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PubMed1987

Effects of increasing enflurane concentrations on intraocular pressure.

The effects of enflurane at various concentrations on intraocular pressure (IOP) were studied. In 15 healthy patients, intubated and mechanically ventilated, IOP was measured the day before surgery, after premedication and during anaesthesia, after administration of 0.5%, 1.0% or 1.5% enflurane. Enflurane in combination with general anaesthesia and controlled ventilation (PCO2 4.7-5.3 kPa) caused a significant decrease in IOP. The decrease was more marked (44%) with 1% enflurane than with 0.5% enflurane (21%). The change in IOP was comparable with 1.0% and 1.5% enflurane; however, systolic arterial pressure decreased more with enflurane 1.5%. Increasing the inspired concentration of enflurane from 1% to 1.5% did not appear to be associated with any further decrease in IOP.

Adult↗
PubMed1980

Effects of enflurane on functionally skinned myocardial fibers from rabbits.

Enflurance, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20 C). The [Ca2+]--tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10 per cent decrease at 5 per cent enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85 per cent decrease at 2.5-7.5 per cent enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5 per cent), but was decreased at high concentration (25 per cent decrease at 7.5 per cent enflurane). Enflurane (1-7.5 per cent), however, increased (13-44 per cent) the submaximum caffeine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.

Animals↗
PubMed1982

The enflurane sparing effect of morphine, butorphanol, and nalbuphine.

The potencies of morphine and of the narcotic analgesic agonist-antagonists butorphanol and nalbuphine in terms of their ability to decrease enflurane MAC were studied. Following the determination of control MAC for enflurane in each dog, an intravenous bolus dose of either butorphanol tartrate, nalbuphine hydrochloride, morphine, or placebo was administered and enflurane MAC was redetermined. A higher dose of the same drug was then administered and enflurane MAC was redetermined up to a total of four doses in each animal. The successive doses for morphine and nalbuphine were 0.5, 1.5, 5.0, and 20.0 mg/kg; for butorphanol, 0.1, 0.3, 1.0, and 4.0 mg/kg; lactated Ringer's solution was used as a placebo. Both butorphanol and nalbuphine produced significant reductions of enflurane MAC (11 and 8%, respectively) at their lowest doses. No further reductions were produced by three- to forty-fold larger doses of either agonist-antagonist. Morphine produced a 17% reduction of enflurane MAC at the lowest dose with progressive decreases of enflurane MAC up to 63% at a dose of 5 mg/kg morphine. A fourfold increase in the morphine dose did not further decrease MAC. No change in enflurane MAC occurred in the animals given placebo. It was concluded that there is a "ceiling" to the potency of butorphanol and nalbuphine as anesthetic supplements. There is also a limit to the anesthetic sparing effect of morphine, but it is considerably greater than that of the agonist-antagonist narcotic analgesics.

Anesthetics↗
PubMed1985

Chemistry of halothane-enflurane mixtures applied to anesthesia.

The authors obtained boiling point-composition data and vapor pressure-composition data for the halothane-enflurane system at 20 degrees C and 25 degrees C. This was used to demonstrate the existence of an azeotropic mixture of halothane and enflurane and to predict the output of an enflurane vaporizer contaminated with different amounts of halothane and a halothane vaporizer contaminated with different amounts of enflurane. The study was undertaken because the information allows a comprehensive description of the behavior of a contaminated vaporizer and the required data were not previously available. It was shown that an enflurane vaporizer contaminated with halothane delivers potentially dangerous mixtures of the two agents, whereas an enflurane-contaminated halothane vaporizer does not pose a serious problem. It was concluded that when halothane and enflurane vaporizers are mounted in series, the halothane should be downstream. It is explained why the halothane-enflurane azeotrope is unlikely to be useful clinically.

Anesthesia, Inhalation↗
PubMed1990

Effects of ketamine, halothane, enflurane, and isoflurane on systemic and splanchnic hemodynamics in normovolemic and hypovolemic cirrhotic rats.

The effects of ketamine, halothane, enflurane, and isoflurane on systemic and splanchnic hemodynamics in cirrhotic rats that were either normovolemic or hypovolemic following hemorrhage were characterized. Rats received at random either ketamine (30 mg/kg iv, 1.5 mg.kg-1.min-1 iv), halothane, enflurane, or isoflurane (1 MAC). Conscious rats were considered the control group. Four weeks before hemodynamic studies bile duct ligation was performed in all rats to induce cirrhosis. Hemodynamic measurements were performed using the radioactive microsphere method 1 h after the onset of anesthesia and 30 min after hemorrhage. Anesthetized rat lungs were mechanically ventilated with room air. Before hemorrhage cardiac index was higher in conscious rats and in rats receiving isoflurane than in the other groups (P less than 0.001). Hepatic arterial blood flow was similar in conscious rats and in those receiving isoflurane or halothane and was higher than in those receiving ketamine or enflurane. The lowest splanchnic and portal venous tributary blood flows were observed in rats receiving enflurane. After hemorrhage cardiac index was significantly less than before hemorrhage in all groups, except in rats receiving enflurane. After hemorrhage portal venous tributary blood flow decreased significantly in all groups except in enflurane group. During halothane and enflurane anesthesia hepatic arterial blood flow and hepatic arterial fraction of cardiac output decreased (P less than 0.01) and they were maintained in the other groups. After hemorrhage hepatic arterial fraction of cardiac output in conscious rats was higher than in those receiving ketamine, halothane, or enflurane (P less than 0.05) and was similar to those receiving isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Repetitive post-training exposure to enflurane modifies spatial memory in mice.

BACKGROUND: Previously the authors found that a single post-training exposure to enflurane or isoflurane, but not halothane, enhanced memory storage in an active avoidance task, which is a behavior with underlying mechanisms that are poorly understood and still debated. In contrast, spatial tasks are known to depend on hippocampal functions. This study investigated the effects of repetitive post-training exposure to enflurane on spatial memory in mice. METHODS: Using an eight-arm radial maze, 80 mice were trained to eat a pellet placed on the end of each of the eight arms. Training occurred on four consecutive days with one trial per day. The number of errors in the first eight choices was recorded to determine performances for each day of training. Immediately after each training session, mice in the enflurane group received 1 h exposure to 0.5%, 1%, or 2% enflurane in air through a calibrated vaporizer. The performance ratios (the ratio of errors on each day compared with the first day of the 4 days) in the control and the enflurane groups were compared. RESULTS: The performance ratios (which equals the mean of the error in the fourth day/the error in the first day) in the control, and 0.5%, 1%, and 2% enflurane groups were 0.66, 0.65, and 0.32 (P < 0.01, vs. control), and 0.46 (P < 0.05, vs. control), respectively. CONCLUSIONS: Repetitive post-training exposure to 1% and 2% enflurane significantly enhanced spatial memory in the eight-arm radial maze task. Enflurane enhances consolidation of spatial memory, possibly by affecting hippocampal activity.

Anesthetics, Inhalation↗
PubMedDate not supplied

Comparative metabolic effects of halothane and enflurane in rat heart cell culture.

The effects of halothane and enflurane on the oxygen consumption rates and substrate utilization by beating and nonbeating rat heart myocytes in cell culture were compared. Halothane, on an equal dose and equal MAC (minimum alveolar concentration producing immobilization of 50% of subjects) basis, was significantly more effective than enflurane in reducing total myocyte oxygen consumption and contractile rate. The greater effect of halothane on oxygen consumption was not due entirely to its effect on myocyte contractile rate, since quiescent (nonbeating) cells and cells rendered nonbeating by large doses of halothane also showed greater reductions in oxygen consumption than with large doses of enflurane. Both halothane and enflurane reduced glucose and palmitic acid metabolism by myocytes when compared with controls. However, there were no significant differences between halothane or enflurane with regard to glucose metabolism. Halothane was significantly more effective than enflurane in reducing cellular palmitic acid metabolism. Although palmitic acid uptake by myocytes was reduced to the same extent by both anesthetics when compared with control uptake values, halothane reduced myocyte uptake of glucose to a greater degree than enflurane. The results of this study indicate that halothane is a more potent myocardial metabolic depressant than enflurane.

Animals↗
PubMed1981

Enflurane anesthesia in living donor renal transplantation.

Two groups of patients undergoing elective living donor renal transplantation were studied during enflurane or halothane supplemented anesthesia. The duration of anesthesia was similar in both groups. The mean administered enflurane dose was 243 vol % min; the corresponding halothane dose was 56 vol % min. In the enflurane group, the mean serum inorganic fluoride level peaked at 21.0 mumol/l 3 h after the end of anesthesia. The inorganic fluoride level in urine produced by the renal graft increased continuously, but did not peak, during the first 24 postanesthetic hours. The renal graft quickly started to function in all patients in both groups. The frequency of rejection reactions was higher in the enflurane group than in the halothane group. Serum creatinine levels decreased rapidly in both groups. Urine flow was high on the day of transplantation, but normalized on the first postanesthetic day. Renal sodium clearance decreased earlier in the enflurane group than in the halothane group. This difference was statistically significant on the first postanesthetic day. In the enflurane group, the required pancuronium dose was significantly lower than in the halothane group. In one patient in the enflurane group, the serum inorganic fluoride level increased to 37.5 mumol/l. In this patient renal tubular function may have been affected, but the change was not conclusive since a pronounced rejection of the graft became evident. Since increases in serum inorganic fluoride level approaching 75% of the threshold level for nephrotoxicity in normal kidneys may occur, enflurane should not be routinely used in anesthesia for renal transplantation.

Anesthesia, General↗
PubMed1985

Cardiovascular effects of enflurane and asphyxia during long-term beta 1-adrenoceptor blockade.

The haemodynamic effects of enflurane (1.7% and 3.4% expiratory concentrations) were investigated in sheep (n = 6) pretreated with an infusion of metoprolol (0.2 mg X kg-1 X h-1 for 5 days) and in control animals (n = 6). Chloralose was used as basal anaesthetic. A 90 s apnoea period was included in the experiment to evaluate further the possible side-effects of long-term metoprolol treatment in combination with enflurane anaesthesia. MAC 1.0 for enflurane in the sheep was found at 1.45% end-tidal concentration by separate measurements. Before enflurane administration, the only significant differences between the two groups of animals were a lower systemic vascular resistance and a higher stroke volume during metoprolol treatment. Enflurane abolished these discrepancies in a dose-dependent fashion and similar cardiovascular depression was observed in both groups of animals at 3.4% expiratory concentration of enflurane. Metoprolol did not significantly affect the hypertensive response to apnoea during chloralose anaesthesia alone. At enflurane 1.7% expiratory concentration the apnoea response was small and only the metoprolol-treated animals showed a significant increase in left ventricular end-diastolic pressure. We conclude that 5 days of pretreatment with metoprolol in the sheep model does not significantly impair cardiovascular performance during enflurane anaesthesia.

Adrenergic beta-Antagonists↗
PubMed1987

Pulmonary ventilation and gas exchange in children anaesthetized with halothane, enflurane and isoflurane.

The effects of similar anaesthetic levels of halothane (1.3 MAC), enflurane (1.2 MAC) and isoflurane (1.1 MAC) on pulmonary ventilation and gas exchange were investigated in 24 children subjected to minor and intermediate paediatric surgical procedures. Eight children were anaesthetized with each agent, pneumotachography and capnography were used, and airway as well as oesophageal pressures were measured. Minute ventilation (VE) was lower with enflurane than with halothane (P less than 0.001) and isoflurane (ns). Tidal volumes were, however, similar and variations in VE were thus caused by lower respiratory rates with enflurane than with the two other agents. Alveolar ventilation (VABohr) and carbon dioxide elimination (VCO2) were smaller and end-tidal CO2 tension higher with enflurane. Ventilatory efficiency was, however, somewhat better with enflurane as indicated by lower VDBohr/VT (ns) and VE/VCO2 (P less than 0.05) ratios compared with the two other agents. The effects of all three agents on dynamic compliance were similar, while total pulmonary resistance was less with isoflurane than with halothane and enflurane. It is concluded that although minute ventilation was smaller with enflurane than with halothane and isoflurane, ventilatory efficiency was similar due to a smaller dead space ventilation as a result of the lower respiratory rates in children anaesthetized with enflurane.

Airway Resistance↗
PubMed1988

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.

Anesthesia, Inhalation↗
PubMed1992

Effects of propofol and enflurane on action potentials, membrane currents and contraction of guinea-pig isolated ventricular myocytes.

1. The effects of two general anaesthetics, propofol and enflurane, on electrical activity and contractions were investigated in single myocytes isolated from guinea-pig ventricles. 2. Propofol and enflurane depressed the plateau and shortened the duration of action potentials. 3. Under voltage-clamp conditions, propofol and enflurane reduced the amplitude of inward calcium current and of additional inward current activated by cytosolic calcium. 4. Contractions (measured with an optical technique) accompanying either action potentials or second inward currents (in response to depolarizations to 0 mV) were reduced by both anaesthetics. The mechanisms for calcium entry during contractions accompanying pulses to positive potentials such as +60 mV are thought to differ from those accompanying second inward currents which are evoked by pulses from -40 to 0 mV. Enflurane enhanced the amplitudes of contractions accompanying pulses to positive potentials; in contrast these contractions were depressed by propofol. 5. In experiments where recovery processes were investigated by use of pairs of voltage-clamp pulses with a variable interval between them, enflurane but not propofol slowed the recovery of contractions and calcium-activated 'tail' currents. These observations are consistent with the hypothesis that enflurane may impair calcium handling by the sarcoplasmic reticulum whereas propofol has little, if any, effect at this site. 6. In conclusion, the actions of propofol and enflurane on second inward currents contribute to their effects on action potentials and contraction. The negative inotropic effect of both anaesthetics may result partly from reduced calcium influx to trigger contraction, and for enflurane, partly from an impairment of calcium handling by the sarcoplasmic reticulum.

Animals↗
PubMed1993

Effect of enflurane and isoflurane on norepinephrine kinetics: a new approach to assessment of sympathetic function during anesthesia.

We investigated the effects of enflurane [1.0 and 1.5 minimum alveolar concentration (MAC)] and isoflurane (1.0, 1.5, and 2.0 MAC) on norepinephrine (NE) spillover (a measure of NE release rate) and NE clearance in 16 dogs, by using an isotope (3H-NE) dilution technique. During anesthesia with either enflurane or isoflurane, endogenous NE concentrations decreased markedly. In contrast, 3H-NE concentrations increased or remained unchanged. There was a significant (P < 0.05) reduction in NE spillover with both anesthetics at all doses studied. NE spillover decreased by 54% +/- 6% and 68% +/- 4% at 1.0 MAC enflurane and 1.5 MAC enflurane, respectively. Isoflurane decreased NE spillover by 54% +/- 8%, 59% +/- 9%, and 71% +/- 8% at 1.0 MAC, 1.5 MAC, and 2.0 MAC isoflurane, respectively. NE clearance was reduced by both anesthetics; enflurane reduced NE clearance (P < 0.05) at all concentrations studied, whereas NE clearance was reduced by 24% +/- 8% from awake values only at the highest dose of isoflurane (P < 0.05, 2.0 MAC). For enflurane, NE clearance was decreased by 17% +/- 5% at 1.0 MAC and 37% +/- 7% at 1.5 MAC enflurane. Because decreased NE clearance would otherwise have increased NE plasma concentration, our measured decreases in endogenous plasma NE concentrations probably did not reflect the actual extent of sympathetic inhibition produced by enflurane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed2000

Comparative effects of diltiazem with enflurane or desflurane on myocardial contractility and heart rate in the isolated rat hearts.

BACKGROUND: The volatile anesthetics may reduce cardiac contractility by limiting both membrane Ca2+ entry and altering intracellular Ca2+ release. Additional pharmacological effects of calcium channel blockers could potentially enhance anesthetic-induced depression. The aim of this study was to compare the direct cardiac effects of enflurane and a new volatile anesthetic, desflurane, in combination with diltiazem on the isolated Sprague-Dawley rat heart. METHODS: After stabilization period isolated rat hearts (n = 40) were perfused with an oxygenated modified Krebs' solution at 55 mmHg equilibrated with 1, 2 and 3 MAC of enflurane (1.7, 3.4 and 5.1 vol% respectively) or desflurane (6, 12 and 18 vol% respectively) in combination with 100 ng/mL diltiazem at 36 degrees C. Isovolumetric left ventricular pressure (LVP), rate of change of ventricular pressure (dp/dt), spontaneous heart rate and coronary flow were measured. To examine the indirect metabolic effect due to autoregulation of coronary flow, O2 delivery (DO2), myocardial O2 consumption (MVO2) and percent O2 extraction (POE) were also monitored. RESULTS: Diltiazem plus enflurane or desflurane depressed LVP and dp/dt dose-dependently. Enflurane plus diltiazem significantly decreased heart rate more than desflurane plus diltiazem in a dose-dependent manner. Desflurane plus diltiazem significantly increased coronary flow more than enflurane plus diltiazem and oxygen delivery increased proportionally with coronary flow. But there were statistically insignificant dose-dependent increases in both groups. Myocardial oxygen consumption and percentage of oxygen extraction were also decreased dose-dependently in both groups. Bradydysrhythmia that accompanied atrioventricular dissociation occurred with diltiazem plus high enflurane or desflurane concentration at an incidence of 46% and 40% respectively. CONCLUSIONS: These in vitro results demonstrate that diltiazem plus enflurane or desflurane depresses left ventricular contractile function and diltiazem plus enflurane causes higher incidence of bradydysrhythmia more than equivalent levels of diltiazem plus desflurane.

Anesthetics, Inhalation↗
PubMed1992

[Interaction of nicardipine and inhalational anesthetics--comparison between enflurane and isoflurane].

The effects of nicardipine 1 mg bolus injection under enflurane anesthesia were compared with those under isoflurane anesthesia. Twelve neurosurgical patients were divided into 2 groups, enflurane group (n = 6) and isoflurane group (n = 6). In all patients anesthesia was induced with midazolam, thiamylal, fentanyl and vecuronium. Anesthesia was maintained with fentanyl, nitrous oxide, pancuronium plus enflurane (enflurane group) or plus isoflurane (isoflurane group). After incision of dura mater, nicardipine 1 mg was given through forearm venous line. For about 30 minutes before and after nicardipine injection, concentration of inhalational anesthetics was kept constant and no drugs were given. Blood pressure (BP), heart rate (HR), rate pressure product (RPP), and serum concentrations of catecholamine and nicardipine were monitored for 30 minutes after nicardipine injection. In isoflurane group, BP decreased more and longer, and increases of HR and serum concentration of catecholamine continued longer compared with enflurane group. Elimination half life of nicardipine was shorter, area under the curve (AUC) was smaller and clearance of nicardipine was larger in isoflurane group than in enflurane group. It was concluded that isoflurane increased the effects of nicardipine, which were BP depression and reflex sympathetic stimulation, than enflurane and that metabolism and elimination of nicardipine were accelerated more by isoflurane than by enflurane.

Anesthesia, Inhalation↗
PubMed1988

The increase in urinary alanine aminopeptidase excretion associated with enflurane anesthesia is increased further by aminoglycosides.

Urinary excretion of alanine aminopeptidase (AAP) is an extremely sensitive indicator of drug-induced renal tubular damage. The urinary excretion of AAP was determined in patients after enflurane anesthesia with or without concurrent aminoglycoside administration to determine if enflurane enhances the nephrotoxic potential of aminoglycosides. Twenty-two patients with normal renal function were studied. Ten received enflurane alone, eight received enflurane plus gentamicin or tobramycin, and four patients who underwent nitrous oxide and narcotic anesthesia were the control group. Preoperative values ranged from 1010 to 2461 microU/24 hour. Urinary AAP excretion increased significantly in both enflurane groups 2 days postoperatively (P less than 0.025). Patients who received both enflurane and aminoglycosides had significantly greater urinary AAP excretion on postoperative day 2 than did patients given enflurane alone: 21,342 +/- 4074 microU/24 hour and 6336 +/- 1496 microU/24 hour, respectively (mean +/- SEM, P less than 0.005). There was no change in AAP excretion in the control group compared to baseline; on day 3 AAP was 1412 +/- 710 microU/24 hour. No changes in blood urea nitrogen or serum creatinine levels were observed. These data suggest that enflurane increases the renal tubular effects of aminoglycosides, possibly increasing the risk of aminoglycoside renal toxicity.

Adult↗
PubMed1995

Retinal tissue oxygen tension in normoxic cats under enflurane anesthesia.

PURPOSE: General anesthesia reduces systemic blood pressure and, thus, ocular perfusion pressure (at constant intraocular pressure). Whether this reduction in ocular perfusion pressure produces retinal hypoxia is unknown. To answer this question, the authors measured inner retinal oxygen tension in cats under general enflurane anesthesia at three clinically relevant levels of anesthesia under normoxic conditions. METHODS: Polarographic oxygen microelectrodes were used to measure inner retinal oxygen tension in cats under enflurane anesthesia at 21% inspired oxygen tension. Measurements were made in the preretinal vitreous body within 100 to 200 microns of the internal limiting membrane of the retina. Three levels of enflurane anesthesia were used: 1.2%, 2.4%, and 3.6%, corresponding to 0.5, 1.0, and 1.5 minimal alveolar concentration. Intraocular pressure of the cats was maintained at a constant normal level throughout the experiments. RESULTS: Under normoxic conditions, inner retinal oxygen tension remained unchanged or increased slightly as ocular perfusion pressure decreased with deeper levels of enflurane anesthesia. CONCLUSION: Commonly used surgical levels of enflurane general anesthesia do not cause hypoxia of the inner retina in cats breathing 21% inspired oxygen. This may be the result of preservation of retinal vascular autoregulation under enflurane anesthesia, retinal vasodilatation secondary to a direct smooth muscle relaxing effect of enflurane, or decreased retinal oxygen use under enflurane anesthesia.

Anesthesia, Inhalation↗
PubMed1977

Inhibition of adrenal medullary catecholamine secretion by enflurane: II. Investigations in isolated bovine adrenals--site and mechanism of action.

To determine the site and mechanism of action underlying the inhibition of adrenal medullary catecholamine release by enflurane, the authors measured the effects of enflurane on catecholamine secretion evoked by various secretagogues in isolated bovine adrenals perfused with Locke's solution. Catecholamine concentrations in the perfusate were measured spectrofluorometrically. Enflurane caused concentration-dependent inhibition of catecholamine release in response to activation of the nicotinic receptors in the chromaffin cells with acetylcholine or dimethylphenylpiperazinium (DMPP). An enflurane concentration of 0.88 mM caused 50 per cent inhibition of the DMPP-induced secretion. The inhibition induced by enflurane was shown to be noncompetitive. The catecholamine release evoked by activation of the muscarinic receptors with pilocarpine was only slightly decreased by 3.74 mM enflurane. At this concentration the release in response to KCl, 56 mM, was partially inhibited, whereas the output in response to tyramine (from glands perfused with calcium-free Locke's solution) was unaffected. It is concluded that the site of action of enflurane is the cell membrane. At concentrations above 1 mM, enflurane may impair calcium ion influx, but at lower concentrations it probably interacts with hydrophobic regions of the nicotinic receptor.

Acetylcholine↗