The effects of sevoflurane, isoflurane, halothane, and enflurane on hemodynamic responses during an inhaled induction of anesthesia via a mask in humans

A rapid increase in isoflurane or desflurane concentration induces tachycardia and hypertension and increases-plasma catecholamine concentration. Little information is available as to whether sevoflurane, halothane, and enflurane induce similar responses during anesthesia induction via mask. Fifty ASA physical status I patients, aged 20-40 yr, and scheduled for elective minor surgery, received one of four volatile anesthetics: sevoflurane, isoflurane, halothane, or enflurane. Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask. The inspired concentration of anesthetic was increased by 0.9 MAC every 5 min to a maximum of 2.7 MAC. Heart rate (HR) and systolic blood pressure (SBP) were measured before and every minute for 15 min during anesthetic inhalation. In the sevoflurane and isoflurane groups, venous blood samples were drawn to determine the concentrations of plasma epinephrine and norepinephrine 3 min after each increase in anesthetic concentration. Sustained increments in HR were observed after increases in inspired isoflurane concentration to 1.8 MAC and 2.7 MAC (peak changes of 15 +/- 3 and 17 +/- 3 bpm, respectively). Isoflurane also increased SBP transiently after the inspired concentration was increased to 2.7 MAC (peak change of 10 +/- 4 mm Hg). Enflurane increased HR after the inspired concentration was increased to 2.7 MAC (peak change of 9 +/- 2 bpm). In contrast, changes in sevoflurane and halothane concentrations did not induce hyperdynamic responses. Plasma norepinephrine concentration in the isoflurane group was significantly higher than that in the sevoflurane group during 2.7 MAC (P = 0.022). We propose that there is a direct relationship between airway irritation of the anesthetic and immediate cardiovascular change during an inhaled induction of anesthesia.     

Generalised mitochondrial cytopathy is an absolute contraindication to orthotopic liver transplant in childhood

OBJECTIVE: To compare mask anesthesia induction and recovery characteristics between 2 inhalant anesthetic agents: isoflurane and sevoflurane. ANIMALS: 16 clinically normal, young adult Beagles. PROCEDURE: Using a cross-over design, dogs were randomly selected to receive sevoflurane or isoflurane via a face mask and a circle anesthetic system. Vaporizer setting concentrations were increased in stepwise, equal minimum alveolar concentrations (MAC) for each anesthetic until the vaporizer setting of 2.6% for isoflurane or 4.8% for sevoflurane (2 MAC) was reached. Concentration was kept constant until the dog had a negative tail clamp response and was intubated. End-tidal concentration was maintained at 1.8 to 2.0% or 3.3 to 3.8% for isoflurane or sevoflurane, respectively (1.4 to 1.6 MAC) for 30 minutes. Dogs were allowed to recover with only tail clamp stimulation until a positive response was obtained. Extubation was performed when a spontaneous swallow reflex was observed. Dogs were allowed to achieve sternal recumbency and stand unassisted without further stimulation. RESULTS: Sevoflurane induction resulted in shorter time to loss of palpebral reflex, negative tail clamp response, and time to tracheal intubation, and was of better quality than isoflurane induction. Both anesthetics were associated with rapid and smooth recovery. CONCLUSIONS: Sevoflurane mask induction is faster and of better quality, compared with isoflurane, in adult dogs. Recovery time and quality are comparable. CLINICAL RELEVANCE: On the basis of these results, sevoflurane is a suitable inhalant anesthetic for mask induction and recovery in adult dogs and appears to have some advantages over isoflurane, including faster and smoother mask induction.     

Effects of sevoflurane or halothane on contractile responses of isolated canine basilar artery

