Desflurane and errors of gas selection on vaporizer analyzer

With monochromatic infrared gas spectrometers (MIS), the displayed concentration is computed from measured IR absorption and a gain factor specific for the selected volatile agent (VA). As MIS cannot detect which VA is actually present, the displayed concentration can be very different from the actual one. As bottles and vaporizers are very specific for desflurane, it is impossible to misfill a vaporizer; however an erroneous selection of VA on MIS remains possible. The aim of this study was to assess the displayed concentrations after erroneous vapour selection on the monitor. When either desflurane, or isoflurane or enflurane were delivered at constant concentrations, all VA measured by the MIS, namely desflurane, sevoflurane, isoflurane, enflurane and halothane were successively selected and the displayed concentrations compared with the actual vapour concentration using a Capnomac Ultima (Datex) monitor. Consequences of erroneous selection can be included in three categories: 1) dangerous error, when a displayed concentration is much lower than the actual one, e.g. desflurane or sevoflurane erroneously selected; 2) evident error, when displayed concentration is much higher than 10 vol%; 3) uncomfortable situation, when displayed and actual concentrations are similar, e.g. isoflurane erroneously selected instead of desflurane. This error can only be detected by a careful checking of the device.     

Effects of three different types of management on the elimination kinetics of volatile anaesthetics. Implications for malignant hyperthermia treatment

The effectiveness of three types of management on the elimination kinetics of volatile anaesthetics was studied prospectively in 45 patients randomised to one of three groups. Patients were anaesthetised using isoflurane. Inspiratory and expiratory isoflurane concentrations were measured. After reaching a steady-state isoflurane concentration, the vaporizer was turned off. In group 1, only the fresh gas flow was increased from 40 to 120 ml.kg-1 x min-1. Patients in group 2, in addition to the increase in the fresh gas flow, had a charcoal filter connected in the inspiratory limb of the circuit. Patients in group 3 had the fresh gas flow increased and the anaesthetic machine and breathing system changed. There was a statistically significant difference in the isoflurane washout from the anaesthetic machines between group 1 (90% elimination time 39 [10] s) and group 2 (90% elimination time 25 [5] s) (p < 0.01). However, there was no significant difference in the isoflurane washout from the patients in any of the groups. Thus the use of a charcoal filter or a change of the anaesthetic machine and breathing system proved to be of no clinical advantage.     

Dependence of surgical trauma in aortic interventions on the approach chosen. A prospective study

A study was undertaken to assess the performance of the Komesaroff vaporizer, placed within the circuit, in ventilated patients during maintenance of closed circuit anaesthesia with halothane or isoflurane. Following intravenous induction, anaesthesia was maintained by inhalation. This was achieved using a conventional vaporizer outside the circle for the first 10 minutes to manage the fast uptake phase. The fresh gas flow was then reduced to the basal oxygen requirement with the Komesaroff vaporizer within the circle maintaining inhalational anaesthesia. Complete isolation of the circuit was achieved by returning all anaesthetic gases to the circuit following analysis and using a bag-in-bottle ventilator. The Komesaroff vaporizer dial was positioned at between the first and second division and end-tidal volatile anaesthetic agent levels were measured. This study demonstrated that at dial positions 1 or 1.5 with either agent, the end-tidal volatile concentration plateaued at clinically acceptable levels. The Komesaroff vaporizer can therefore be used safely in ventilated patients to maintain closed circuit anaesthesia provided clinical observation and monitoring are meticulous.     

Accuracy of 94 anaesthetic agent vaporizers in clinical use

Using the Brüel & Kjaer Anaesthetic Gas Monitor type 1304, we have monitored the output of 94 anaesthetic agent vaporizers (Fluotec 3:58, Enfluratec 3:24, Isotec 3:12), in seven departments of anaesthesia, at different dial settings and flow rates. The range of output, for one type of vaporizer and dial setting (flow: 6 litre min-1) was largest with the Fluotec 3 (0.85-1.55% when dial set to 1%) and smallest with the Isotec 3 (0.85-1.15% when dial set to 1%). In determining the number of vaporizers with unacceptable inaccuracy, we applied acceptance limits of +/- 15% relative on each vaporizer and each dial setting. Using a flow of oxygen 6 litre min-1 17% of Fluotec 3.8% of Isotec 3 and 71% of Enfluratec 3 vaporizers had outputs outside those limits. Even when some specific conditions (vaporizers giving output beyond the limits at any two or more dial settings; output beyond the limits in the clinically relevant range (0.5-2%)) were added, a substantial number of vaporizers did not perform within the limits. We found a significantly greater accuracy of the vaporizers after 3-monthly calibration checks (P < 0.05) compared with vaporizers undergoing service and calibration only annually. Using a questionnaire, we found that fewer than 30% of the anaesthetists using the vaporizers would accept aberrance beyond +/- 10% relative of the dial setting.     

