Effects of enflurane and isoflurane on resistance to reabsorption of cerebrospinal fluid in dogs

Using the technique of ventriculocisternal perfusion, resistance to reabsorption of cerebrospinal fluid (Ra) was calculated from determinations of the rate of reabsorption of cerebrospinal fluid (Va) at differing cerebrospinal fluid pressures in dogs. Ra was examined during prolonged anesthesia (5.0-6.0 h) with enflurane (2.2%, end expired) or isoflurane (1.4%, end expired). Compared with previously reported normal values for Ra in dogs (220-224 cmH2O . ml-1 . min), enflurane increased Ra to 274 +/- 4 cmH2O . ml-1 . min (mean +/- SEM), and isoflurane decreased Ra to 104 +/- 1 cmH2O . ml-1 . min. The alterations of cerebrospinal fluid (CSF) dynamics caused by enflurane, namely increase of both Ra and the rate of production of cerebrospinal fluid (Vf), may contribute to the sustained increase of intracranial pressure observed during prolonged anesthesia with enflurane. In contrast, the different alterations of CSF dynamics caused by isoflurane, namely decrease of Ra with no change in Vf, may explain, in part, why minimal increase of intracranial pressure is observed during prolonged anesthesia with isoflurane. Because decreased Ra improves spatial compensation by cerebrospinal fluid volume for increased intracranial pressure, isoflurane may offer an advantage over enflurane in patients at risk because of increased intracranial pressure.     

Effect of sevoflurane on intracranial pressure, sagittal sinus pressure, and the intracranial volume-pressure relation in cats

The effect of sevoflurane on intracranial pressure (ICP), sagittal sinus pressure (SSP), and the intracranial volume-pressure (V-P) relation was examined in cats. In experiment 1, on nine cats, changes in ICP and SSP were studied for 180 min during anesthesia with 1 MAC sevoflurane (2.6%, inspired) and 50% nitrous oxide (N2O) in oxygen (O2). ICP significantly (p <0.01) increased from 8.4 +/- 3.8 cm H2O (mean +/- SD), the control level to 10.6 +/- 5.1 cm H2O immediately after the administration of sevoflurane. ICP was unchanged for the subsequent 120 min but then increased significantly (p <0.05) 140 min after administration, being 15.5 +/- 9.0 cm H2O at 180 min. There were no changes in SSP or blood gases. In experiment 2, the rapid injection technique of mock cerebrospinal fluid was used to determine the intracranial V-P relation in ten cats. Measures of V-P relationships included (a) ICP before volume injection (Po), (b) peak ICP caused by volume injection (Pp), (c) intracranial compliance (C) calculated as the ratio of change of intracranial volume Delta V) to change of ICP (Delta P), and (d) the pressure volume index (PVI) calculated as the ratio of Delta V to log Pp/Po. The subjects were divided into two groups, one administered 2.6% sevoflurane and 50% N2O in O2 (n = 6) and the other 50% N2O in O2 (n = 4). Each cat in both groups was given two bolus injections into the lateral ventricle at 180 min after the start of anesthesia. Then, C and PVI were calculated. C and PVI in the group treated with sevoflurane were significantly (p <0.05) lower than in the other group. These findings suggest that prolonged use of sevoflurane increases the intracranial elastance.     

Effects of 0.5 and 1.0 MAC isoflurane,sevoflurane and desflurane on intracranial and cerebral perfusion pressures in children