Although volatile anesthetic is known as a cerebral vasodilator, its mechanism is not clear. The purpose of this study was to investigate effects of sevoflurane or halothane on contractions induced by high K+ and serotonin in the isolated canine basilar artery. Cylindrical segments of canine basilar artery were placed in Krebs solution oxygenated with 95% O2 and 5% CO2 at 37 degrees C. They were then constricted with cumulative administration of 10 to 60 mM KCl, or with 10(-9) to 10(-6) M serotonin and exposed to either sevoflurane or halothane at concentration of 1.0 and 2.0 MAC. Halothane and sevoflurane at concentration of 1.0 and 2.0 MAC decreased contractile responses evoked by KCl to a similar degree. The attenuation by either of the two anesthetics at concentration of 2.0 MAC were equivalent to the inhibitions by diltiazem 2 x 10(-7) M. Contractile responses to serotonin above 3 x 10(-7) M were depressed by halothane 1.0 MAC, but not by sevoflurane 1.0 MAC. Sevoflurane and halothane at concentration of 2.0 MAC decreased contractile responses evoked by serotonin at concentrations above 3 x 10(-8) M and 10(-8) M. Removal of the endothelium did not alter the response of the basilar artery contracted by serotonin to either anesthetic. These findings suggest that sevoflurane and halothane depress the voltage-dependent Ca2+ channels due to decreases of contractile responses to high K+. Our results also demonstrate that sevoflurane is a less potent vasodilator of the basilar artery contracted by serotonin than halothane.     

Sevoflurane or halothane anesthesia: can we tell the difference?

This study was performed to evaluate the ability of anesthesiologists to differentiate between sevoflurane, a newer, more expensive anesthetic, and halothane. A total of 113 assessments were made by 36 anesthesiologists on 58 children, aged 6 mo to 6 yr, scheduled for bilateral myringotomy and tube placement. All patients received midazolam (0.5 mg/kg per os) approximately 30 min before the induction of anesthesia. Sevoflurane or halothane was randomly selected for anesthetic induction and maintenance. The anesthesiologists, who were unaware of the anesthetic being used, were asked to identify the anesthetic based on clinical signs and to assess the quality of induction, speed of induction, and speed of emergence using a visual analog scale (VAS; minimum score = 0, maximum score = 100). The anesthesiologists correctly identified the anesthetic only 56.6% of the time. This was not significantly different from the 50% that would result from random guessing (P = 0.08). Further, there were no significant differences in VAS scores between the two groups. This study suggests that in premedicated pediatric patients undergoing brief surgical procedures, anesthesiologists cannot correctly differentiate between sevoflurane and halothane. The lack of significant differences in VAS scores suggests that the speed of induction, the speed of emergence, and the quality of induction are similar under these clinical conditions. Any purported benefits of sevoflurane seem to be of minor consequence under the circumstances studied. Implications: When the anesthetic halothane or sevoflurane is administered in a blind, randomized fashion, anesthesiologists could not reliably identify which drug was being used to anesthetize children for a brief surgical procedure. These results suggest that the differences between the two drugs in clinical practice are small and may not justify the additional cost of sevoflurane.     

Ultrasound-guided 1.2-mm cutting-needle biopsies of head and neck tumours

BACKGROUND: The direct effect of halothane on vascular smooth muscle is mediated in part via its effects on the sarcoplasmic reticulum (SR). Little information is available concerning the effects of other volatile anesthetics including isoflurane and sevoflurane, whose vascular effects differ from those of halothane. The aim of the present study was to compare the effects of halothane, isoflurane and sevoflurane on the SR by testing the contraction induced by caffeine in vascular smooth muscle. METHODS: Rings without endothelium from isolated canine mesenteric artery were mounted in physiological saline solution (PSS) for isometric tension recording. After complete depletion of Ca2+ from the SR by adding 35 mM caffeine, the rings were exposed to normal Ca2+ containing PSS (Ca2+ loading), to Ca(2+)-free PSS for 10 min, and then to 15 mM caffeine to induce contraction. Anesthetics were administered during Ca2+ loading, the Ca(2+)-free phase and simultaneously with caffeine administration. RESULTS: Halothane (0.5-2%) attenuated the caffeine-induced contraction of canine mesenteric artery when administered during Ca2+ loading in the SR (P < 0.001), whereas isoflurane and sevoflurane (1-4%) failed to affect the contraction. When given simultaneously with caffeine, halothane (1-2%) potentiated the caffeine-induced contraction (P < 0.05), but isoflurane and sevoflurane had no effect. When given before caffeine administration, halothane (0.5-2%), isoflurane (2-4%) and sevoflurane (4%) all potentiated the caffeine-induced contraction (P < 0.05). CONCLUSION: It has been shown that halothane not only potentiates caffeine-induced Ca2+ release from the SR, but also induces contraction by releasing Ca2+ from the SR. We conclude that halothane decreases Ca2+ accumulation in the SR while exerting facilitative and additive effects on caffeine-induced Ca2+ release from the SR when applied before caffeine administration and simultaneously with caffeine, respectively, whereas isoflurane and sevoflurane lack both the ability to decrease Ca2+ accumulation and an additive effect on caffeine-induced Ca2+ release from the SR, but are able to facilitate Ca2+ release by caffeine.     

