venous blood flows (1) before the inhalation of each anesthetic (base line); (2) 1 h after the start of inhalation of 1.5 minimum alveolar concentration (MAC) anesthetic; (3) 1 h after hepatolobectomy with the same MAC of anesthesia; and (4) 2 h after the discontinuation of anesthesia. Measurements of systemic hemodynamics, blood gas tensions, plasma enzyme leaks and arterial ketone body ratio were made at the same time. Results Sevoflurane maintained hepatic arterial blood flow better than halothane anesthesia, both before and after hepatolobectomy. Hepatic arterial vascular resistance increased in the halothane group but did not change in the sevoflurane group after hepatolobectomy. No significant difference was found in oxygen metabolism and arterial ketone body ratio between two groups. Serum enzyme leakage was less in the sevoflurane group. Conclusion Sevoflurane has less adverse effects on liver circulation, especially hepatic arterial blood flow, and hepatic function than halothane in the case of hepatolobectomy.     

Relaxation by sevoflurane, desflurane and halothane in the isolated guinea-pig trachea via inhibition of cholinergic neurotransmission

We have studied relaxation of airway smooth muscle by sevoflurane, desflurane and halothane in the isolated guinea-pig trachea. Ring preparations were mounted in tissue baths filled with physiological salt solution (PSS), aerated continuously with 5% carbon dioxide in oxygen. Electrical field stimulation (EFS) elicited cholinergic contractions that were abolished by tetrodotoxin, indicating nerve- mediated responses. Anaesthetics were added to the gas aerating the tissue baths. Halothane, sevoflurane and desflurane at 0.5-1.0 MAC markedly attenuated cholinergic contractions to EFS. Initiation of contractile responses to acetylcholine (ACh) were not affected by volatile anaesthetics, suggesting prejunctional inhibition (i.e. inhibition of acetylcholine release). When added to a maintained submaximal contraction to ACh, volatile anaesthetics induced relaxation, indicating postjunctional inhibition. We conclude that sevoflurane, desflurane and halothane inhibited postganglionic cholinergic neuroeffector transmission in the trachea. The effect was probably exerted via pre- and postjunctional mechanisms (i.e. inhibition of acetylcholine release and direct muscle actions). Sevoflurane and desflurane were more potent than halothane both pre- and postjunctionally.      

Behavioural effects of chronic exposure to sub-anesthetic concentrations of halothane, sevoflurane and desflurane in rats

BACKGROUND: A double-blind, randomized trial was conducted to determine the behavioural effects of chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane in rats. METHODS: Halothane, sevoflurane and desflurane group rats received 0.1%, 0.3%, and 0.6% concentrations in a flow rate of 3 L.min(-1) O(2) respectively. Control animals also received 3 L.min(-1) O(2) in another investigation room, which had the same properties as the study group rooms. Rats breathed inhaled agents or oxygen between 09:00-13:00 hr every day for 30 days. After 30 days of inhalation of subanesthetic doses of inhaled agents or oxygen, behavioural tests were applied. RESULTS: Tests of exploratory activity and curiosity (hole-board test), anxiety (elevated plus maze test) and learning and memory functions (multiple T maze test), demonstrated that chronic exposure to subanesthetic concentrations of all three anesthetics alters behavioural functions in rats. However, impairment of learning (P<0.05) and memory function (P<0.05) were greater in association with desflurane, in comparison to halothane and sevoflurane-treated rats. CONCLUSION: Chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane is associated with behavioural change in rats. Of the three drugs, desflurane was associated with the lowest learning and memory function test scores.     

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     

Effects of halothane and sevoflurane on inhibitory neurotransmission to medullary expiratory neurons in a decerebrate dog model

BACKGROUND: In canine expiratory bulbospinal neurons, 1 minimum alveolar concentration (MAC) halothane and sevoflurane reduced the glutamatergic excitatory drive at a presynaptic site and enhanced the overall gamma-aminobutyric acid (GABA)-mediated inhibitory input. The authors investigated if this inhibitory enhancement was mainly caused by postsynaptic effects. METHODS: Two separate anesthetic studies were performed in two sets of decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs during hypercapnic hyperoxia. The effect of 1 MAC halothane or sevoflurane on extracellularly recorded neuronal activity was measured during localized picoejection of the GABAA receptor agonist muscimol and the GABAA receptor antagonist bicuculline. Complete blockade of GABAA-mediated inhibition with bicuculline was used to assess the prevailing overall inhibitory input to the neuron. The neuronal response to muscimol was used to estimate the anesthetic effect on postsynaptic GABAA receptor function. RESULTS: Halothane at 1 MAC depressed the spontaneous activity of 12 expiratory neurons 22.2 +/- 14.8% (mean +/- SD) and overall glutamatergic excitation 14.5 +/- 17.9%. Overall GABA-mediated inhibition was enhanced 14.1 +/- 17.9% and postsynaptic GABAA receptor function 74.2 +/- 69.2%. Sevoflurane at 1 MAC depressed the spontaneous activity of 23 neurons 20.6 +/- 19.3% and overall excitation 10.6 +/- 21.7%. Overall inhibition was enhanced 15.4 +/- 34.0% and postsynaptic GABAA receptor function 65.0 +/- 70.9%. The effects of halothane and sevoflurane were not statistically different. CONCLUSION: Halothane and sevoflurane at 1 MAC produced a small increase in overall inhibition of expiratory premotor neuronal activity. The increase in inhibition results from a marked enhancement of postsynaptic GABAA receptor function that is partially offset by a reduction in presynaptic inhibitory input by the anesthetics.     

