Diaphragmatic activity during isoflurane anaesthesia in dogs

The effect of isoflurane administration on diaphragmatic activity was investigated in six anaesthetized mechanically ventilated dogs. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure (Pdi) generated during supramaximal stimulation of both cervical phrenic nerves at frequencies of 0.5, 10, 20, 50 and 100 Hz under partially isometric conditions at 1, 1.5 and 2 minimum alveolar anaesthetic concentrations (MAC), after maintaining 1 h of stable conditions. Pdi measurements were made at the start of the stimulation (initial) and at the end of a 2-s period (2-s). The force-frequency relationship was compared at each anaesthetic level. For single twitch (0.5 Hz) stimulation, the time constant of diaphragmatic relaxation was also assessed. The sequence of changing anaesthetic depth was altered in random fashion between animals. Pdi amplitude at single twitch stimulation was unchanged at the three anaesthetic concentrations. There was no significant difference in initial Pdi at various stimulus frequencies with increasing depth of isoflurane anaesthesia. In addition, no change in 2-s Pdi during low frequency stimulation (10 and 20 Hz) was noted during any of the three levels of anaesthesia. By contrast, 2-s Pdi with 50 Hz stimulation during 2 MAC isoflurane exposure decreased significantly below Pdi levels seen at 1 and 1.5 MAC (P<O.O1). Furthermore, 2-s Pdi at 100 Hz stimulation decreased significantly in a dose-dependent fashion. From these results, we conclude that isoflurane reduces diaphragmatic activity at higher stimulation frequencies of 50 and 100 Hz.     

Distribution of diaphragm blood flow during sevoflurane anaesthesia in dogs

Purpose

The purpose of this study was to determine the effect of increasing the concentrations of sévoflurane anaesthesia on the distribution of diaphragm blood flow (Qdi) in ten dogs during mechanical ventilation.

Methods

Animals were divided into two groups, sévoflurane (n = 6) and time control (n = 4) groups. Blood flow to the crural and the costal diaphragm (Qcru, Qcost) was determined by the hydrogen clearance technique at 0, 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC) of sévoflurane after a 30 min period of steady-state conditions. Cardiac output (CO) and the mean arterial blood pressure (MBP) were also measured.

Results

Sevoflurane anaesthesia caused a reduction in CO (L · min^?1) from a control value of 1.51 ± 0.21 to 1.38 ±0.1 (0.5 MAC), 1.09 ± 0.15 (1.0 MAC) and 0.98 ± 0.12 (1.5 MAC) (Mean ± SD). Mean blood pressure, Qcru and Qcost also decreased with increasing depth of anaesthesia. In addition, the decrease of Qcru was greater than that of Qcost at all levels of MBP and CO. No change occurred in these variables in the lime control group.

Conclusion

Sevoflurane anaesthesia changes the distribution of Qdi with a greater reduction occurring in Qcru than in Qcost.     

Leucocyte distribution during sevoflurane anaesthesia

We have examined if sevoflurane anaesthesia per se modified the number of circulating leucocytes in humans. Fifty-nine patients undergoing elective surgery were anaesthetized with sevoflurane in oxygen. The inhaled concentration was increased gradually to 5% and maintained for 20 min. Arterial blood samples were obtained before induction of anaesthesia and at 20 min. While the total number of leucocytes remained constant, circulating neutrophils decreased (mean 3370 (SD 1030) mm-3 to 3170 (940) mm-3; P < 0.01) and lymphocytes increased (1870 (520) mm-3 to 2040 (580) mm-3; P < 0.01). We conclude that high concentrations of sevoflurane modified the distribution of leucocytes in anaesthetized patients.      

Excitation phenomena during sevoflurane anaesthesia in children

The advantages of rapid induction of and emergence from sevoflurane anaesthesia may be more than offset by the frequent occurrence of agitation during induction and recovery, and a possible epileptogenic effect. The mechanisms and possible strategies to prevent these drawbacks are reviewed, on the basis of the most recent literature.     