Sevoflurane (SEVOrane) as an inhalation anesthetic in dogs in comparison with halothane and isoflurane

1969 Sevofluran was synthesized and in December 1995 licensed for clinical use in Germany. The low blood/gas partition coefficient is responsible for the fast uptake and elimination of sevoflurane. Sevoflurane does not irritate the airway. In human medicine no side effect of liver- and kidney function have been seen after sevofluran anaesthesia. There is low cardiovascular and respiratory depression caused by sevoflurane. In this study the use of sevoflurane in dogs should be tested and compared with isoflurane and halothane anaesthesia. All dogs were premedicated with /-methadon and diazepam. No significant depression of the cardiovascular system was seen. Neither kidney-nor hepatotoxic side effects could be found after sevoflurane, isoflurane and halothane anaesthesia. After sevoflurane anaesthesia the dogs woke up quietly and without any excitation and were able to stand on average ten minutes earlier after sevoflurane anaesthesia than after isoflurane and 85 minutes earlier than after halothane anaesthesia.     

Subtalar staple arthroereisis for planovalgus foot deformity in children with neuromuscular disease

This double-blinded study was undertaken to prospectively evaluate the role of halothane and sevoflurane and the use of IV ketorolac on the anesthetic emergence in a group of children undergoing bilateral myringotomy with pressure equalization tube procedures. Two-hundred ASA physical status I and II patients were premedicated with nasal midazolam (0.2 mg/kg) and randomized to one of four groups (Group 1 - halothane and ketorolac; Group 2 - halothane and placebo; Group 3 - sevoflurane and ketorolac; Group 4 - sevoflurane and placebo). A blinded nurse observer characterized the quality of the anesthetic emergence and recorded the incidence of emesis and the use of pain medications in the recovery room. There were no differences in age, weight, previous anesthetic experience, or duration of anesthesia among the four groups. There was no difference in the incidence of emergence agitation for patients anesthetized with sevoflurane compared with halothane, regardless of whether they received ketorolac or placebo. Regardless of the anesthetic, the incidence of emergence agitation was significantly less in patients who received ketorolac compared with patients who received placebo. The incidence of emesis in the recovery room, the total 24-h incidence of emesis, and the use of at-home pain medications were similar in all four groups. IMPLICATIONS: We conclude that the incidence of emergence agitation in children undergoing ultrashort anesthetic procedures is similar for sevoflurane and halothane and that ketorolac markedly diminishes emergence agitation and/or pain behavior.     

Evidence for regulation of the NADH peroxidase gene (npr) from Enterococcus faecalis by OxyR

To evaluate residual effects of inhalational anesthetics after reversal of neuromuscular blocking agent, neuromuscular function was monitored after halothane or sevoflurane anesthesia in thirty-seven patients (ASA physical status I or II) for elective surgery after obtaining informed consent. Electromyograph of the adductor pollicis muscle in response to train of four (TOF) stimulation was monitored throughout the study. The first twitch of TOF (T1; % of its control) and the ratio of the fourth twitch to the first twitch of TOF (T4/T1; TR) were recorded at 0, 2, 5, 10, and 15 min after reversal. The patients were divided into five groups; 1) the fentanyl group (n = 7) received fentanyl/N2O; 2) in the halothane stop group (n = 6), halothane was discontinued at least fifteen minutes before neostigmine administration; 3) in the halothane stable group (n = 7), 0.7% halothane was maintained until fifteen minutes after neostigmine; 4) in the sevoflurane stop group (n = 12), sevoflurane was discontinued fifteen minutes before the reversal; 5) in the sevoflurane stable group (n = 5), 3% sevoflurane was maintained until fifteen minutes after the reversal. Anesthesia was induced by thiopental 4 mg.kg-1 and suxamethonium 1 mg.kg-1 and the patients were intubated. After initial dose of vecuronium 0.1 mg.kg-1, the additional dose of 0.02 mg.kg-1 was administered to maintain T1 under 10% of the control value. At the end of the surgery atropine 0.015 mg.kg-1 and neostigmine 0.04 mg.kg-1 were administered to reverse vecuronium when T1 had recovered to 25% of its control. Halothane groups did not differ from fentanyl group. Recovery of T1 at 15 min was suppressed after discontinuation of sevoflurane (86.0 +/- 8.2%) in comparison with fentanyl (97.0 +/- 8.3%). Both T1 (75.4 +/- 12.2%) and TR (68.0 +/- 12.6%) at 15 min after the reversal during 3% sevoflurane inhalation were below those of the stable group. We conclude that the residual sevofulrane after discontinuation of inhalation may impair the neuromuscular transmission after the reversal of neuromuscular blockade. Neuromuscular function should be monitored after the end of anesthesia even though the patient is fully awake.     