BACKGROUND: Isoflurane has been a commonly used agent for neuroanesthesia, but newer agents, sevoflurane and desflurane, have a quicker onset and shorter emergence from anesthesia and are increasingly preferred for general pediatric anesthesia. But their effects on intracranial pressure (ICP) and cerebral perfusion pressure (CPP), especially in pediatric patients with already increased ICP, have not been well documented. METHODS: We studied 36 children scheduled for elective implantation of an intraparenchymal pressure device for 24 h monitoring for suspected elevated ICP. After a standardized intravenous anesthesia, the patients were moderately hyperventilated with 60% nitrous oxide (N2O) in oxygen. The patients were then randomized to receive 0.5 and 1.0 MAC of isoflurane (Group I, n = 12), sevoflurane (Group S, n = 12) or desflurane (Group D, n = 12) in 60% N2O in oxygen. Respiratory and hemodynamic variables, ICP and CPP were recorded at baseline and after exposure to a target level of test drug for 10 min or until CPP fell below 30 mmHg (recommended lower ICP level is 25 mmHg in neonates, rising to 40 mmHg in toddlers). RESULTS: When comparing baseline values with values at 1.0 MAC, mean arterial pressure (MAP) decreased (P < 0.001) in all groups, with no differences between the groups. ICP increased (P < 0.001) with all agents, mean +2, +5, and +6 mmHg in Group I, S and D, respectively, with no differences between the groups. Regression analyzes found no relationship between baseline ICP and the increases in ICP from baseline to 1.0 MAC for isoflurane or sevoflurane. However, increased baseline ICP tended to cause a higher ICP increase with 1.0 MAC desflurane; regression coefficient +0.759 (P = 0.077). The difference between regression coefficients for Group I and Group D were not significant (P = 0.055). CPP (MAP-ICP) decreased (P < 0.001) in all groups, mean -18, -14 and -17 mmHg in Group I, S and D, respectively, with no significant difference between the groups. CONCLUSIONS: 0.5 and 1.0 MAC isoflurane, sevoflurane and desflurane in N2O all increased ICP and reduced MAP and CPP in a dose-dependent and clinically similar manner. There were no baseline dependent increases in ICP from 0 to 1.0 MAC with isoflurane or sevoflurane, but ICP increased somewhat more, although statistically insignificant, with higher baseline values in patients given desflurane. The effect of MAP on CPP is 3-4 times higher than the effect of the increases in ICP on CPP and this makes MAP the most important factor in preserving CPP. In children with known increased ICP, intravenous anesthesia may be safer. However, maintaining MAP remains the most important determinant of a safe CPP.     

The nonlinear contribution of nitrous oxide at sub-MAC concentrations to enflurane MAC in rats

The presumed linear relationship describing the contribution of nitrous oxide (N2O) to the enflurane requirement necessary to achieve a 1.0 MAC level of anesthesia was tested in rats (N = 84). Each rat received one of six different concentrations of N2O, and enflurane was adjusted to attain 1.0 MAC with the use of a standard tail clamp method. The resultant group MAC anesthetic concentrations were Group I-N2O = 0.0%, enflurane = 2.30%; Group II-N2O = 10.4%, enflurane = 2.19%; Group III-N2O = 30.7%, enflurane = 1.85%; Group IV-N2O = 61.8%, enflurane = 1.75%; Group V-N2O = 70.9%, enflurane = 1.56%; and Group VI-N2O = 80.3%, enflurane = 1.54%. Increasing the N2O concentration from 0-10%, from 30-60%, or 70-80% did not significantly decrease the enflurane requirement; however, increasing the N2O concentration from 10-30% or 60-70% produced a significant decrease (P less than 0.05) in the concentration of enflurane required for 1.0 MAC of anesthesia. Thus, in rats, increasing the concentration of N2O in sub-MAC ranges did not produce a linear decrease in the enflurane concentration required to add up to 1.0 MAC of anesthesia. These results are consistent with a dose-dependent interaction between N2O and the excitatory properties of enflurane; this interaction could represent synergism at low concentrations or antagonism at higher concentration of N2O.     

The effects of sevoflurane and isoflurane on intracranial pressure and cerebral perfusion pressure after diffuse brain injury in rats

Twenty-four adult male Wistar rats, weighing 220 to 290 g, were anesthetized with 30 mg/kg intraperitoneal sodium thiopental, then underwent a tracheostomy. After diffuse impact-acceleration brain injury (BI) was induced, each rat was paralyzed and mechanically ventilated with 30% O2 in nitrous oxide (N2O). The rats were assigned randomly to two groups, each of which received one of the two volatile anesthetic agents, sevoflurane or isoflurane. The anesthetics were administered at 0.5, 0.75, 1.0, and 1.25 minimal alveolar concentration (MAC) for 30 minutes each, respectively, and anesthesia was maintained at 0.75 MAC during the last hour of the study period. Intracranial pressure (ICP), mean arterial pressure (MAP), rectal and intrahemispheric temperatures, and end-tidal volatile anesthetic concentrations were monitored continuously throughout the 3 hours, with measurements recorded every 15 minutes. At baseline, there were no significant differences between the two groups regarding the monitored physiologic values. In the sevoflurane group, MAP fell significantly after 45 minutes, and a similar change was observed in the isoflurane group after 30 minutes (P < .05, P < .01, and P < .001, respectively). Intracranial pressure increased significantly at 45 minutes in the sevoflurane group (P < .01) and remained elevated from 60 minutes until the end of the study period (P < .01, P < .001). Although ICP increased in the isoflurane group, the change was not significant. Cerebral perfusion pressure (CPP) decreased in parallel with MAP, with the reduction in the sevoflurane group being more pronounced than that in the isoflurane group. The results demonstrated that, under the conditions of diffuse BI, animals that were anesthetized with sevoflurane had higher ICP and lower CPP levels than those anesthetized with isoflurane.     