Emergency physician-performed portable bedside ultrasonography demonstrating periportal brightness in a patient with hepatitis A

We report a serious dysfunction of 19 halothane vaporisers Vapor 19.3 (Dr?ger) which delivered a much higher concentration of agent than indicated on the dial. This inaccuracy was linked to a major corrosion of the inner layers of the vaporiser, with a deposit of zinc bromide and chloride in the bypass channel. The main cause for this dysfunction was the absence of an adequate maintenance of the vaporisers since their purchase 3 years before.     

Changing from isoflurane to desflurane toward the end of anesthesia does not accelerate recovery in humans

BACKGROUND: In an attempt to combine the advantage of the lower solubilities of new inhaled anesthetics with the lesser cost of older anesthetics, some clinicians substitute the former for the latter toward the end of anesthesia. The authors tried to determine whether substituting desflurane for isoflurane in the last 30 min of a 120-min anesthetic would accelerate recovery. METHODS: Five volunteers were anesthetized three times for 2 h using a fresh gas inflow of 2 l/min: 1.25 minimum alveolar concentration (MAC) desflurane, 1.25 MAC isoflurane, and 1.25 MAC isoflurane for 90 min followed by 30 min of desflurane concentrations sufficient to achieve a total of 1.25 MAC equivalent ("crossover"). Recovery from anesthesia was assessed by the time to respond to commands, by orientation, and by tests of cognitive function. RESULTS: Compared with isoflurane, the crossover technique did not accelerate early or late recovery (P > 0.05). Recovery from isoflurane or the crossover anesthetic was significantly longer than after desflurane (P < 0.05). Times to response to commands for isoflurane, the crossover anesthetic, and desflurane were 23 +/- 5 min (mean +/- SD), 21 +/- 5 min, and 11 +/- 1 min, respectively, and to orientation the times were 27 +/- 7 min, 25 +/- 5 min, and 13 +/- 2 min, respectively. Cognitive test performance returned to reference values 15-30 min sooner after desflurane than after isoflurane or the crossover anesthetic. Isoflurane cognitive test performance did not differ from that with the crossover anesthetic at any time. CONCLUSIONS: Substituting desflurane for isoflurane during the latter part of anesthesia does not improve recovery, in part because partial rebreathing through a semiclosed circuit limits elimination of isoflurane during the crossover period. Although higher fresh gas flow during the crossover period would speed isoflurane elimination, the amount of desflurane used and, therefore, the cost would increase.     

Environmental and biological control in a population exposed to isoflurane in the operating room

OBJECTIVE: To measure the level of occupational exposure to isoflurane in the operating room, and to determine the relation between isoflurane concentration in atmospheric and exhaled air. PATIENTS AND METHODS: One hundred seventy-eight samples were obtained from 60 male and female subjects who work in the operating room of our hospital. To monitor workplace exposure we used passive diffusion samplers. Biological monitoring (isoflurane in exhaled air) was accomplished with standard adsorption tubes to collect exhaled air samples. Gases were thermically separated and analyzed by gas chromatography. RESULTS: Atmospheric isoflurane concentrations ranged between 1.14 and 157.23 mg/m3 (geometric mean 16.23 mg/m3). Exhaled isoflurane concentrations ranged from 0.15 to 26.09 mg/m3 (geometric mean 2.85 mg/m3). Atmospheric and exhaled isoflurane concentrations were strongly related (r = 0.82; p < 0.0001). Linearity was determined by the following equation: log of exhaled isoflurane concentration = -0.69 + 0.95 log of atmospheric isoflurane concentration. CONCLUSIONS: The concentrations of isoflurane in atmospheric and exhaled air found in our study exceed the maximum levels for halogenated gases recommended by the National Institute for Occupational Safety and Health, although they do not exceed the levels stipulated by Swiss authorities. In order to adequately assess operating room antipollution measures, atmospheric and biologic monitoring of isoflurane and other inhaled anesthetic gas concentrations is necessary.     