Cerebral autoregulation in children during sevoflurane anaesthesia

Introduction. Little is known about cerebral autoregulationin children. The aim of this study was to examine cerebral autoregulationin children. Methods. Cerebral autoregulation testing was performed duringless than 1 MAC sevoflurane anaesthesia in children (from 6months to 14 yr) and in adults (18–41 yr). Mean middlecerebral artery flow velocities (V_MCA) were measured using transcranialDoppler ultrasonography. Mean arterial pressure (MAP) was increasedto whichever was greater: 20% above baseline or (i) 80 mm Hgfor less than 9 yr, (ii) 90 mm Hg for 9–14 yr, and (iii)100 mm Hg for adults. Cerebral autoregulation was consideredintact if the autoregulatory index was     

Glucose intolerance during prolonged sevoflurane anaesthesia

Purpose

The effects of prolonged sevoflurane anaesthesia on insulin sensitivity were investigated by two successive intravenous glucose tolerance tests (IVGTT) in eight patients who underwent prolonged surgery.

Methods

The first IVGTT was administered (25 g glucose as 20% dextrose in water iv) over two minutes 35 min after initiation of surgery. Arterial blood samples were obtained at 0, 5, 10, 30, 60, and 120 min after glucose administration for blood glucose and plasma insulin determination. A second IVGTT was performed six hours following the initiation of surgery.

Results

The disappearance rate of glucose (k-value) for the first IVGTT was 0.887 ± 0.436 (mean ± SD) % · min^?1, and 0.784 ± 0.289 for the second IVGTT. Both k-values are lower than the normal value. The maximum insulin response to glucose (ΔIRI · ΔBS^?1) of the second IVGTT was lower than the first IVGTT (0.124 ± 0.092 vs 0.071 ± 0.056, P < 0.05). The total insulin output of the first IVGTT was higher than the second IVGTT (1,161 ± 830 vs 568 ± 389 μU · min · ml^?1, P < 0.05).

Conclusion

Glucose intolerance is enhanced by diminished insulin output in response to blood glucose elevation during prolonged anaesthesia and surgery.     

The uptake of sevoflurane during anaesthesia

The rate of uptake of sevoflurane during clinical anaesthesia (1.3 MAC) was measured by computer-controlled injection of liquid anaesthetic into a closed breathing system. The cumulative uptake of sevoflurane was 4.8 ml, 7.4 ml. 9.5 ml and 11.5 ml at 30, 60, 90 and 120 min, respectively. The ratio of inspired to end-expired sevoflurane was greater than similar measurements we have made for desflurane in the past, but the absolute rate of sevoflurane uptake was less than the rate of uptake of desflurane in these cases. The rate of uptake was equivalent to 0.59e^{−0.32 t}  + 0.039e^{−0.036 t}  + 0.105e^{−0.0034 t}  mlmin⁻¹ liquid sevoflurane. Plasma urea and creatinine measured on the first postoperative day were not significantly different from pre-operative values.     

Degradation products of sevoflurane during low-flow anaesthesia

Low-flow (1 litre min^–1) sevoflurane anaesthesia was usedin 16 patients undergoing laparoscopic cholecystectomy (groupLSC, n = 8) or tympano-plasty (group TP, n = 8), and concentrationsof sevoflurane degradation products were measured. Degradationproducts in the circuit were measured hourly, and end-tidalcarbon dioxide concentration, inspired and end-tidal sevofluraneconcentrations, and carbon dioxide elimination were monitored.The only degradation product detected was CF₂=C(CF₃)-O-CH₂F(compound A). The mean maximum concentrations of compound Awere 21.6 (SEM 1.6) ppm and 1 9.6 (0.8) ppm in the LSC and TPgroups, respectively (ns). The maximum temperatures of sodalime were 46.4 (0.5) °C, and 44.8 (0.5) °C, respectively(P < 0.05). Hourly end-tidal sevoflurane concentrations andconcentrations of sevoflurane degradation products were thesame for both groups. Carbon dioxide elimination was the samefor both groups 1 h after the start of anaesthesia, but washigher in group LSC after 2 h (P < 0.05). Intraperitonealcarbon dioxide insufflation associated with laparoscopic cholecystectomyhad no effect on the concentration of sevoflurane degradationproducts.     

Liver function after sevoflurane or isoflurane anaesthesia in neurosurgical patients

Purpose

Although both sevoflurane and isoflurane are thought to be less hepatotoxic than halothane or enflurane, recent case reports have described liver injury after sevoflurane or isoflurane anaesthesia. There are no studies comparing liver function after sevoflurane or isoflurane anaesthesia. The purpose of this study was to compare serum liver enzyme concentrations in patients receiving either sevoflurane or isoflurane anaesthesia prospectively.

Methods

Ninety patients scheduled for elective neurosurgery were studied. Serum concentrations of aspartame aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBil), alkaline phosphatase (ALP), γ- glutamyl transpeptidase (GTP), and lactate dehydrogenase (LDH) were measured before and, 1, 2, 3, 7, and 14 days after either sevoflurane (45 patients) or isoflurane (45 patients) anaesthesia.

Results

AST ALT and GTP increased peaking seven days after anaesthesia, especially in the isoflurane group. The numbers of patients with abnormal values in AST and ALT were not different in the isoflurane from that in the sevoflurane group. The increase in TBil peaked one day after anaesthesia in both groups.

Conclusion

Even in a small number of patients, isoflurane induced an elevation of serum levels of liver enzymes more frequently than did sevoflurane three to 14 days after anaesthesia.     

Convulsions associated with epidural analgesia during sevoflurane anaesthesia

A three-year-old girl who underwent an operation for adrenal neuroblastoma was anaesthetized with sevoflurane and epidural analgesia. In the immediate recovery period she had convulsions. The convulsions were successfully treated with thiopentone and sevoflurane, there were no neurological sequelae. The convulsions were considered to be a manifestation of mepivacaine toxicity because of a high plasma mepivacaine concentration. Complications of paediatric regional analgesia and manifestations of mepivacaine toxicity under sevoflurane anaesthesia are discussed.     

Mivacurium-induced neuromuscular blockade during sevoflurane and halothane anaesthesia in children

The neuromuscular blocking effects of mivacurium during sevoflurane or halothane anaesthesia was studied in 38 paediatric patients aged 1–12 yr. All received premedication with midazolam, 0.5 mg · kg⁻¹ po and an inhalational induction with up to 3 MAC of either agent in 70% N₂O and O₂. The ulnar nerve was stimulated at the wrist by a train-of-four stimulus every ten seconds and the force of adduction of the thumb recorded with a Myotrace force transducer. Anaesthesia was maintained with a one MAC end-tidal equivalent of either volatile agent for five minutes before patients received mivacurium (0.2 mg · kg⁻¹) iv. The onset of maximal blockade occurred in 2.4 ± 1.26 (mean ± SD) min with halothane and 1.8 ± 0.54 min with sevoflurane (NS). Four patients failed to achieve 100% block (3 halothane, 1 sevoflurane). The times from injection to 5, 75, and 95% recovery during sevoflurane (9.8 ± 2.6, 19.5 ± 4.4, and 24.2 ± 4.8 min) were greater than during halothane anaesthesia (7.2 ± 2.2, 15.0 ± 4.0, 19.2 ± 4.9 min, respectively (P < 0.005). All patients demonstrated complete spontaneous recovery of neuromuscular function (T₁ > 95%, T₄/T₁ > 75%) during the surgery which lasted 24–63 min. All patients showed clinical signs of full recovery of neuromuscular blockade (i.e., headlift, gag, or cough). Pharmacological reversal was not required. It is concluded that following a single intubating dose of mivacurium, the time to maximum relaxation was not different during halothane and sevoflurane anaesthesia; recovery times to 5, 75 and 95% twitch height were longer during sevoflurane anaesthesia and neuromuscular reversal was not necessary. L’activité neurobloquante du mivacurium pendant l’anesthésie au sévoflurane ou à l’halothane fait l’objet de cette étude réalisée chez 38 enfants de 1 à 12 ans. Tous ont été prémédiqués au midazolam 0,5 mg · kg⁻¹ et l’anesthésie est induite avec un agent volatil jusqu’à MAC 3 de l’un des agents dans du N₂O à 70%. Le nerf cubital était stimulé au poignet au train de quatre aux dix seconds et la force de l’adduction du pouce mesurée avec un transducteur de force Myotrace. L’anesthésie était entretenue avec l’équivalent MAC I d’un des deux agents volatils pendant cinq minutes avant l’administration de mivacurium (0,2 mg · kg⁻¹). Le début du bloc maximum est survenu dans 2,4 ± 1,26 (moyenne ± SD) min avec l’halothane et 1,8 ± 0,54 min avec le sévoflurane (NS). Quatre patients n’ont pas été bloqués à 100% (trois avec l’halothane, un avec le sévoflurane). L’intervalle séparant l’injection à 5; 75, et 95% de la récupération pendant l’anesthésie au sévoflurane (9,8 ± 2,6, 19,5 ± 4,4 et 24,2 ± 4,8 min) a été plus long que pendant l’anesthésie à l’halothane (7,2 ± 2,2, 15,0 ± 4,0, 19,2 ± 4,9 min, respectivement (P < 0,005). An moniteur, chez tous les patients, la fonction neuromusculaire a récupéré spontanément (T₁ > 95%, T₄/T₁ > 75%) au cours de la chirurgie qui a duré de 24–63 min. Tous les patients montraient aussi les signes cliniques d’une récupération complète (par ex., levée de la tête, réflexe pharyngé ou toux). Aucun antagoniste pharmacologique n’a été requis. Il est conclu que le délai jusqu’à la relaxation maximum après une seule dose d’intubation de mivacurium ne diffère pas entre l’anesthésie à l’halothane et l’anesthésie au sévoflurane; les délais de retour à 5, 75 et 95% de la hauteur du twitch sont plus longs pendant l’anesthésie au sévoflurane et il n’est pas nécessaire d’antagoniser le bloc neuromusculaire.

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Supported in part by a grant from Abbott Laboratories, Chicago, Illinois.     

Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs

Background. In this study we aimed to clarify the role of endothelinin arterial pressure regulation during anaesthesia with increasingconcentrations of sevoflurane (1–3 MAC) and compare itwith those of vasopressin and angiotensin. Methods. After an awake control period, on different days, sixdogs underwent each of the following four interventions: sevofluraneanaesthesia alone (1–3 MAC), sevoflurane after block ofeither endothelin receptors using tezosentan (3 mg kg^–1followed by 3 mg kg^–1 h^–1), vasopressinV_1a receptors using [d(CH₂)₅Tyr(Me²)]AVP (40 µg kg^--1)or angiotensin receptors using losartan (6 mg kg^–1 h^–1).Plasma concentrations of endothelin, big endothelin, vasopressinand renin were measured. Effects of sevoflurane in the presenceand absence of the respective receptor block were analysed andcompared using analysis of variance for repeated measures (ANOVAfollowed by Fisher’s PLSD (protected least significantdifference) (P<0.05)). Results. Mean arterial pressure decreased in a dose-dependentmanner with sevoflurane during all interventions. At 1 MAC,this decrease was greatest during angiotensin receptor block(mean (SEM), –41 (3) mm Hg), intermediate duringvasopressin and endothelin receptor block (–31 (4) and–30 (2) mm Hg respectively), and least during sevofluranealone (–24 (3) mm Hg). The course of systemic vascularresistance mirrored the course of arterial pressure, while cardiacoutput did not differ between groups. Plasma concentrationsof endothelin, big endothelin and renin did not change duringany intervention, whereas vasopressin concentration increasedfrom     

Vecuronium-induced neuromuscular block during xenon or sevoflurane anaesthesia in humans

Twitch response using accelerometry and plasma concentrations, of vecuronium and its metabolite were studied in 27 surgical patients during xenon or sevoflurance anaesthesia after administration of vecuronium 0.05 mg kg-1. Anaesthesia was maintained using oxygen-xenon (MAC = 71%) or oxygen-sevoflurane (MAC = 2%) at an end-tidal concentration equal to 0.8 MAC (i.e. 57% xenon and 1.6% sevoflurane). Mean time from administration of vecuronium to 25% recovery of the first twitch of the train-of-four response was significantly shorter in the xenon group than in the sevoflurane group (12.9 (SD 2.5) min vs 19.4 (6.0) min, respectively). Plasma concentrations of vecuronium at 25% recovery were significantly higher during xenon than during sevoflurane anaesthesia (187 (49) ng ml-1 vs 136 (40) ng ml-1, respectively), while those of 3-desacetylvecuronium were similar in both groups.      

Alterations in the biochemical markers of renal function after sevoflurane anaesthesia

AIM: This study has been carried out to see whether renal function is acutely altered in patients undergoing sevoflurane anaesthesia. For this purpose, the urinary levels of markers of renal tubular function, namely leucine amino peptidase (LAP), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and beta-2 microglobulin (beta-2M), and urinary albumin as a predictor of renal glomerular function were measured before and after sevoflurane anaesthesia. METHODS: This study was comprised of 20 patients (11 males and nine females) aged 18-55, who underwent various elective surgical procedures under general anaesthesia. Urine samples of all patients were collected before and 1, 2 and 8 h after the anaesthesia. The levels of LAP, GGT, beta-2M, and albumin were then expressed as factored by urinary creatinine. In all patients, the anaesthesia was maintained with sevoflurane (2% end-tidal) at a high flow-rate (6 L/min). RESULTS: Urinary beta-2M and LAP levels after anaesthesia were unchanged (P > 0.05). While urinary GGT and ALP levels were found elevated in the first hour, LDH levels were higher in the second hour (P < 0.05). They returned to normal levels in the later periods after the anaesthesia. Urinary albumin excretion (UAE) was significantly elevated in the second hour after the anaesthesia (P < 0.001). Although UAE was decreased in the eighth hour after the anaesthesia, it still remained higher than the pre-anaesthesia level (P < 0.001). CONCLUSIONS: These results suggest that a 2% end-tidal concentration of sevoflurane at a high flow-rate (6 L/min) acutely alters renal glomerular function but does not have a significant acute effect on biochemical markers of renal tubular damage.     

Pulmonary mechanics during isoflurane,sevoflurane and desflurane anaesthesia

This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n = 22), sevoflurane (n = 23), or desflurane (n = 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.     

Liver and renal function after repeated sevoflurane or isoflurane anaesthesia

Purpose

To compare retrospectively liver and renal function after repeated exposure (twice) to sevoflurane or isoflurane.

Methods

Sixty patients were studied for liver and renal function after repeated exposure within 30 to 180 days to sevoflurane (30 patients) or isoflurane (30 patients). Serum concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBil), alkaline phosphatase (ALP), γ-glutamyl transpeptidase (GTP), blood urea nitrogen (BUN) and creatinine (Cr) were measured before and, 1, 3, 7, and 14 days after surgery. Qualitative analyses of urinary protein and glucose were done 1, 3, and 7 days after surgery.

Results

The number of patients with abnormal values in AST ALT and GTP was larger in the isoflurane than in the sevoflurane group. BUN and Cr were within normal range after anaesthesia in either group. Renal excretion of protein and glucose increased one and three days after anaesthesia with no difference between the anaesthetics. None of the variables showed differences between the first and second anaesthesia after either anaesthetic.

Conclusion

Repeat exposure to sevoflurane or isoflurane within 30 to 180 days had no additional risk of increasing serum concentration of liver enzymes or increasing urinary excretion of protein and glucose compared with the first exposure to the same anaesthetic.     

Decrease in minimum alveolar concentration of sevoflurane during anaesthesia and arthroscopy

BACKGROUND AND OBJECTIVE: Although the MACtetanus (minimum alveolar concentration that prevents movement in response to electrical tetanus stimulation in 50% of patients) of isoflurane decreases during anaesthesia and surgery, it is not known whether this occurs to the same extent with other inhalational anaesthetics. We determined the MACtetanus of sevoflurane before and after surgery. METHODS: Eleven patients who underwent arthroscopy of the shoulder underwent inhalational induction of anaesthesia with sevoflurane and tracheal intubation by succinylcholine. MACtetanus was determined in each patient by testing the response to a 10 s, 50 Hz, 80 mA transcutaneous tetanic electrical stimulus to the ulnar nerve at varying concentrations of sevoflurane. The end-tidal concentration of sevoflurane was kept constant for 15 min before each stimulus and the concentration of sevoflurane varied in increments of 0.1% until a sequence of three alternate responses (move, not move, move) or (not move, move, not move) was obtained. After arthroscopy of the shoulder, individual MACtetanus were measured as described above. RESULTS: The mean MACtetanus decreased from 2.22 +/- 0.29% before arthroscopy to 1.82 +/- 0.26% after arthroscopy (P < 0.01). CONCLUSIONS: It is concluded that the MACtetanus of sevoflurane decreases during anaesthesia and surgery.     

Soda lime temperatures during low-flow sevoflurane anaesthesia and differences in dead-space

BACKGROUND: Sevoflurane degrades during low-flow anaesthesia to compound A, and high carbon dioxide absorbent temperatures cause increased degradation. The purpose of this investigation was to determine if larger tidal volumes, without increasing alveolar ventilation, decrease the temperature in the carbon dioxide absorber during low- and minimal-flow sevoflurane anaesthesia. METHODS: Prospective, randomized study, including 45 patients (ASA 1-2), scheduled for elective general or urology surgery. The patients were randomly assigned to one of three treatments. Patients in group 1 (NDS) received fresh gas flow of 1 litre/min without using additional dead-space volumes. In group 2 (DS + 1.0), the patients received fresh gas flow of 1 litre/min using additional dead-space volumes, placed between the Y-piece and the HME, and patients in group 3 (DS + 0.5) received the same technique with a fresh gas flow of 0.5 litre/min. The soda lime temperatures, dead-space volumes, end-tidal carbon dioxide, sevoflurane concentrations, ventilation volumes and pressures, absorbent weight and ear temperatures were measured. RESULTS: The maximum temperature of the soda lime was 44.1 +/- 1.1 degrees C in the NDS group, 37.8 +/- 0.8 degrees C in the DS + 1.0 group and 38.5 +/- 2.7 degrees C in the DS + 0.5 group (P<0.0001). The dead-space volume between the Y-piece the tracheal tube was 164 +/- 69 ml in the DS + 1.0 group and 196 +/- 15 ml in the DS + 0.5 group (P<0.05). The ventilator pressure were higher in the DS groups compared with the NDS group (P<0.001). Soda lime weight increased in all groups. End-tidal carbon dioxide, sevoflurane concentrations and ear temperatures were similar between the groups. CONCLUSION: Increasing dead-space volumes can reduce carbon dioxide absorber temperature during low- and minimal-flow sevoflurane anaesthesia.