Failure of enflurane in altering renal responses to acute intracranial pressure increases

The effects of acute increases of intracranial pressure (ICP) on renal function before and during enflurane and enflurane-N2O anesthesia were determined in 12 mongrel dogs. Prior to anesthesia, acute elevations of 10 and 20 torr in ICP significantly increased urine osmolarity (Uosm), mean arterial blood pressure (MAP), and renal vascular resistance (RVR); significantly decreased urine volume (U vol), para-aminohippurate clearance (Cpah), and free water clearance (C/20); and had no effect on inuline clearance (Cin) or plasma levels of antidiuretic hormone (ADH). Thirty minutes of enflurane (2.2 percent end-tidal concentration) in 70 percent nitrogen and O2 in the presence of normal ICP caused significant increases in Uosm while MAP, CPAH, UVOL CH20, CIN, and osmolar clearance (CosM) were significantly decreased and ADH was unchanged. Substituting 70 percent N2O for nitrogen had no significant effect on any variable measured. Increasing ICP 10 torr during enflurane-N-2O anesthesia caused significant increases (compared to enflurane-N2O values in the presence of normal ICP) in UosM, RVR, and CosM, as well as significant decreases in UVOL, CH2O, AND CPAH, but had no effect on ADH, CIN, or MAP. Enflurane and N2O anesthesia moderates the elevation MAP in response to an acute increase in ICP but fails to alter the renal response to increased ICP.     

比较七氟醚、异氟醚和安氟醚对颅内压的影响

目的：为了观察七氟醚对颅内压的影响。方法：选择２４例颅内肿胶病人,测定七氟醚麻醉的时颅内压变化并与异氟醚和安氟醚进行比较。术前用药、麻醉诱导及维持的静脉用药相同。于Ｌ３－４穿刺蛛网膜睛腔测脑脊液压（代表颅内压,ＩＣＰ）。依吸入药不同随机分为七的氟醚（Ｓ）组,异氟醚（１）组和安氟醚（Ｅ）组,监测ＢＰ、ＭＡＰ、ＥＣＧ、ＳｐＯ２、ＰＥＴ、ＣＯ２和ＭＡＣ,调整ＶＴ和ＲＲａＣＯ２维持在４～４．６６ＫＰＡ。三     

Concentrations of sevoflurane with and without nitrous oxide to block vasomotor reflexes to incision (MACBVR)

The minimum alveolar concentration of an anesthetic that blocks the skin vasomotor reflex to surgical incision (MACBVR) for sevoflurane was determined in 37 patients aged 30-60 years scheduled for laparotomies with or without nitrous oxide. Thirty seven patients were randomly allocated to one of the two groups: a sevoflurane group and a sevoflurane/N2O (50 vol%) group. The skin blood flow of the finger tip was measured using a laser Doppler flowmeter. Anesthesia was induced with sevoflurane and N2O and tracheal intubation was facilitated with vecuronium 0.1 mg.kg-1. Predetermined end tidal concentrations of sevoflurane and N2O were maintained for at least 15 min before incision. The MACBVR values of sevoflurane in O2 and in the presence of 50% N2O were 3.07% and 1.63%, respectively. The MACBVR level in the total anesthetic MAC multiple was 1.75 MAC for sevoflurane alone and the value decreased to 1.43 MAC when 50% N2O was used. There were no relations between the amplitude of the reduction in skin blood flow and the changes of hemodynamic variables in each group. However, the changes in SBP and HR at incision were significantly suppressed by addition of N2O (changes in SBP and HR: 41.6 +/- 20.4 mmHg and 35.4 +/- 12.5 bpm in the sevoflurane group vs. 24.6 +/- 10.2 mmHg and 18.1 +/- 9.5 bpm in the sevoflurane/N2O group, P < 0.01). The results suggest that N2O is useful to suppress adrenergic responses to a surgical stimulus during sevoflurane anesthesia.     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