Effects of halothane and sevoflurane on the paediatric respiratory pattern

Using a respiratory inductive plethysmograph, we investigated the effects of halothane and sevoflurane on the paediatric respiratory pattern under spontaneous breathing. We measured tidal volume per weight, respiratory rate, partial pressure of end-expiratory carbon dioxide (Pet_CO2), rib cage contribution to ventilation (%RC) and phase shift between rib cage and abdominal movements at 0.5, 1.0 and 1.5 MAC of these inhalational anaesthetics in oxygen. Both of these anaesthetics increased Pet_CO2 significantly with increase in depth of anaesthesia; sevoflurane produced more profound respiratory depression than halothane at high MAC. Both agents decreased %RC significantly with increase in depth of anaesthesia; paradoxical respiration occurred in the halothane group at high MAC. The profound respiratory depression of sevoflurane is due to both decreased tidal volume and decreased respiratory rate. The paradoxical respiration under halothane may be attributed to the potent suppression of intercostal muscle function and may be partly due to compensatory sparing effect on respiratory rate, which leads to the increase in airway flow and airway resistance.     

Volatile anaesthetics and the atmosphere: atmospheric lifetimes and atmospheric effects of halothane, enflurane, isoflurane, desflurane and sevoflurane

The atmospheric lifetimes of the halogenated anaesthetics halothane, enflurane, isoflurane, desflurane and sevoflurane with respect to reaction with the hydroxyl radical (OH.) and UV photolysis have been determined from observations of OH. reaction kinetics and UV absorption spectra. Rate coefficients for the reaction with OH radicals for all halogenated anaesthetics investigated ranged from 0.44 to 2.7 x 10(-14) cm3 molec-1 s-1. Halothane, enflurane and isoflurane showed distinct UV absorption in the range 200-350 nm. In contrast, no absorption in this wavelength range was detected for desflurane or sevoflurane. The total atmospheric lifetimes, as derived from both OH. reactivity and photolysis, were 4.0-21.4 yr. It has been calculated that up to 20% of anaesthetics enter the stratosphere. As a result of chlorine and bromine content, the ozone depletion potential (ODP) relative to chlorofluorocarbon CFC-11 varies between 0 and 1.56, leading to a contribution to the total ozone depletion in the stratosphere of approximately 1% for halothane and 0.02% for enflurane and isoflurane. Estimates of the greenhouse warming potential (GWP) relative to CFC-12 yield values of 0.02-0.14, resulting in a relative contribution to global warming of all volatile anaesthetics of approximately 0.03%. The stratospheric impact of halothane, isoflurane and enflurane and their influence on ozone depletion is of increasing importance because of decreasing chlorofluorocarbons globally. However, the influence of volatile anaesthetics on greenhouse warming is small.      

Carbon monoxide production from desflurane, enflurane, halothane, isoflurane, and sevoflurane with dry soda lime.

BACKGROUND: Previous studies in which volatile anesthetics were exposed to small amounts of dry soda lime, generally controlled at or close to ambient temperatures, have demonstrated a large carbon monoxide (CO) production from desflurane and enflurane, less from isoflurane, and none from halothane and sevoflurane. However, there is a report of increased CO hemoglobin in children who had been induced with sevoflurane that had passed through dry soda lime. Because this clinical report appears to be inconsistent with existing laboratory work, the authors investigated CO production from volatile anesthetics more realistically simulating conditions in clinical absorbers. METHODS: Each agent, 2.5 or 5% in 2 l/min oxygen, were passed for 2 h through a Dr?ger absorber canister (bottom to top) filled with dried soda lime (Dr?gersorb 800). CO concentrations were continuously measured at the absorber outlet. CO production was calculated. Experiments were performed in ambient air (19-20 degrees C). The absorbent temperature was not controlled. RESULTS: Carbon monoxide production peaked initially and was highest with desflurane (507 +/- 70, 656 +/- 59 ml CO), followed by enflurane (460 +/- 41, 475 +/- 99 ml CO), isoflurane (176 +/- 2.8, 227 +/- 21 ml CO), sevoflurane (34 +/- 1, 104 +/- 4 ml CO), and halothane (22 +/- 3, 20 +/- 1 ml CO) (mean +/- SD at 2.5 and 5%, respectively). CONCLUSIONS: The absorbent temperature increased with all anesthetics but was highest for sevoflurane. The reported magnitude of CO formation from desflurane, enflurane, and isoflurane was confirmed. In contrast, a smaller but significant CO formation from sevoflurane was found, which may account for the CO hemoglobin concentrations reported in infants. With all agents, CO formation appears to be self-limited.