Regional vasodilating properties of isoflurane in normal swine myocardium

BACKGROUND: Studies of the coronary vasodilating properties of isoflurane have produced inconsistent results. Isoflurane has been reported to cause minimal or no coronary vasodilation, mild dose-related vasodilation, or even near-maximal coronary vasodilation. The current study was performed to clarify the direct coronary vasodilating potency of isoflurane. METHODS: We determined the vasodilating properties of isoflurane in regionally perfused swine myocardium. Six domestic swine were anesthetized with pentobarbital and fentanyl. The left anterior descending artery (LAD) was cannulated and perfused with blood drawn from the carotid artery and passed thorough a membrane oxygenator. LAD arterial flow was controlled by a calibrated roller pump with continuous digital readout, and LAD arterial pressure was measured directly. The anterior interventricular vein was cannulated and dimension crystals placed in the LAD-perfused myocardium. The vasodilation response to 0, 1, 2, and 3% isoflurane administered via the membrane oxygenator was determined and compared to maximal vasodilation produced by regional intracoronary administration of adenosine. RESULTS: Systemic blood pressure and heart rate remained constant throughout the experiment. With 3% isoflurane, systolic shortening and regional myocardial oxygen consumption decreased by 60 and 20%, respectively. The same concentration increased coronary blood flow by 51 +/- 34% and reduced coronary vascular resistance by 32.9 +/- 11.0%. Neither coronary blood flow nor coronary vascular resistance was affected with 1% isoflurane. Regional coronary administration of adenosine produced much greater changes in both coronary blood flow (+591%) and coronary vascular resistance (-92.5%). Isoflurane increased the venous oxygen content of the anterior interventricular vein in a dose-dependent fashion from 4.85 vol% at control to 6.17, 7.01, and 8.63 vol% at 1, 2, and 3% isoflurane, respectively. CONCLUSIONS: We conclude that isoflurane is a mild dose-dependent coronary vasodilator. At a 1% concentration, the coronary vasodilating properties of isoflurane are minimal.     

Respiratory gas exchange. Anesthesia with enflurane or isoflurane in nitrous oxide during spontaneous and controlled ventilation

The estimation of oxygen consumption and carbon dioxide elimination is essential for predicting the metabolic activity and needs of any patient having anaesthesia. During anaesthesia oxygen consumption can be measured and compared to a predicted value. However, oxygen uptake is affected by anaesthetic agents, which complicates the interpretation of measured oxygen uptake rate. The purpose of this study was to investigate whether there are any differences in respiratory gas exchange during anaesthesia with enflurane and isoflurane and also to assess the effects of spontaneous versus controlled ventilation. METHODS. Forty orthopedic patients were randomized to enflurane or isoflurane anaesthesia in nitrous oxide with either spontaneous or controlled ventilation. A fresh low-gas-flow technique was used. Inspiratory oxygen and end-tidal carbon dioxide concentrations and expiratory minute ventilation were measured in a circle absorber system between the y-piece and the endotracheal tube with a sampling analyser. Between the mixing box and the absorption canister, carbon dioxide concentration was continuously measured. The carbon dioxide elimination was calculated from mixed expired concentration and expiratory minute ventilation. Excess gas was collected every 10 min in a non-permeable mylar plastic bag connected to the excess valve. The excess gas flow was calculated and the oxygen uptake rate was assumed to be the difference between the oxygen fresh gas flow and the oxygen excess gas flow. RESULTS. The grand mean oxygen uptake rate was 2.5 ml.kg-1 x min-1 or 100 ml.min-1 x m-2. There were no statistically significant differences in oxygen uptake between enflurane and isoflurane anaesthesia or between spontaneous and controlled ventilation. The mean oxygen uptake rate at 10 min was between 2.0 and 2.2 ml.kg-1 x min-1 in all groups. At 30 min the mean oxygen uptake rates were 2.6 to 2.8 ml.kg-1 x min-1. Carbon dioxide elimination was closely associated with expired minute ventilation, with a carbon dioxide excretion of about 30 ml per litre gas exhaled, irrespective of ventilatory mode employed.     