The anticonvulsant effects of volatile anesthetics on lidocaine-induced seizures in cats

Large concentrations of sevoflurane and isoflurane, but not halothane, induce spikes in the electroencephalogram. To elucidate whether these proconvulsant effects affect lidocaine-induced seizures, we compared the effects of sevoflurane, isoflurane, and halothane in cats. Fifty animals were allocated to 1 of 10 groups: 70% nitrous oxide (N2O), 0.6 minimum alveolar anesthetic concentration (MAC) + 70% N2O, 1.5 MAC + 70% N2O, and 1.5 MAC of each volatile agent in oxygen. Lidocaine 4 mg x kg(-1) x min(-1) was infused IV under mechanical ventilation with muscle relaxation. Electroencephalogram in the cortex, amygdala, and hippocampus and multiunit activities in the midbrain reticular formation (R-MUA) were recorded. Lidocaine induced spikes first from the amygdala or hippocampus in the 70% N2O and halothane groups and from the cortex in the sevoflurane and isoflurane groups. Lidocaine induced seizures in all cats in the 70% N2O and 0.6 MAC + N2O groups. Seizure occurrence was reduced in the 1.5 MAC + N2O group (P < 0.05 versus 70% N2O). The onset of seizure was delayed in the 0.6 MAC + N2O and 1.5 MAC groups for sevoflurane and isoflurane, but not for halothane, compared with the 70% N2O group (P < 0.05). Lidocaine increased R-MUA with seizure by 130%+/-56% in the 70% N2O group. The increase of R-MUA with seizure was more suppressed in the volatile anesthetic groups than in the 70% N2O group (P < 0.05). In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased. IMPLICATIONS: Increasingly, epidural blockade is combined with general anesthesia to achieve stress-free anesthesia and continuous pain relief in the postoperative period. In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased.     

Rate of CSF formation and resistance to reabsorption of CSF during sevoflurane or remifentanil in rabbits

Information on the effects of sevoflurane on the rate of cerebrospinal fluid (CSF) formation (Vf) and resistance to reabsorption of CSF (Ra) is incomplete, and no such information is available for remifentanil. The present study examined the dose-related effects of sevoflurane and remifentanil on Vf and Ra in rabbits. Eight rabbits were studied during isoflurane 1.4% (baseline) and sevoflurane 1.4%, 2.5%, and 3.7%, and eight were studied during isoflurane 1.4% (baseline) and remifentanil 0.30, 0.67, and 1.00 microg x kg(-1) x min(-1) in randomized order. Ventriculocisternal perfusion at two CSF pressure states for each experimental condition was used to determine Vf and Ra. There was no dose-response relation for Vf (10.4+/-2.5, 9.0+/-2.0, and 10.0+/-3.0 microl x min(-1)) or Ra (0.81+/-0.33, 1.35+/-0.54, and 0.84+/-0.27 cm H2O x microl(-1) x min) between the three sevoflurane concentrations. There also was no dose-response relation for Vf (7.8+/-1.2, 8.8+/-3.0, and 6.5+/-2.3 microl x min(-1)) or Ra (1.07+/-0.54, 1.23+/-0.50, and 1.13+/-0.51 cm H2O x microl(-1) x min) between the three remifentanil doses. Vf and Ra during either sevoflurane or remifentanil were not significantly different from Vf and Ra during the two isoflurane baseline conditions (Vf = 8.5+/-2.5 and 9.8+/-1.3 microl x min(-1), and Ra = 0.97+/-0.36 and 1.38+/-0.55 cm H2O x microl(-1) x min, mean +/- SD). Vf and Ra are of interest because they influence CSF volume, intracranial pressure, and/or intracranial elastance. In our model, sevoflurane or remifentanil did not significantly alter Vf or Ra.     