Preservation of the ration of cerebral blood flow/metabolic rate for oxygen during prolonged anesthesia with isoflurane, sevoflurane, and halothane in humans

BACKGROUND: In several animal studies, an increase in cerebral blood flow (CBF) produced by volatile anesthetics has been reported to resolve over time during prolonged anesthesia. It is important to investigate whether this time-dependent change of CBF takes place in humans, especially in clinical situations where surgery is ongoing under anesthesia. In this study, to evaluate the effect of prolonged exposure to volatile anesthetics (isoflurane, sevoflurane, and halothane), the CBF equivalent (CBF divided by cerebral metabolic rate for oxygen (CMRO2) was determined every 20 min during anesthesia lasting more than 4h in patients. METHODS: Twenty-four surgical patients were assigned to three groups at random to receive isoflurane, sevoflurane, or halothane (8 patients each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 MAC before surgery and then 1.5 MAC for the 3 h of surgical procedure. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 60 mmHg, using phenylephrine infusion, if necessary. CBF equivalent was calculated every 20 min as the reciprocal of arterial-jugular venous oxygen content difference. RESULTS: CBF equivalent at 0.5 MAC of isoflurane, halothane, and sevoflurane was 21 +/- 4, 20 +/- 3, and 21 +/- 5 ml blood/ml oxygen, respectively. All three examined volatile anesthetics significantly (P<0.01) increased CBF equivalent in a dose-dependent manner (0.5, 1.0, 1.5 MAC). AT 1.5 MAC, the increase of CBF equivalent with all anesthetics was maintained increased with minimal fluctuation for 3 h. The mean value of CBF equivalent at 1.5 MAC in the isoflurane group (45 +/- 8) was significantly (P<0.01) greater than those in the halothane (32 +/- 8) and sevoflurane (31 +/- 8) groups. Electroencephalogram was found to be relatively unchanged during observation periods at 1.5 MAC. CONCLUSIONS: These results demonstrate that CBF/CMRO2 ratio is markedly increased above normal and maintained during prolonged inhalation of volatile anesthetics in humans. It is impossible to determine whether these data indicate a stable CBF or whether CBF and CMRO2 are changing in parallel during the observation period. The unchanging electroencephalographic pattern suggests that the former possibility is more likely and that the increase of CBF produced by volatile anesthetics is maintained over time without decay, which has been reported in several animal studies. It also is suggested that isoflurane possesses greater capability to maintain global CBF relative to CMRO(2) than does halothane or sevoflurane. time.)     

Relationships between Müller cells and neurons in a primitive tetrapod, the Australian lungfish

BACKGROUND: The cardiovascular side effects of volatile anesthetics are one of the chief causes of postoperative complications in children, and infants seem to be at the greatest risk for this. This study compared cardiovascular changes at equipotent concentrations of sevoflurane and halothane in infants. METHODS: Thirty infants classified as American Society of Anesthesiologists physical status I or II who required elective surgery were randomized to receive either halothane or sevoflurane for inhalation induction. Cardiovascular and echocardiographic data were recorded in both groups at baseline and at end-tidal concentrations of 1 and 1.5 minimum alveolar concentration (MAC). RESULTS: Sevoflurane did not alter heart rate or cardiac index at all concentrations compared with awake values. Sevoflurane significantly decreased blood pressure and systemic vascular resistance compared with awake values at all concentrations. Shortening fraction and rate-corrected velocity of circumferential fiber shortening decreased at 1.5 but not at 1 MAC. Myocardial contractility assessed by stress-velocity index and stress-shortening index decreased significantly at all concentrations, but did not fall into the abnormal range at any concentration. Halothane caused a greater decrease in heart rate, shortening fraction, stress-shortening index, velocity of circumferential fiber shortening, stress-velocity index, and cardiac index at all concentrations than did sevoflurane. CONCLUSION: Sevoflurane causes a lesser decrease in cardiac output than does halothane in infants.     

Sevoflurane has less effect than halothane on pulmonary afferent activity in the rabbit

We have compared the effects of sevoflurane and halothane on the discharge frequencies of 19 slowly adapting and four rapidly adapting lung receptors in the rabbit by recording from single vagal fibres. Both agents reduced the discharge frequency of slowly adapting receptors during expiration (P < 0.0005), halothane having a greater effect than sevoflurane (P < 0.0005). Neither agent had any effect on discharge frequency at the end of inspiration when discharge frequency is at a maximum. Neither agent affected the discharge frequency of rapidly adapting receptors.     

Effects of halothane on the phrenic nerve responses to carbon dioxide mediated by carotid body chemoreceptors in vagotomized dogs

BACKGROUND: Previous studies in dogs showed that the phrenic nerve response to an acute hypoxic stimulus was dose dependently depressed by 0.5-2.0 minimum alveolar concentration (MAC) of halothane but not abolished. Because a carbon dioxide stimulus is transduced by a different mechanism in the carotid body chemoreceptors (CBCRs) than is a hypoxic stimulus, inhalational anesthetics may preferentially depress one of these transduction processes, the central neuronal processing, or both, of the integrated responses to these two types of inputs. METHODS: Carotid body chemoreceptor stimulation was produced by short (1-1.5 s), bilateral, 100% carbon dioxide in saline infusions into the carotid arteries during neural inspiration in unpremedicated, halothane-anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. The phrenic neurogram quantified the neural inspiratory response. Four protocols were performed in the study: (1) the dose-dependent effects of halothane anesthesia (0.5-2.0 MAC) during hyperoxic hypercapnia on phrenic nerve activity, (2) the effects of three background levels of the partial pressure of carbon dioxide (PaCO2) on the magnitude of the carbon dioxide infusion responses at 1 MAC halothane, (3) the effects of anesthetic type on the magnitude of the carbon dioxide infusion response, and (4) the effects of CBCR denervation. RESULTS: Peak phrenic nerve activity (PPA) increased significantly during the carbon dioxide-stimulated phrenic burst in protocols 1-3; after denervation there was no response (protocol 4). Halothane produced a dose-dependent reduction in the PPA of control and carbon dioxide infusion-stimulated phrenic bursts and in the net carbon dioxide response. The net PPA responses for the different PaCO2 background levels were not different but were somewhat larger for sodium thiopental anesthesia than for 1.0 MAC halothane. CONCLUSIONS: The phrenic nerve response to an acute, severe carbon dioxide stimulus was dose dependently depressed by surgical doses of halothane. The observed responses to carbon dioxide infusion were mediated by the CBCRs because they were eliminated by CBCR denervation. These results suggest that the CBCR transduction and central transmission of the carbon dioxide signal in terms of inspiratory excitatory drive are not abolished at surgical levels of halothane anesthesia.     

No effects of high-dose omeprazole in patients with severe airway hyperresponsiveness and (a)symptomatic gastro-oesophageal reflux

Uptake of inhaled anesthetics may be measured as the amount of anesthetic infused to maintain a constant alveolar concentration of anesthetic. This method assumes that the patient absorbs all of the infused anesthetic, and that none is lost to circuit components. Using a standard anesthetic circuit with a 3-L rebreathing bag simulating the lungs, and simulating metabolism by input of carbon dioxide, we tested this assumption for halothane, isoflurane, and sevoflurane. Our results suggest that after washin of anesthetic sufficient to eliminate a material difference between inspired and end-tidal anesthetic, washin to other parts of the circuit (probably the ventilator) and absorbent (soda lime) continued to remove anesthetic for up to 15 min. From 30 min to 180 min of anesthetic administration, circuit components absorbed trivial amounts of isoflurane (12 +/- 13 mL vapor at 1.5 minimum alveolar anesthetic concentration, slightly more sevoflurane (39 +/- 15 mL), and still more halothane (64 +/- 9 mL). During this time, absorbent degraded sevoflurane (321 +/- 31 mL absorbed by circuit components and degraded by soda lime). The amount degraded increased with increasing input of carbon dioxide (e.g., the 321 +/- 31 mL increased to 508 +/- 48 mL when carbon dioxide input increased from 250 mL/min to 500 mL/min). Measurement of anesthetic uptake as a function of the amount of anesthetic infused must account for these findings. Implications: Systems that deliver inhaled anesthetics may also remove the anesthetic. Initially, anesthetics may diffuse into delivery components and the interstices of material used to absorb carbon dioxide. Later, absorbents may degrade some anesthetics (e.g., sevoflurane). Such losses may compromise measurements of anesthetic uptake.     

Prolonged sevoflurane, isoflurane and halothane anaesthesia in oxygen using rebreathing or non-rebreathing system in cats

Effects of prolonged sevoflurane, isoflurane and halothane anaesthesia in oxygen on clinical, cardiopulmonary, haematologic, and serum biochemical findings were compared in healthy, premedicated cats breathing spontaneously during 6 h of anaesthesia using rebreathing (semi-closed circuit) or non-rebreathing (Bain coaxial circuit) system. Recovery from anaesthesia with sevoflurane was more rapid than that with halothane or isoflurane in both systems. Respiration and heart rates during sevoflurane anaesthesia were similar to those during isoflurane rather than halothane anaesthesia in both systems. The degree of respiratory acidosis during prolonged sevoflurane anaesthesia was similar to that during isoflurane anaesthesia, and was less than that during halothane anaesthesia in both rebreathing and non-rebreathing systems. Prolonged sevoflurane anaesthesia induced mean arterial pressure similar to isoflurane or halothane anaesthesia in the non-rebreathing system, but it depressed mean arterial pressure less than isoflurane or halothane anaesthesia in the rebreathing system. Time related increase in the arterial carbon dioxide partial pressure was observed during halothane anaesthesia especially in the rebreathing system, however, no significant time-related changes in cardiopulmonary variables were observed during either sevoflurane or isoflurane anaesthesia in both systems. There were no significant differences among sevoflurane, isoflurane and halothane anaesthesia in serum biochemical values in both systems.     

Subjective, psychomotor, cognitive, and analgesic effects of subanesthetic concentrations of sevoflurane and nitrous oxide

BACKGROUND: Sevoflurane is a volatile general anesthetic that differs in chemical nature from the gaseous anesthetic nitrous oxide. In a controlled laboratory setting, the authors characterized the subjective, psychomotor, and analgesic effects of sevoflurane and nitrous oxide at two equal minimum alveolar subanesthetic concentrations. METHODS: A crossover design was used to test the effects of two end-tidal concentrations of sevoflurane (0.3% and 0.60%), two end-tidal concentrations of nitrous oxide (15% and 30%) that were equal in minimum alveolar concentration to that of sevoflurane, and placebo (100% oxygen) in 12 healthy volunteers. The volunteers inhaled one of these concentrations of sevoflurane, nitrous oxide, or placebo for 35 min. Dependent measures included subjective, psychomotor, and physiologic effects, and pain ratings measured during a cold-water test. RESULTS: Sevoflurane produced a greater degree of amnesia, psychomotor impairment, and drowsiness than did equal minimum alveolar concentrations of nitrous oxide. Recovery from sevoflurane and nitrous oxide effects was rapid. Nitrous oxide but not sevoflurane had analgesic effects. CONCLUSIONS: Sevoflurane and nitrous oxide produced different profiles of subjective, behavioral, and cognitive effects, with sevoflurane, in general, producing an overall greater magnitude of effect. The differences in effects between sevoflurane and nitrous oxide are consistent with the differences in their chemical nature and putative mechanisms of action.     

Relationship between anhedonia, affective dependency and autonomy in health subjects

OBJECTIVE: Medical mass spectrometers are configured to detect and measure specific respiratory and anesthetic gases. Unrecognized gases entering these systems may cause erroneous readings. We determined how the Advantage 1100 (Perkin-Elmer, now Marquette Gas Systems, Milwaukee, WI) and PPG-SARA (PPG Biomedical Systems, Lenexa, KS) systems that were not configured to measure desflurane or sevoflurane respond to increasing concentrations of these new potent volatile anesthetic agents. METHODS: Desflurane 0% to 18% in 3% increments or sevoflurane 0% to 7% in 1% increments in 5-L/min oxygen was delivered to the Advantage and PPG-SARA mass spectrometry systems. For each concentration of each agent, the displayed gas analysis readings and uncompensated collector plate voltages were recorded. RESULTS: The Advantage 1100 system read both desflurane and sevoflurane mainly as enflurane and, to a lesser extent, as carbon dioxide and isoflurane. For enflurane(E) readings < 9.9%, the approximate relationships are: %Desflurane = 1.6E; %Sevoflurane = 0.3E. These formulas do not apply if E > 9.9% because of saturation of the summation bus. PPG-SARA read desflurane mainly as isoflurane(I) and, to a lesser extent, as nitrous oxide. PPG-SARA read sevoflurane mainly as enflurane(E) and, to a lesser extent, as nitrous oxide and halothane. The approximate relationships are: %Desflurane = 1.11 (for I < 9%); %Sevoflurane = 2.1E. CONCLUSIONS: Advantage 1100 and PPG-SARA systems not configured for desflurane or sevoflurane display erroneous anesthetic agent readings when these new agents are sampled. Advantage 1100 also displays falsely elevated carbon dioxide readings when desflurane is sampled.     

Pulmonary vasodilator response to adenosine triphosphate-sensitive potassium channel activation is attenuated during desflurane but preserved during sevoflurane anesthesia compared with the conscious state

BACKGROUND: The objective of this study was to investigate the effects of sevoflurane and desflurane anesthesia on the pulmonary vasodilator response to the adenosine triphosphate-sensitive potassium channel agonist, lemakalim, compared with the response measured in the conscious state. In addition, the authors assessed the extent to which sympathetic alpha1-adrenoreceptor inhibition and cyclooxygenase pathway inhibition modulate the vasodilator response to lemakalim. METHODS: Twenty-four conditioned male mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow relationship. After preconstriction with the thromboxane analogue, U46619, dose-response relationships to lemakalim were assessed on separate days in the conscious state and during sevoflurane (approximately 3.5% end-tidal) and desflurane (approximately 10.5% end-tidal) anesthesia (approximately 1.5 minimum alveolar concentration for each anesthetic agent). The effects of sympathetic alpha1-adrenoreceptor inhibition (prazosin) and cyclooxygenase inhibition (indomethacin) on the pulmonary vasodilator response to lemakalim also were assessed in the conscious and desflurane-anesthetized states. RESULTS: Neither sevoflurane nor desflurane had a net effect on the baseline left pulmonary vascular pressure-flow relationship compared with the conscious state. The magnitude of the pulmonary vasodilator response to lemakalim was preserved during sevoflurane anesthesia but was attenuated (P < 0.05) during desflurane anesthesia compared with the conscious state. The attenuated lemakalim-induced vasodilator response during desflurane anesthesia was partially reversed (P < 0.05) by pretreatment with prazosin but not indomethacin. CONCLUSION: These results indicate that adenosine triphosphate-sensitive potassium channel-mediated pulmonary vasodilation is preserved during sevoflurane anesthesia but is attenuated during desflurane anesthesia. The attenuated response to adenosine triphosphate-sensitive potassium channel activation during desflurane anesthesia is partially mediated by reflex sympathetic alpha1-adrenoreceptor vasoconstriction.     

Roles of Rho-associated kinase in cytokinesis; mutations in Rho-associated kinase phosphorylation sites impair cytokinetic segregation of glial filaments

The effects of sevoflurane on myocardial contraction and relaxation are poorly understood. Therefore, we studied the effects of equianaesthetic concentrations (0.5, 1, 1.5, 2 and 2.5 MAC) of sevoflurane, isoflurane and halothane on inotropic and lusitropic (myocardial relaxation) variables, and post-rest potentiation in rat left ventricular papillary muscles in vitro. Sevoflurane and isoflurane caused comparable concentration-dependent negative inotropic effects which were significantly lower than those induced by halothane (P < 0.05). Sevoflurane and isoflurane did not modify lusitropic variables under low or high load, whereas halothane showed a negative lusitropic effect at high concentrations. Halothane suppressed post-rest potentiation, whereas isoflurane and sevoflurane did not. Post-rest recovery was unaffected by halothane, isoflurane or sevoflurane at any concentration. Thus in rat myocardium, sevoflurane and isoflurane caused comparable negative inotropic effects, had no significant lusitropic effects and did not alter post-rest potentiation, suggesting that they did not significantly modify the functions of the sarcoplasmic reticulum.     

