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PubMedDate not supplied

Methoxyflurane biotransformation and renal function following methoxyflurane administration for vaginal delivery or cesarean section.

Methoxyflurane (MOF) administration for conscious analgesia during vaginal delivery (range 5 to 70 min, mean 23 min) or for anesthesia following delivery of the infant at cesarean section (range 25 to 70 min, mean 44 min) was studied in 18 healthy parturients. Serum ionic fluoride increased significantly in both groups 2 hours after discontinuing MOF with peak concentrations of 11.2 and 14.1 mumol/L in the vaginal delivery and cesarean section groups, respectively. Individual peak serum ionic fluoride levels in the 2 groups of 21 and 25 mumol/L were well below reported levels for subclinical toxicity. Significant ionic fluoride elevations in fetal umbilical venous blood (mean 5.3 mumol/L) were measured in the vaginal-delivery group. Maternal urinary ionic fluoride and oxalate were elevated 24 and 48 hours postpartum. BUN, creatinine, urine volume, and urine osmolality remained within normal range. These data indicate that hazardous elevations of serum ionic fluoride with subsequent renal dysfunction are unlikely following low-dose MOF administration for vaginal delivery or cesarean section.

Adult↗

PubMed1975

The influence of age on the distribution, metabolism and excretion of methoxyflurane in Fischer 344 rats: a possible relationship to nephrotoxicity.

Age as a factor in methoxyflurane nephrotoxicity was evaluated in Fischer 344 rats of various ages by determination of: 1) serum inorganic fluoride and methoxyflurane concentrations, and urinary inorganic fluoride excretion in methoxyflurane-exposed rats; 2) liver microsomal methoxyflurane defluorinase activity; and 3) distribution of injected sodium fluoride. Only rats in the youngest age group (6 weeks) did not develop nephrotoxicity after anesthesia. Older rats had a biphasic rather than a monophasic decay in serum methoxyflurane concentration and also had increased serum inorganic fluoride concentration and urinary inorganic fluoride excretion. Older rats also excreted a greater proportion of an injected dose of sodium fluoride compared to young rats. Microsomal methoxyflurane defluorinase specific activity was similar among rats of all ages. It is likely that increased availability of methoxyflurane due to its greater storage in fat led to more inorganic fluoride production in older compared to younger rats. Bone sequestration of inorganic fluoride in younger rats probably accounts for decreased serum inorganic fluoride levels in that group. Both factors cause significant differences in renal exposure to inorganic fluoride; thus the risk of nephrotoxicity is less in younger animals.

Aging↗

PubMed1976

Toxicity following methoxyflurane anaesthesia. IV. The role of obesity and the effect of low dose anaesthesia on fluoride metabolism and renal function.

Seven obese and five normal weight patients were studied before, during and after one hour of methoxyflurane-nitrous oxide anaesthesia during peripheral surgical operations and compared with eight patients of normal weight anaesthetized with nitrous oxide-meperidine and d-tubocurare. Estimates were made of renal function, including serum and urinary electrolytes, osmolarity, uric acid, urea and creatinine. Renal clearances for the latter three substances were also calculated. Serum and urinary inorganic and organic fluoride concentrations were measured, as were renal clearances. This low dose methoxyflurane anaesthesia resulted only in a decrease in uric acid clearance among all the measures, when compared to the meperidine-nitrous oxide controls. The clearance of uric acid remained depressed for longer in the obese patients, but otherwise they did not differ from the normal weight patients. It is possible but not proven that depressed uric acid clearance may be related to the organic fluoride metabolite and an early indicator of methoxyflurane renal toxicity. The previously documented biotransformation of methoxyflurane was seen in this study. A double peak in serum inorganic fluoride was shown in all patients but one. Rather large differences in peak levels of serum inorganic fluoride occurred. The only significant difference between the obese and normal weight patients as far as fluoride metabolism was concerned was a greater variability in the serum inorganic fluoride levels in the obese patients. It would appear that the obese patient metabolizes methoxyflurane in a quantitatively if not qualitatively different fashion than the normal weight patient, perhaps because of fatty infiltration of the liver. Caution is advised in the use of methoxyflurane for more than 90 minutes of low concentration administration in view of the unpredictability of the biotransformation.