Respiratory effects of nitrous oxide during halothane or enflurane anaesthesia in children

The respiratory effects of nitrous oxide (N2O) were studied during halothane and enflurane anaesthesia in 12 children (mean age 46.4 +/- 29.3 months, mean weight 15.3 +/- 4.2 kg) during surgery under continuous extradural anaesthesia. Four equipotent anaesthetic states were studied in random order: 1) halothane 1 MAC in oxygen, 2) halothane 0.5 MAC + 50% N2O, 3) enflurane 1 MAC in oxygen, 4) enflurane 0.5 MAC +50% N2O. End-tidal fractions of CO2 (PetCO2) and halothane and enflurane were measured using infrared analysers. The respiratory variables (tidal volume VT, minute ventilation VE, respiratory frequency F, inspiratory time Ti, mean inspiratory flow VI, effective inspiratory time Ti/Ttot) were measured using a pneumotachograph. Significant changes were observed between the four states for VE, VI, F and PetCO2, whereas the values of VT, Ti and Ti/Tot did not differ significantly. The respiratory depressant effect of 1 MAC of either halothane alone or of the mixture of halothane and N2O was very similar. During enflurane anaesthesia, PetCO2 was less increased when N2O was substituted for enflurane, owing to a significant increase in respiratory frequency. A marked decrease in VE together with an increase in PetCO2 was observed during enflurane anaesthesia (states 3 and 4) when compared to the corresponding states during halothane anaesthesia (states 1 and 2). The respiratory depressant effect of enflurane is greater than that of halothane in unpremedicated children, even when substituting N2O for an equal MAC fraction of enflurane.2+ The effect of N2O on respiratory patterns seems to depend on the inhalational agent used and/or on the vesting respiratory frequency.     

Xenon suppresses the hypnotic arousal in response to surgical stimulation.

STUDY OBJECTIVE: To evaluate the suppressive effects of xenon (Xe) on hypnotic arousal at skin incision. DESIGN: Prospective, randomized study. SETTING: Operating rooms at a university hospital. PATIENTS: 35 ASA physical status I and II patients presenting for elective lower abdominal surgery. INTERVENTIONS: Patients were randomly assigned to receive one of the following regimens: 1.3 minimum alveolar concentration (MAC) isoflurane, 1.3 MAC sevoflurane, 0.7 MAC Xe with 0.6 MAC sevoflurane, 1 MAC Xe with 0.3 MAC sevoflurane, or 0.7 MAC nitrous oxide (N2O) with 0.6 MAC sevoflurane (n = 7 each group). MEASUREMENTS AND MAIN RESULTS: The bispectral index (BIS) was measured at baseline, during anesthesia, and after skin incision. BIS increased significantly at skin incision from the values noted during anesthesia in the sevoflurane and N2O groups, whereas it remained stable at incision in the other three groups (mean change in BIS: 0 +/- 9 for isoflurane, 15 +/- 8 for sevoflurane, 5 +/- 6 for 0.7 MAC Xe, 4 +/- 11 for 1 MAC Xe, and 9 +/- 5 for N2O). CONCLUSIONS: Unlike N2O, Xe was able to suppress hypnotic arousal in response to surgical stimulation when administered with sevoflurane.     

Single-breath induction of anesthesia: comparison of enflurane and sevoflurane

In this study induction of anesthesia using the single-breath technique with either enflurane or sevoflurane in oxygen was compared. Each group consisted of 16 unpremedicated volunteers who breathed approximately 1.7 minimum alveolar concentration (MAC) equivalents of either vapor. There were no significant differences in the cardiovascular and respiratory variables monitored. The induction of anesthesia with enflurane (141±41 s) required significantly more time than with sevoflurane (118±25 s). The enflurane group was associated with significantly more problems during induction, and showed moderate or sometimes severe excitatory movements of the extremities and/or coughing. Subjects in the enflurane group described the induction of anesthesia as less pleasant than in the sevoflurane group. We concluded that enflurane was less suitable for single-breath induction of anesthesia compared with sevoflurane.     

Effects of sevoflurane and isoflurane on electrocorticographic activities in patients with temporal lobe epilepsy.