Preservation of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane anesthesia compared to the conscious state in chronically instrumented dogs

BACKGROUND: The authors' objective was to assess the extent to which sevoflurane and desflurane anesthesia alter the magnitude of hypoxic pulmonary vasoconstriction compared with the response measured in the same animal in the conscious state. METHODS: Left pulmonary vascular pressure-flow plots were generated in seven chronically instrumented dogs by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right main pulmonary artery. Pressure-flow plots were generated during normoxia and hypoxia on separate days in the conscious state, during sevoflurane (approximately 3.5% end-tidal), and during desflurane (approximately 10.5% end-tidal) anesthesia. Values are mean+/-SEM. RESULTS: In the conscious state, administration of the hypoxic gas mixture by conical face mask decreased (P < 0.01) systemic arterial PO2 from 94+/-2 mmHg to 50+/-1 mmHg and caused a leftward shift (P < 0.01) in the pressure-flow relationship, indicating pulmonary vasoconstriction. The magnitude of hypoxic pulmonary vasoconstriction in the conscious state was flow-dependent (P < 0.01). Neither anesthetic had an effect on the baseline pressure-flow relationship during normoxia. The magnitude of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane was also flow-dependent (P < 0.01). Moreover, at any given value of flow the magnitude of hypoxic pulmonary vasoconstriction was similar during sevoflurane and desflurane compared with the conscious state. CONCLUSION: These results indicate that hypoxic pulmonary vasoconstriction is preserved during sevoflurane and desflurane anesthesia compared with the conscious state. Thus, inhibition of hypoxic pulmonary vasoconstriction is not a general characteristic of inhalational anesthetics. The flow-dependent nature of the response should be considered when assessing the effects of physiologic or pharmacologic interventions on the magnitude of hypoxic pulmonary vasoconstriction.     

Neuromuscular effects of rocuronium during sevoflurane, isoflurane, and intravenous anesthesia

The potency and time course of action of rocuronium were studied in patients anesthetized with 66% nitrous oxide in oxygen and 1.5 minimum alveolar anesthetic concentration of sevoflurane or isoflurane, or a propofol infusion. Potency was estimated by using the single-bolus technique. Neuromuscular block was measured by stimulation of the ulnar nerve and by recording the force of contraction of the adductor pollicis muscle. The mean (95% confidence limits) of the 50% and 95% effective doses were estimated tobe 142 (129-157) and 265 (233-301) microg/ kg, 165 (146-187) and 324 (265-396) microg/kg, and 183 (163-207) and 398 (316-502) microg/kg during sevoflurane, isoflurane, and propofol anesthesia, respectively (P < 0.05 for sevoflurane versus propofol). The mean +/- SD times to onset of maximal block after rocuronium 0.6 mg/kg were 0.96 +/- 0.16, 0.90 +/- 0.16, and 1.02 +/- 0.15 min during sevoflurane, isoflurane, and propofol anesthesia, respectively. The respective times to recovery of the first response in the train-of-four (TOF) stimulation (T1) to 25% and 90% were 45 +/- 13.1 and 83 +/- 29.3 min, 35 +/- 6.1 and 56 +/- 15.9 min, and 35 +/- 9.2 and 55 +/- 19.4 min. The times to recovery of the TOF ratio to 0.8 were 103 +/- 30.7, 69 +/- 20.4, and 62 +/- 21.1 min, and the 25%-75% recovery indices were 26 +/- 11.7, 12 +/- 5.0, and 14 +/- 6.9 min, respectively. There were no differences among groups in the times for onset of action or to recovery of T1 to 25%. However, the times for recovery of T1 to 90%, TOF ratio to 0.8, and recovery index in the sevoflurane group were all significantly longer compared with the other two groups (P < 0.05, < 0.01, and < 0.01, respectively). We conclude that the effects of rocuronium, especially duration of action, are significantly enhanced during sevoflurane compared with isoflurane and propofol anesthesia. IMPLICATIONS: In routine clinical use, the effects of rocuronium are enhanced by sevoflurane, in comparison with isoflurane and propofol anesthesia, and the recovery is slower. Particular attention should be paid to monitoring of neuromuscular block during sevoflurane anesthesia.