Economic considerations of the use of new anesthetics: a comparison of propofol, sevoflurane, desflurane, and isoflurane

Cost control in anesthesia is no longer an option; it is a necessity. New anesthetics have entered the market, but economic differences in comparison to standard anesthetic regimens are not exactly known. Eighty patients undergoing either subtotal thyroidectomy or laparoscopic cholecystectomy were randomly divided into four groups, with 20 patients in each group. Group 1 received propofol 1%/sufentanil, Group 2 received desflurane/sufentanil, Group 3 received sevoflurane/sufentanil, and Group 4 received isoflurane/sufentanil (standard anesthesia) for anesthesia. A fresh gas flow of 1.5-2 L/min and 60% N2O in oxygen was used for maintenance of anesthesia, and atracurium was given for muscle relaxation. Concentrations of volatile anesthetics, propofol, and sufentanil were varied according to the patient's perceived need. Isoflurane, desflurane, and sevoflurane consumption was measured by weighing the vaporizers with a precision weighing machine. Biometric data, time of surgery, and time of anesthesia were similar in the four groups. Times for extubation and stay in the postanesthesia care unit (PACU) were significantly longer in the isoflurane group. Use of sufentanil and atracurium did not differ among the groups. Propofol patients required fewer additional drugs in the PACU (e.g., antiemetics), and thus showed the lowest additional costs in the PACU. Total (intra- and postoperative) costs were significantly higher in the propofol group ($30.73 per patient; $0.24 per minute of anesthesia). The costs among the inhalational groups did not differ significantly (approximately $0.15 per minute of anesthesia). We conclude that in today's climate of cost savings, a comprehensive pharmacoeconomic approach is needed. Although propofol-based anesthesia was associated with the highest cost, it is doubtful whether the choice of anesthetic regimen will lower the costs of an anesthesia department. IMPLICATIONS: Cost analysis of anesthetic techniques is necessary in today's economic climate. Consumption of the new inhaled drugs sevoflurane and desflurane was measured in comparison to a standard anesthetic regimen using isoflurane and an IV technique using propofol. Propofol-based anesthesia was associated with the highest costs, whereas the costs of the new inhaled anesthetics sevoflurane and desflurane did not differ from those of a standard, isoflurane-based anesthesia regimen.     

Recovery from sevoflurane anesthesia: a comparison to isoflurane and propofol anesthesia

BACKGROUND: Sevoflurane has a lower blood:gas partition coefficient than isoflurane, which may cause a more rapid recovery from anesthesia; it also might cause faster emergence times than for propofol-based anesthesia. We evaluated a database that included recovery endpoints from controlled, randomized, prospective studies sponsored by Abbott Laboratories that compared sevoflurane to isoflurane or propofol when extubation was planned immediately after completion of elective surgery in adult patients. METHODS: Sevoflurane was compared to isoflurane in eight studies (N=2,008) and to propofol in three studies (N=436). Analysis of variance was applied using least squares method mean values to calculate the pooled mean difference in recovery endpoints between primary anesthetics. The effects of patient age and case duration also were determined. RESULTS: Sevoflurane resulted in statistically significant shorter times to emergence (-3.3 min), response to command (-3.1 min), orientation (-4.0 min) and first analgesic (-8.9 min) but not time to eligibility for discharge (-1.7 min) compared to isoflurane (mean difference). Times to recovery endpoints increased with increasing case duration with isoflurane but not with sevoflurane (patients receiving isoflurane took 4-5 min more to emerge and respond to commands and 8.6 min more to achieve orientation during cases longer than 3 hr in duration than those receiving sevoflurane). Patients older than 65 yr had longer times to orientation, but within any age group, orientation was always faster after sevoflurane. There were no differences in recovery times between sevoflurane and propofol. CONCLUSIONS: Recovery from sevoflurane was 3-4 min faster than with isoflurane in all age groups, and the difference was magnified in longer-duration surgical cases (> 3 hr).     