To compare the neuroexcitatory effects of sevoflurane and isoflurane, we recorded electrocorticograms (ECoG) during wakefulness and during sevoflurane and isoflurane anesthesia in six patients with temporal lobe epilepsy (TLE). These patients had subdural grid electrodes chronically implanted in the temporal region. During sevoflurane anesthesia at 1.5 minimum alveolar concentration (MAC) of the combination with 67% nitrous oxide (N2O), a marked increase in interictal paroxysmal activities was observed in four patients. Two patients had a slight increase in paroxysmal activities. Activated areas were widely distributed, not being confined to the ictal onset zone of spontaneous seizures. However, isoflurane anesthesia at 1.5 MAC of the combination with 67% N2O was associated with less increased paroxysmal activity. While the neuroexcitatory properties of sevoflurane proved greater than those of isoflurane, the widespread irritative response to sevoflurane administration was not helpful in localizing the epileptogenic area.     

Decreased respiratory depression during emergence from anesthesia with sevoflurane/N2O than with sevoflurane alone

PURPOSE: To investigate ventilation and gas elimination during the emergence from inhalational anesthesia with controlled normoventilation with either sevoflurane/N2O or sevoflurane alone. METHODS: Twenty-four ASA I-II patients scheduled for abdominal hysterectomy were randomly allocated to receive either 1.3 MAC sevoflurane/N2O (n = 12) or equi-MAC sevoflurane (n = 12) in 30% oxygen (O2). Expired minute ventilation volumes (V(E)), end-tidal (ET) concentrations of O2, carbon dioxide (CO2), sevoflurane and N2O as well as pulse oximetry saturation (SpO2) and CO2 elimination rates (VCO2) were measured. The ET concentrations of sevoflurane and N2O were converted to total MAC values and gas elimination was expressed in terms of MAC reduction. Time to resumption of spontaneous breathing and extubation were recorded and arterial blood gas analysis was performed at the end of controlled normoventilation and at the beginning of spontaneous breathing. RESULTS: Resumption of spontaneous breathing and extubation were 8 and 13 min less, respectively, in the sevoflurane/N2O than in the sevoflurane group. Spontaneous breathing was resumed in both groups when pH had decreased by 0.07-0.08 and PaCO2 increased by 1.3-1.5 kPa. Depression of V(E) and VCO2 were less, and MAC reduction more rapid in the sevoflurane/N2O than in the sevoflurane group. CONCLUSIONS: Respiratory recovery was faster after sevoflurane/N2O than sevoflurane anesthesia. Changes in pH and PaCO2 rather than absolute values were important for resumption of spontaneous breathing after controlled normoventilation. In both groups, the tracheas were extubated at about 0.2 MAC.     

Effects of enflurane, isoflurane, and sevoflurane on renal tubular functions]

Twenty-seven patients without renal disease were divided randomly into three groups of each nine patients. Each group received either enflurane, isoflurane or sevoflurane. The renal tubular functions were examined during anesthesia and on the first postoperative day. By inhalation of 1.49 MAC hours of enflurane, 2.17 MAC hours of isoflurane or 1.29 MAC hours of sevoflurane, creatinine clearance, Na excretion rate, urine beta 2-microglobulin and urine N-acetyl-beta-D-glucosaminidase showed no significant changes during anesthesia and the during postoperative period among anesthetic agents used. These results indicate that enflurane, isoflurane or sevoflurane does not affect renal tubular function specifically under anesthesia when each was given for less than four hours.     

The dose-response relationship of mivacurium chloride in humans during nitrous oxide-fentanyl or nitrous oxide-enflurane anesthesia

The dose-response relationships of mivacurium chloride during N2O/fentanyl or N2O/enflurane anesthesia were compared in 70 patients intraoperatively. Responses were defined in terms of percentage changes in the evoked twitch tension of the adductor pollicis muscle, and dose-response curves were constructed following probit transformation of the responses. End-tidal concentrations of enflurane during the were study were 0.9-1.2%. When compared with the dose-response curve determined during N2O/fentanyl anesthesia the curve determined during N2O/enflurane anesthesia was displaced significantly to the left (P less than 0.05). As a result, the doses of mivacurium that depressed twitch tension by 50% (ED50) and 95% (ED95) were 39 and 67 micrograms/kg, respectively, during N2O/fentanyl anesthesia, and 27 and 52 micrograms/kg during N2O/enflurane anesthesia. Regression lines describing the relationship between the maximum depression of twitch tension (response) and the time interval between the injection of mivacurium and the return of twitch tension to 90% of the control value (duration) were constructed. The response-duration line for N2O/enflurane anesthesia was displaced significantly to the left of the line for N2O/fentanyl (P less than 0.05), indicating that enflurane anesthesia was associated with a prolongation of mivacurium-induced neuromuscular blockade. The neuromuscular blocking effect of mivacurium is both enhanced by and prolonged during N2O/enflurane compared with that during N2O/fentanyl anesthesia.     