Anesthesia↗

PubMed1976

Methoxyflurane nephropathy.

Investigations of methoxyflurane-induced nephrotoxicity in man have been extensively aided by the use of an animal model. To be of value the animal model must share similar metabolic pathways with man and have the same clinical manifestations of the diseases process. The Fischer 344 rat appears to meet these criteria. The predominant factors in the production of methoxyflurane nephrotoxicity appear to be high methoxyflurane dosage and serum inorganic fluoride concentration. It is likely that secondary factors include: (1) a high rate of methoxyflurane metabolism and sepsitivity of the kidney to inorganic fluoride toxicity: (2) concurrent treatment with other nephrotoxic drugs; (3) preexisting renal disease; (4) surgery of the urogenital tract, aorta, or renal vasculative; (5) repeat administration of methoxyflurane due to accumulation of inorganic fluoride and, perhaps, methoxyflurane induction of its own metabolism: and (6) concurrent treatment with enzyme-inducing drugs such as phenobarbital.

Age Factors↗

PubMed1979

Effect of phenytoin (DPH) treatment on methoxyflurane metabolism in rats.

The toxicity and metabolism of the fluorinated anesthetic methoxyflurane were compared in Fischer 344 rats pretreated with phenytoin or phenobarbital. Treatment with either drug potentiated the polyuric effects of methoxyflurane by more than 100%. Also, serum inorganic fluoride (F-) levels and urinary F- excretions after methoxyflurane exposure were comparable in phenytoin- and phenobarbital-treated rats, a 26 to 49% increase as compared to rats treated with methoxyflurane alone. In vitro, 10-fold increases in the rate of hepatic microsomal methoxyflurane defluorination were observed after treatment of rats with either phenytoin or phenobarbital. Kinetic studies with microsomes demonstrated inhibition of methoxyflurane defluorination in the presence of phenytoin. Defluorination of three additional fluorinated ether anesthetics, enflurane, isoflurane and sevoflurane, also was examined in vitro. Phenytoin and phenobarbital treatment resulted in similar enhancement of defluorination of the latter two anesthetics, but not enflurane. Phenytoin and phenobarbital treatment increase defluorination of fluorinated ether anesthetics to approximately the same extent in vitro and in vivo in Fischer 344 rats.

Anesthetics↗

PubMed1979

Serum and urine inorganic fluoride concentrations and urine oxalate concentrations following methoxyflurane anesthesia in the dog.

Plasma fluoride, urine fluoride and urine oxalate concentrations were measured before administering an anesthetic to 8 dogs, and at 0, 3, 9, 24, 48, and 72 hours following 1.5 hours of anesthesia with 1% methoxyflurane. Plasma and urine osmolalities were measured and compared with fluoride and oxalate values. Fluoride concentration increased in both plasma and urine following anesthesia when compared with the preanesthetic concentrations. Maximum mean plasma inorganic fluoride was 106.71 mumoles per liter (+/- 25.44 SE) at 9 hours after exposure to methoxyflurane was completed. By 72 hours after exposure to methoxyflurane the plasma fluoride concentration was 23.47 microM/L (+/- 5.74 SE). Mean urine inorganic fluoride concentration was highest at 9 hours after exposure to methoxyflurane and reached 6047.03 microM/L (+/- 1378.46 SE) as compared to the mean preanesthetic base-line concentration of 542.68 microM/L (+/- 132.93 SE), and the 72 hour mean urine fluoride concentration which was 1593.78 microM/L (+/- 579.46 SE). Urine oxalate concentrations, when compared with urine osmolality (mg/mOsm), increased throughout the study. The 72-hour concentration after exposure to methoxyflurane was 2.5 times the preanesthetic (mg/mOsm) oxalate concentration. Plasma osmolality did not change markedly during the study. Urine osmolalities varied between animals and collection times, but a consistent pattern did not occur. Clinical and laboratory signs of renal dysfunction were not observed in any animal during the study.

Anesthesia↗

PubMed1976

[The uterotropismus of halothane, chloroform or methoxyflurane in clinical use (author's transl)].

To perform episiotomy, 89 women after childbirth were anaesthetized with either halothane (50 patients), methoxyflurane (24 patients) or chloroform (15 patients). The activity of the uterus was registered tocodynamographically. To examine the alternate influence of narcotics and uterotonica, 57 patients were pre-medicated with sintocinon and methergin i.m. as a prophylaxis. The second group (32 patients) received no premedication to stimulate labor activity, however in 18 cases towards the end of narcosis oxytocin and methergin were given i.v. In addition to these examinations 5 vaginal deliveries were anaesthetised with halothane only. Concerning our own experimental study it can be observed: 1. The relaxative properties of halothane wich suppresses completly the activity of myometrium during the deep stages of anaesthesia are superior to chloroform and methoxyflurane. 2. More rapid relaxation of the uterus with halothane compared with chloroform and methoxyflurane. 3. After the use of halothane a quicker return of the activity of the uterus compared with chloroform and methoxyflurane. 4. The value of a prophylaxis with uterotonica can be demonstrated by a comparatively reduced slowing-down of labour-activity during anaesthesia. 5. In every one of the cases, an interuption of the labour-suppressing, caused by the anaesthesia, can be obtained by injecting intravenously oxytocin or methergin. 6. During vaginal delivery, compared to the post placentar phase, there is no need for higher concentrations of halothane to be used to suppress labour contractions. The discussion deals with the intensity of reduction of the uterus contraction caused by the above mentioned narcotics, the dangers of the atony of the uterus, and the indications and contra-indications of obstetrical anaesthesia with halothane or methoxyflurane.

Adult↗

PubMed1977

Maternal and neonatal effects of methoxyflurane, nitrous oxide and lumbar epidural anaesthesia for Caesarean section.

General anaesthetic techniques continue to be used for Caesarean section despite the possible increased incidence of foetal acidosis and neonatal depression. Two techniques of general anaesthesia (methoxyflurane-oxygen and nitrous oxide-oxygen) and lumbar epidural anaesthesia were compared in 37 patients under-going elective Caesarean section. Apgar scores at birth were similar in all three groups. Neurophysiological testing of the neonates at six hours and twenty-four hours of age revealed a superiority for the methoxyflurane-oxygen and lumbar epidural techniques, although the babies in the epidural group tended to be hypotonic. Cord blood gas analysis showed the babies in the methoxyflurane group to have a higher PaO2 with less metabolic acidosis than the babies from the other two groups. The maternal effects of the three anaesthetic techniques were similar, with only a small rise in serum fluroide levels noted in the methoxyflurane group.

Anesthesia, Epidural↗

PubMed1978

Biodegradation of halothane, enflurane and methoxyflurane.

The biodegradation of halothane, enflurane and methoxyflurane was studied in 22 patients undergoing abdominal surgery, by measuring the uptake and elimination of each agent and the fluoride excretion in urine. Six control patients were anaesthetized with nitrous oxide in oxygen together with neuromuscular blocking drugs, five patients with nitrous oxide in oxygen and 0.93% halothane, five with nitrous oxide in oxygen and 1.30% enflurane, and six with nitrous oxide in oxygen and 0.31% methoxyflurane. The ratio of the fluoride excretion in urine to the total amount of fluoride contained in the amount of each anaesthetic agent absorbed during anaesthesia was estimated to be 17.7% for halothane, 2.3% for enflurane and 46.3% for methoxyflurane. The serum fluoride concentration increased to a maximum of 15.8 +/- 3.8 mumol litre-1 (mean +/- SD) at 6 h after anaesthesia with methoxyflurane, while it did not exceed 8 mumol litre-1 with the other anaesthetic agents.

Adult↗

PubMed1975

The action of ether and methoxyflurane on synaptic transmission in isolated preparations of the mammalian cortex.

1. The actions of ether and methoxyflurane on the evoked potentials of in vitro preparations of the guinea-pig olfactory cortex were studied. Following stimulation of the lateral olfactory tract (l.o.t.) evoked potentials could be recorded from the cortical surface; these potentials consisted of an initial wave (the compound action potential of the l.o.t.) followed by a negative field potential which was associated with the synchronous excitation of many superficial excitatory synapses (population e.p.s.p.). Superimposed on the population e.p.s.p. was a number of positive peaks. These positive peaks reflect the synchronous discharge of many neurones and so have been called population spikes. 2. When ether or methoxyflurane was added to the gas stream that superfused the surface of the preparations, the population e.p.s.p.s. and population spikes were depressed at lower concentrations than those required to depress the compound action potential of the afferent fibres. 3. The evoked activity of individual cells in the cortex was depressed by ether and methoxyflurane. However, five of the twelve cells tested in ether showed an increase in their evoked activity at concentrations below 4-5%, but at higher concentrations these cells also became depressed. 4. Both ether and methoxyflurane depressed the sensitivity of cortical neurones to iontophoretically applied L-glutamate and may similarly depress the sensitivity of the post-synaptic membrane to the released transmitter substance. 5. Neither anaesthetic appeared to increase the threshold depolarization required for nerve impulse generation. Thus, the decrease of the discharge of the post-synaptic cells was primarily caused by a depression of chemical transmission. 6. Ether caused some cells in the cortex to alter their normal pattern of synaptically evoked discharge and both anaesthetics induced similar changes during excitation by glutamate.

Animals↗

PubMed1977

Autoregulation of renal blood flow during ether, halothane and methoxyflurane anesthesia in dogs.

The effects of ether, halothane and methoxyflurane (0.5-1.5 MAC) on renal blood flow and its autoregulation were studied in 24 dogs. The left renal artery was perfused with the animals' own blood by a constant pressure perfusion system. The perfusion pressure ranged from 60 to 200 mmHg. Renal blood flow at the perfusion pressure of 100 mmHg was changed neither by ether nor by halothane, while it was decreased dose-dependently by methoxyflurane. At equipotent anesthetic concentrations the autoregulation of renal blood flow was only slightly impaired by ether, but significantly by halothane and methoxyflurane. Adenosine (100 mug/min) or calcium chloride (10 mg/min) which was infused directly into the renal artery resulted in a restoration of autoregulation impaired by MAC-1 of each anesthetic when perfusion pressure was raised stepwise from 100 to 200 mmHg, but no restoration was observed at low perfusion pressure below 100 mmHg. The results indicate that methoxyflurane exerts a direct constrictive effect on the renal vasculature. Adenosine and calcium may play a significant role on the response of the renal vasculature to raised perfusion pressure.

Adenosine↗

PubMed1976

Fluoride in bone of rats anesthetized during gestation with enflurane or methoxyflurane.

Fluoride concentrations in maternal and fetal bones were measured following exposure of pregnant rats to methoxyflurane and enflurane anesthesia. Fluoride content in fetal bone increased significantly only after exposure to methoxyflurane, and then only when methoxyflurane was administered after 12 days of gestation, when ossification of fetal bone begins. Fluoride concentrations in maternal bone increased following both anesthetics, except in rats exposed to methoxyflurane after 15 days of gestation, when ossification of many fetal skeletal parts is in progress and fluoride is preferentially deposited in the fetal skeleton.

Anesthesia, Inhalation↗

PubMed1975

Maternal and foetal effects of methoxyflurane anaesthesia in the pregnant ewe.

Maternal and foetal cardiovascular, blood gas and acid-base changes were studied during 90 minutes of methoxyflurane anaesthesia. At 1.0 and 1.5 MAC anaesthesia, despite slight to moderate falls in maternal blood pressure, cardiac output and uterine blood flow, no serious foetal deterioration was seen. 2.0 MAC methoxyflurane was associated with marked falls in maternal blood pressure, cardiac output and uterine blood flow. Foetal hypoxaemia and a mixed respiratory and metabolic acidosis developed. Little foetal cardiovascular depression was seen with any level of anaesthesia. There was no direct effect of methoxyflurane on the uterine vasculature.

Acid-Base Equilibrium↗

PubMed1975

Doses of epinephrine causing arrhythmia during enflurane, methoxyflurane and halothane anaesthesia in dogs.

The arrhythmogenic dosage of epinephrine, administered by constant intravenous infusion, was measured in five dogs during enflurane, methoxyflurane and halothane anaesthesia. While premature ventricular contractions were observed in only one of five dogs with enflurane and methoxyflurane, epinephrine-induced arrhythmias were seen in all animals during halothane anaesthesia. Epinephrine dosage and the resultant increase in mean arterial blood pressure at which arrhythmias occurred during halothane anaesthesia were significantly less (p less than 0.05) than with the other anaesthetics. These observations indicate that enflurane and methoxyflurane, as compared to halothane, possess relatively less arrhythmogenic potential as sensitizing agents in the presence of increased circulating catecholamines.

Anesthesia, Inhalation↗

PubMed1979

Preservation of the hypoxic pulmonary vasoconstrictor mechanism during methoxyflurane anaesthesia in the dog.

The effect of methoxyflurane on the hypoxic pulmonary vasoconstrictor response in the dog lung was assessed by measuring the redistribution of pulmonary blood flow in response to two levels of unilateral alveolar hypoxia. Methoxyflurane 0.5% had no significant effect on the redistribution of blood flow resulting from the unilateral administration of oxygen 7% or nitrogen and there were no significant differences in PaO2 between the measurements made during unilateral hypoxia with methoxyflurane and those made during unilateral hypoxia in the control periods.

Anesthesia, Inhalation↗

PubMed1978

Cardiac function during induction and early anesthesia with methoxyflurane. An evaluation using systolic time intervals and pressure time indices.

In addition to the standard monitoring of heart rate and blood pressure, the Systolic Time Intervals were used to evaluate cardiac performance, and the Pressure Time Indices (tension time index = TTI; diastolic pressure time index = DPTI) were used to estimate myocardial oxygen balance. Twelve patients with known heart disease were studied during induction with thiopental, intubation, and early anesthesia with methoxyflurane. Cardiac performance diminished after thiopental; and during methoxyflurane it was reflected in increases in pre-ejection period (PEP) and the ratio PEP/LVET. Intubation resulted in a hyperactive state of the heart, as shown by maximal decreases in PEP and PEP/LVET. Myocardial oxygen balance--estimated from the supply/demand ratio (DPTI/TTI)--was impaired after thiopental. After intubation, DPTI/TTI decreased to its lowest value due to an excess of myocardial oxygen demand (TTI) over myocardial oxygen supply (DPTI), signifying a transitory underperfusion of the subendocardium. During methoxyflurane the oxygen balance was gradually restored towards control value. The Systolic Time Intervals and the Pressure Time Indices provided valuable information on cardiac function not available from standard monitoring alone.

Adult↗

PubMed1978

Recovery from anaesthesia in ponies: a comparative study of the effects of isoflurane, enflurane, methoxyflurane and halothane.

The duration and quality of recovery after separate 2 hour anaesthetic periods with equipotent alveolar concentrations of isoflurane, enflurane, halothane and methoxyflurane were evaluated in experimental ponies. Recovery was shortest after isoflurane anaesthesia, followed by enflurane, halothane and finally methoxyflurane, although standing was achieved more rapidly after enflurane than after isoflurane. This sequence of recovery times was compatible with the respective solubilities of the 4 agents. The smoothest recovery was obtained after isoflurane anaesthesia, followed by methoxyflurane, halothane and then enflurane. The isoflurane recovery was characterized by very quiet and prolonged sternal recumbency with excellent coordination upon standing. The chief difficulties with halothane recovery were shivering and delayed coordination upon standing. Enflurane anaesthesia was followed by a very brief period of sternal recumbency but there was considerable shivering and incoordination upon standing. This may have been due to central nervous stimulation during anaesthesia producing a residual excitatory effect. On the basis of this investigation, isoflurane was considered to be the most satisfactory volatile anaesthetic for the horse.

Anesthesia, Inhalation↗

PubMed1979

Fluoride concentrations in urine of delivery ward personnel following exposure to low concentrations of methoxyflurane.

Midwives and other delivery ward personnel exposed to methoxyflurane do not have measurable traces of the agent in expired air when examined soon after exposure. This may imply a rapid uptake of the anesthetic. If this is the case, then the products of the metabolism of methoxyflurane, such as fluoride, may appear in the urine of such personnel. The present study investigated urinary fluoride levels in 24 delivery ward personnel and compared the values found after methoxyflurane/nitrous oxide analgesia with those measured in the same individuals after exposure to nitrous oxide alone. A highly significant difference was observed. Thus it would appear that, in spite of an apparently adequate system of environmental ventilation, there is a significant uptake of methoxyflurane by delivery ward personnel when this agent is employed for obstetrical analgesia.

Anesthesia, Obstetrical↗