Nitrous oxide has different effects on the EEG and somatosensory evoked potentials during isoflurane anaesthesia in patients

BACKGROUND: Electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) are altered by inhalation anaesthesia. Nitrous oxide is commonly used in combination with volatile anaesthetics. We have studied the effects of nitrous oxide on both EEG and SEPs simultaneously during isoflurane burst-suppression anaesthesia. METHODS: Twelve ASA I-II patients undergoing abdominal or orthopaedic surgery were anaesthetized with isoflurane by mask. After intubation and relaxation the isoflurane concentration was increased to a level at which an EEG burst-suppression pattern occurred (mean isoflurane end-tidal concentration 1.9 (SD 0.2) %. With a stable isoflurane concentration, the patients received isoflurane-air-oxygen and isoflurane-nitrous oxide-oxygen (FiO2 0.4) in a randomized cross-over manner. EEG and SEPs were simultaneously recorded before, and after wash-out or wash-in periods for nitrous oxide. The proportion of EEG suppressions as well as SEP amplitudes for cortical N20 were calculated. RESULTS: The proportion of EEG suppressions decreased from 53.5% to 34% (P < 0.05) when air was replaced by nitrous oxide. At the same time, the cortical N20 amplitude was reduced by 69% (P < 0.01). CONCLUSION: The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.     

Reduction of the minimum alveolar concentration of isoflurane by dexmedetomidine

BACKGROUND: alpha 2-Adrenergic agonists have been shown to reduce anesthetic requirements of other anesthetics, and they may even act as complete anesthetics by themselves at high doses in animal models. The present study was designed to define the interaction of intravenous infusion of dexmedetomidine, an alpha 2-adrenergic agonist, and isoflurane in patients having surgery by using the minimum alveolar concentration (MAC) of isoflurane as the measure of anesthetic potency. METHODS: Forty-nine women scheduled for abdominal hysterectomy were randomly allocated to receive either a placebo infusion (n = 16) or a two-stage infusion of dexmedetomidine with target plasma concentration of 0.3 ng/ml (n = 17) or 0.6 ng/ml (n = 16). The study drug infusion was commenced 15 min before induction of anesthesia with thiopental and alfentanil and was continued until skin incision. The end-tidal concentration of isoflurane for each patient was predetermined according to the "up-down" method of Dixon, and it was maintained for at least 15 min before the patient's response to skin incision was assessed. RESULTS: The MAC of isoflurane was 0.85% end-tidal in the control group, 0.55% end-tidal with the low dose of dexmedetomidine, and 0.45% end-tidal with the high dose of dexmedetomidine. CONCLUSIONS: The MAC of isoflurane in the control group was lower than that reported previously in similar patients having surgery, probably due to anesthesia induction with thiopental and alfentanil. Nevertheless, with the high dose of dexmedetomidine, the MAC of isoflurane was still 47% less than that without dexmedetomidine.     

Arthroscopy in the elderly

The uptake rate of oxygen and nitrous oxide were studied during low flow anaesthesia with enflurane or isoflurane in nitrous oxide with either spontaneous or controlled ventilation. The excess gas flow and composition were analysed. The nitrous oxide uptake rate was in agreement with Severinghaus' formula VN20 1000.t-0.5. The composition of excess gas was predictable and the following formula for oxygen uptake could be derived: VO2 = VfgO2-0.45 (VfgN2(0)-(kg: 70.1000.t-0.5)) where oxygen uptake rate (VO2, ml.min-1) equals oxygen fresh gas flow (VfgO2) minus 0.45 times the difference between the fresh gas flow of nitrous oxide (VfgN2O), ml.min-1 and estimated uptake of nitrous oxide. The equation assumes constant inspired gas concentrations of 30% oxygen and 65-70% nitrous oxide. The oxygen uptake rates calculated from this formula were in good agreement with measured uptake rates. Thus, continuous monitoring of oxygen uptake rates is possible by using only reliable flowmeters and analysis of inspired oxygen concentration.     

Effects of halothane and isoflurane on carbon monoxide-induced relaxations in the rat aorta

BACKGROUND: Halothane and isoflurane previously were reported to attenuate endothelium-derived relaxing factor/nitric oxide-mediated vasodilation and cyclic guanosine monophosphate (cGMP) formation in isolated rat aortic rings. Carbon monoxide has many chemical and physiologic similarities to nitric oxide. This study was designed to investigate the effects of halothane and isoflurane on carbon monoxide-induced relaxations and cGMP formation in the isolated rat aorta. METHODS: Isometric tension was recorded continuously from endothelium denuded rat aortic rings suspended in Krebs-filled organ baths. Rings precontracted with submaximal concentrations of norepinephrine were exposed to cumulative concentrations of carbon monoxide (26-176 microM). This procedure was repeated three times, with anesthetics delivered 10 min before the second procedure. Carbon monoxide responses of rings contracted with the same concentration of norepinephrine (10(-6) M and 2 x 10(-6) M) used in the anesthetic-exposed preparations also were examined. The concentrations of cGMP were determined in denuded rings using radioimmunoassay. The rings were treated with carbon monoxide (176 microM, 30 s) alone, or carbon monoxide after a 10-min incubation with halothane (0.34 mM or 0.72 mM). To determine whether the sequence of anesthetic delivery influenced results, vascular rings pretreated with halothane were compared with nonpretreated rings. RESULTS: Carbon monoxide (26-176 microM) caused a dose-dependent reduction of norepinephrine-induced tension, with a maximal relaxation of 1.51 +/- 0.07 g (85 +/- 7% of norepinephrine-induced contraction). Halothane (0.34 mM and 0.72 mM) significantly attenuated the carbon monoxide-induced relaxations, but only the highest concentration of isoflurane (0.53 mM) significantly attenuated the carbon monoxide-induced relaxations. Carbon monoxide (176 microM) significantly increased cGMP content (+88.1 +/- 7.1%) and preincubation of the aortic rings with halothane (0.34 mM and 0.72 mM) inhibited this increase (-70.7 +/- 6.8% and -108.1 +/- 10.6%, respectively). When aortic rings and carbon monoxide were added simultaneously to Krebs solution equilibrated with halothane (0.72 mM), no inhibition of cGMP formation occurred. CONCLUSION: Carbon monoxide-induced endothelium-independent relaxations of rat aortic rings were decreased by clinically relevant concentrations of halothane and isoflurane. The carbon monoxide-induced elevations of cGMP were attenuated by halothane only when the anesthetic was incubated with aortic rings before carbon monoxide treatment. The possible clinical significance of the actions of the anesthetics on this endogenous vasodilator is yet to be determined.     

Effect of a subanesthetic minimum alveolar concentration of isoflurane on two tests of the hypoxic ventilatory response

BACKGROUND: These experiments were designed to study the effect of 0.1 minimum alveolar concentration isoflurane on the hypoxic ventilatory response as measured by two common methods of hypoxic testing: when normocapnic hypoxia was induced abruptly and when it was induced gradually. We hypothesized that any disparity in results would be due to an isoflurane effect that was manifested differently in the two tests. METHODS: After 20 min for uptake and equilibration of 0.1 minimum alveolar concentration end-tidal isoflurane or carrier gas in hyperoxia, isocapnic hypoxia was induced either abruptly over 60-80 s ("step" test) or gradually over 10 min ("ramp" test), followed by 20 min of isocapnic hypoxia at 45 mmHg end-tidal oxygen. Control of the hypoxic and isocapnic stimuli was accomplished accurately by a computer-controlled dynamic end-tidal forcing system. Eight subjects performed each test in the presence and absence of isoflurane. RESULTS: For both step tests and ramp tests, 0.1 minimum alveolar concentration isoflurane had no effect on minute ventilation during the defined periods of hypoxia. With isoflurane, delta VE45, the acute change in ventilation from hyperoxia to hypoxia, was 97 +/- 20% (mean +/- SEM) of the control response for step tests and 100 +/- 25% of the control response for ramp tests. The step tests produced significantly larger acute hypoxic responses than did the ramp tests, but by the end of 20 min of hypoxia, ventilation was similar for both tests. CONCLUSIONS: Neither method of hypoxic testing demonstrated the level of isoflurane effect reported by others. A comparison of the two methods of hypoxic testing suggests that ramp tests, as commonly performed, do not allow adequate time for full expression of the acute hypoxic ventilatory response. Step tests also better separated the opposing hypoxic effects of carotid body stimulation and central ventilatory depression.     

Effect of differential delivery of isoflurane to head and torso on lumbar dorsal horn activity

BACKGROUND: The spinal cord appears to be the site where anesthetic agents prevent movement in response to noxious stimuli. When isoflurane is differentially delivered to the head and torso (with low torso concentrations), cranial anesthetic requirements increase compared with systemic administration. The aim of the current study was to test the hypothesis that isoflurane action in the brain has descending influences on spinal cord dorsal horn neurons. A secondary aim was to determine the association, if any, of high cranial concentrations of isoflurane (>6%) with dorsal horn activity. METHODS: Ten goats were anesthetized with isoflurane and the carotid arteries and jugular veins isolated and cannulated for cerebral bypass. A laminectomy was performed for recording from single lumbar dorsal horn neurons with hind limb mechanical receptive fields (one cell per goat). A standard noxious mechanical stimulus was applied to the dew claw or hoof bulb during a control period with end-tidal isoflurane at 1.3% and during bypass with the following head/torso isoflurane concentrations: 1.3%/1.3%, 3.2%/1.3%, 9.4%/1.3%, 1.3%/0.2%, 3.0%/0.2% and 8.8%/0.3%. RESULTS: When torso isoflurane concentration was 1.3%, increasing cranial isoflurane concentration to 3% or 9% had no significant effect on the activity of dorsal horn units. When torso isoflurane was 0.2-0.3%, spontaneous activity increased; however, at these torso concentrations, evoked responses were significantly decreased (-60%) only when cranial isoflurane concentration was increased to 9%. CONCLUSIONS: Isoflurane action in the brain had an inhibitory effect on dorsal horn activity with the combination of supraclinical cranial and low torso concentrations.     

Effects of isoflurane on in vivo release of acetylcholine in the rat cerebral cortex and striatum

BACKGROUND: Acetylcholine (ACh) is one of the major excitatory neurotransmitters in the central nervous system, and changes in neural activity induced by anesthesia alter the release of ACh. However, the effects of isoflurane, one of the most widely used volatile anesthetics, on ACh release are not known. The present study attempts to clarify the dose-effect relationship of isoflurane on the in vivo release of ACh in rat brains. METHODS: Changes in the extracellular concentration of ACh and choline in the cerebral cortex and striatum induced by 0.5, 1.0, and 1.5 minimum alveolar concentration (MAC) of isoflurane were determined using a brain microdialysis technique. RESULTS: In the cortex, the ACh release decreased to 30.8+/-10.1 (mean+/-SEM), 10.2+/-4.1, and 8.1+/-2.9% of basal value by increasing doses of isoflurane, and in the striatum, to 73.3+/-4.4, 49.2+/-4.2, and 40.7+/-4.5%. The ACh release rapidly recovered control levels with the discontinuance of isoflurane. Choline concentration was not changed significantly by isoflurane except for a decrease to 74.8+/-4.6% in the striatum by 0.5 MAC. In both the cortex and striatum, the choline concentration decreased with the discontinuance of isoflurane to 70.3+/-13.3, and 68.2+/-5.4%, respectively. CONCLUSION: The fact that all classic anesthetics reported previously, as well as isoflurane, reduce ACh release supports the hypothesis that the suppression of cholinergic cells is, at least in part one of the mechanisms of anesthesia.     

Gastric myoelectric and motor activity in dogs after isoflurane anesthesia

To characterize the effects of isoflurane on gastric motility, gastric electrical and contractile activities were assessed in six healthy adult dogs before and after recovery from anesthesia. Baseline recordings (fasting and fed state) were obtained in unanesthestized dogs 8 days after implantation of serosal electrodes and strain-gauge force transducers. After an overnight fast, dogs were anesthetized with 1.3 minimum alveolar concentration (MAC) isoflurane for 4.5 hours (approximately 6 MAC hours). No other anesthetic or sedative drugs were administered. During anesthesia, ventilation was mechanically controlled to maintain arterial carbon dioxide tension at 36 +/- 4 mm Hg. Gastric electrical and contractile activities (fasting and fed state) were recorded again 18 hours after recovery from isoflurane anesthesia. Recordings were analyzed to determine gastric slow-wave frequency, presence of slow-wave dysrhythmias, slow-wave propagation velocity, coupling of contractions to slow waves, a motility index based on relative contractile amplitudes, and onset and duration of contractions after a standardized meal. The only variable that was significantly decreased 18 hours after 6 MAC hours of isoflurane anesthesia was the gastric motility index during fasting-state phase III. This decrease was not apparent in the fed-state test periods. Our results suggest that, with the exception of gastric motility index during fasting-state phase III, variables for gastric electrical and contractile activities in dogs are unaffected by isoflurane 18 hours after anesthesia.     

Desflurane, sevoflurane, and isoflurane impair canine left ventricular-arterial coupling and mechanical efficiency

BACKGROUND: The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs. METHODS: Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively. RESULTS: Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane. CONCLUSIONS: The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (< 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.