Plasma inorganic fluoride with sevoflurane anesthesia: correlation with indices of hepatic and renal function.

The biotransformation and plasma inorganic fluoride ion production of sevoflurane (the new volatile anesthetic) during and after surgical anesthesia was studied in 50 ASA I or II surgical patients. Twenty-five additional patients served as controls by receiving isoflurane. Sevoflurane or isoflurane was administered with a semiclosed (total gas flow, 2 L/min O2) circle absorption system for durations of 1.0 to greater than 7.0 minimal alveolar concentration (MAC) hours for surgical anesthesia (sevoflurane MAC, 2.05%; isoflurane MAC, 1.15%). Preoperative and postoperative blood urea nitrogen and creatinine concentrations were determined. Blood samples were obtained during and after anesthesia in both groups for determining anesthetic blood concentration analysis and plasma fluoride level. Plasma fluoride concentrations did not significantly increase during isoflurane anesthesia. Sevoflurane biotransformation produced a mean peak plasma inorganic fluoride concentration of 29.3 +/- 1.8 mumol/L, 2 h after anesthesia, which decreased to 18 mumol/L concentration by 8 h after anesthesia. The peak plasma inorganic fluoride ion concentration correlated with duration of sevoflurane anesthetic exposure. Five patients given sevoflurane had peak levels transiently exceeding 50 mumol/L, and one of these had a history of ingesting drugs potentially producing hepatic enzyme induction. No increases in postoperative levels of creatinine, blood urea nitrogen, direct bilirubin, or hepatic transaminase and no changes in serum electrolyte level occurred in either anesthetic group. Indirect bilirubin concentration increased significantly after sevoflurane anesthesia, but the increase was not of clinical significance (from 0.30 +/- 0.03 to 0.38 +/- 0.06 mg/dL). Indirect bilirubin concentrations did not increase after isoflurane anesthesia; the concentrations reached 0.31 +/- 0.04 mg/dL and did not differ significantly from those found with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)     

Recovery of cognitive function after remifentanil-propofol anesthesia: a comparison with desflurane and sevoflurane anesthesia

We compared the recovery characteristics of remifentanil, desflurane, and sevoflurane when used for anesthesia in elective operative procedures. Sixty ASA physical status I and II patients, aged 18-65 yr, were randomly assigned to receive remifentanil-propofol, desflurane-N2O, or sevoflurane-N2O anesthesia. Before the induction of anesthesia, the patients of the desflurane and sevoflurane groups received fentanyl 2 microg/kg. In all groups, anesthesia was induced with propofol and maintained either with remifentanil 0.25 microg x kg(-1) x min(-1), desflurane, or sevoflurane 0.85 MAC with 65% nitrous oxide in oxygen. Anesthetics were titrated to achieve an adequate level of surgical anesthesia and to maintain mean arterial pressure within 20% of baseline values. Early recovery times and a modified Aldrete Recovery Score > 9 were recorded. Trieger Dot Test and Digit Substitution Test (DSST) were performed the day before surgery and in the postanesthesia care unit to evaluate intermediate recovery. The remifentanil-propofol group had a significantly faster emergence than desflurane or sevoflurane, with no difference between both inhaled anesthetics. Thirty min after anesthesia administration, patients in the remifentanil-propofol and in the desflurane groups gave significantly more correct responses in the DSST compared with sevoflurane (remifentanil 87%, desflurane 83%, sevoflurane 56%), the impairment in the sevoflurane patients corresponding to the effects of a blood alcohol level of approximately 0.1% and, thus, being of clinical importance. Ninety minutes after anesthesia administration, no significant difference could be demonstrated among the groups in the DSST scores. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration. IMPLICATIONS: We compared awakening and intermediate recovery times after remifentanil-propofol anesthesia to desflurane-N2O and sevoflurane-N2O anesthesia. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration.