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PubMed1977

Halothane hepatotoxicity and the reduced derivative, 1,1,1-trifluoro-2-chloroethane.

Halothane (1,1,1-trifluoro-2-bromo-2-chloroethane) is a safe, clinically useful inhalation anesthetic. Rare, unpredictable cases of liver necrosis have been reported following its use. Although the mechanism of this reaction in man is unknown the most plausible is biotransformation to reactive intermediates compounds. The oxidative metabolism of halothane appears to be benign. There is early evidence that reductive (nonoxygen dependent) may be harmful. Since the bromine atom of halothane appears to possess weak bond energy, the reduced, debrominated derivative of halothane, 1,1,1-trifluoro-2-chloroethane, was synthesized and tested for hepatotoxicity in the rat. The derivative is unstable and thus was prepared anaerobically and trapped in propylene glycol solvent. Injection of small amounts of this compound into the portal vein of rats produces extensive liver necrosis. It is postulated that biotransformation of halothane via a reductive pathway could produce this reactive intermediate metabolite.

Animals↗
PubMed1995

Inhibitory effects of corticoids on reductive halothane dehalogenation.

The effects of corticoids, hydrocortisone, methylprednisolone, betamethasone and dexamethasone, on the reductive metabolism of halothane to produce chloro-difluoroethylene (CDE) and chlorotrifluoroethane (CTE) in the liver microsomes of guinea-pig were examined. The substrate differential spectrum for methylprednisolone showed a peak at 412 nm and trough at 395 nm, typical modified type II. The other corticoids showed a similar spectral change. The corticoids had no effect on NADPH-cytochrome P450 reductase. All of these corticoids inhibited the reductive dehalogenation of halothane. The concentrations of hydrocortisone, methylprednisolone, betamethasone and dexamethasone causing 50% inhibition of CDE formation from halothane were 5.1 +/- 0.7 mg/ml, 3.1 +/- 1.2 mg/ml, 2.3 +/- 0.4 mg/ml and 2.4 +/- 0.6 mg/ml, respectively, with no significant differences except for hydrocortisone. The concentrations of hydrocortisone, methylprednisolone, betamethasone and dexamethasone causing 50% inhibition of CTE formation from halothane were 4.9 +/- 0.5 mg/ml, 3.1 +/- 1.0 mg/ml, 2.4 +/- 0.3 mg/ml and 28.0 +/- 9.1 mg/ml, respectively, with no significant differences except for dexamethasone. Our results showed that corticoids inhibit halothane metabolism.

Adrenal Cortex Hormones↗
PubMed1997

Volatile cardioplegia: fast normothermic cardiac arrest induction and recovery with halothane in isolated rat hearts.

To study the effect of halothane as a cardioplegic agent, ten Wistar rats were anesthetized by ether inhalation and their hearts were perfused in a Langendorff system with Krebs-Henseleit solution (36 degrees C; 90 cm H2O pressure). After a 15-min period for stabilization the control values for heart rate, force(T), dT/dt and coronary flow were recorded and a halothane-enriched solution (same temperature and pressure) was perfused until cardiac arrest was obtained. The same Krebs-Henseleit solution was reperfused again and the parameters studied were recorded after 1, 3, 5, 10, 20 and 30 min. Cardiac arrest occurred in all hearts during the first two min of perfusion with halothane-bubbled solution. One minute after reperfusion without halothane, the following parameters reported in terms of control values were obtained: 90.5% of control heart rate(266.9 +/- 43.4 to 231.5 +/- 71.0 bpm), 20.2% of the force (1.83 +/- 0.28 to 0.37 +/- 0.25 g), 19.8% of dT/dt (46.0 +/- 7.0 to 9.3 +/- 6.0 g/s) and 90.8% of coronary flow (9.9 +/- 1.5 to 9.4 +/- 1.5 ml/min). After 3 min of perfusion they changed to 99.0% heart rate (261.0 +/- 48.2), 98.9% force (1.81 +/- 0.33), 98.6 dT/dt (45.0 +/- 8.2) and 94.8% coronary flow (9.3 +/- 1.4). At 5 min 100.8% (267.0 +/- 40.6) heart rate, 105.0% (1.92 +/- 0.29) force and 104.4% (48.2 +/- 7.2) dT/dt were recorded and maintained without significant differences (P > 0.01) until the end of the experiment. These data demonstrate that volatile cardioplegia with halothane is an effective technique for fast induction of and prompt recovery from normothermic cardiac arrest of the rat heart.

Anesthetics, Inhalation↗
PubMed1976

Effects of change in concentration of calcium on myocardial contractility depressed by thiamylal and halothane.

The effects of change in the concentration of Ca++ on myocardial contractility depressed by thiamylal and halothane were studied in isolated dog heart muscle. The concentration of Ca++ in the bathing medium was increased stepwise from 1.9 to 20.9 mM. An increase in Ca++ concentration resulted in an increase both in net-shortening (delta1) and in maximum velocity of shortening at 0.4 g preload (V'max) which reached the maximum values at 11.4mM of Ca++. A further increase in Ca++ concentration rather decreased delta1 and V'max. The concentration-response relation curves in the presence of thiamylal (3.3 mg%) shifted to the right almost parallel to the control curve, with the peaks at 15.2 mM of Ca++. The result indicates that the depression of myocardial contractility produced by thiamylal is counteracted competitively by Ca++. However, the curves in the presence of halothane (5.0 +/- 0.4 mg%) were kept lower than those of the control, with the peaks at 7.6 mM of Ca++. The result shows that the counteraction of Ca++ to the depression of myocardial contractility was limited in the presence of halothane. A similar tendency was observed in maximum force of isometric contraction (Fm). Moreover, in the presence of halothane, the administration of higher concentrations of Ca++ almost always accompanied "after-contraction". From the result obtained and the literature concerned it was suggested that the mechanism for producing the depression of myocardial contractility might be different between thiamylal and halothane in relation to Ca++ movements at the Ca++ storage sites within the myocardium.

Animals↗
PubMed1977

Effects of halothane on coronary and systemic circulations, myocardial metabolism and blood flow distribution within the canine heart.

Myocardial metabolism, blood flow distribution within the heart, and coronary and systemic circulations were observed during halothane anesthesia using 15 mongrel dogs. Pao2 and Paco2 were maintained near 100 and 40 torr respectively throughout the study. As arterial halothane content increased, most parameters of systemic circulation were depressed significantly. Coronary blood flow was reduced in parallel with myocardial oxygen consumption (MVo2) (r=+0.89, pless than0.001). Myocardial contractility decreased significantly as anesthesia deepened. MVo2 and myocardial CO2 production were reduced as arterial halothane concentration rose. Arterial-coronary venous difference in blood oxygen content remained unchanged even in deep stage. Lactate and pyruvate were continuously taken up by the myocardium, although the amounts of uptake were reduced as anesthesia progressed. Calculated excess lactate and redox potential did not show any signs of myocardial hypoxia even in deep halothane anesthesia. Among major hemodynamic parameters, left ventricular dp/dt max showed the closest correlation with MVo2. Microsphere injection method was used to observe blood flow distribution within the heart. Halothane did not influence the distribution significantly and I/O ratio of the left ventricular free wall remained near 1.0 during the study.

Animals↗
PubMed1986

Reduction in the myocardial sodium current by halothane and thiamylal.

Effects of two general anesthetics, halothane and thiamylal, on the fast sodium inward current (INa) of enzymatically isolated single rat ventricular cells were studied under current clamp and voltage clamp conditions. A suction pipette technique was used for potential measurement, current injection and internal perfusion of isolated cells. In current clamp experiments, sodium action potential was elicited in a Ca-free Co Krebs solution and the action potential was reduced by 0.5% halothane and 5 X 10(-5) M thiamylal. In voltage clamp experiments, the calcium current was suppressed by replacing Ca with Co and the potassium current was eliminated by replacing K with Cs and adding 4-aminopyridine and tetraethylammonium. Both anesthetics decreased INa, in a dose dependent manner, without changing the shape of the current-voltage curve. Halothane (1%) shifted the steady state inactivation curve in a negative direction along the potential axis by 8.5 +/- 2 mV (mean +/- S.D., n = 4). Thiamylal, 5 X 10(-5) and 10(-4) M, shifted the curve in a negative direction by 4.4 +/- 0.8 mV (n = 5) and 8.6 +/- 3.2 mV (n = 5), respectively. Both agents slightly reduced the maximum sodium conductance (gNa). Halothane (1%) increased half recovery time from inactivation measured at -80 mV from 30 +/- 15 to 80 +/- 25 ms (n = 4). Thiamylal (10(-4) M) prolonged it at - 75 mV from 50 +/- 20 to 110 +/- 15 ms (n = 5). With a test pulse duration of 50 ms, neither drug produced a use-dependent inhibition of INa. Halothane and thiamylal depress the INa of cardiac muscles mainly by shifting the steady state inactivation curve in a negative direction along the potential axis. Relatively small prolongation of half recovery time from inactivation and no sign of use-dependent inhibition suggest a molecular mechanism which differs in some respects from the local anesthetics.

Animals↗
PubMed2004

Influence of morphine sulfate on the halothane sparing effect of xylazine hydrochloride in horses.

OBJECTIVE: To quantitate the dose and time-related effects of morphine sulfate on the anesthetic sparing effect of xylazine hydrochloride in halothane-anesthetized horses and determine the associated plasma xylazine and morphine concentration-time profiles. ANIMALS: 6 healthy adult horses. PROCEDURE: Horses were anesthetized 3 times to determine the minimum alveolar concentration (MAC) of halothane in O2 and characterize the anesthetic sparing effect (ie, decrease in MAC of halothane) by xylazine (0.5 mg/kg, i.v.) administration followed immediately by i.v. administration of saline (0.9% NaCI) solution, low-dose morphine (0.1 mg/kg), or high-dose morphine (0.2 mg/kg). Selected parameters of cardiopulmonary function were also determined over time to verify consistency of conditions. RESULTS: Mean (+/- SEM) MAC of halothane was 1.05 +/- 0.02% and was decreased by 20.1 +/- 6.6% at 49 +/- 2 minutes following xylazine administration. The amount of MAC reduction in response to xylazine was time dependent. Addition of morphine to xylazine administration did not contribute further to the xylazine-induced decrease in MAC (reductions of 21.9 +/- 1.2 and 20.7 +/- 1.5% at 43 +/- 4 and 40 +/- 4 minutes following xylazine-morphine treatments for low- and high-dose morphine, respectively). Overall, cardiovascular and respiratory values varied little among treatments. Kinetic parameters describing plasma concentration-time curves for xylazine were not altered by the concurrent administration of morphine. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of xylazine decreases the anesthetic requirement for halothane in horses. Concurrent morphine administration to anesthetized horses does not alter the anesthetic sparing effect of xylazine or its plasma concentration-time profile.

Adjuvants, Anesthesia↗
PubMed2000

Hepatic effects of halothane and isoflurane anesthesia in goats.

OBJECTIVE: To determine hepatic effects of halothane and isoflurane anesthesia in young healthy goats. DESIGN: Randomized prospective clinical trial. ANIMALS: 24 healthy 9-month-old female goats. PROCEDURE: Goats were sedated with xylazine hydrochloride and ketamine hydrochloride and anesthetized with halothane (n = 12) or isoflurane (12) while undergoing tendon surgery. End-tidal halothane and isoflurane concentrations were maintained at 0.9 and 1.2 times the minimal alveolar concentrations, respectively, and ventilation was controlled. Venous blood samples were collected approximately 15 minutes after xylazine was administered and 24 and 48 hours after anesthesia, and serum aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT) activities and bilirubin concentration were measured. Goats were euthanatized 25 or 62 days after anesthesia, and postmortem liver specimens were submitted for histologic examination. RESULTS: All goats recovered from anesthesia and survived until euthanasia. Serum SDH, GGT, and ALP activities and bilirubin concentration did not increase after anesthesia, but serum AST activity was significantly increased. However, serum hepatic enzyme activities were within reference limits at all times in all except 1 goat in which serum AST activity was high 24 and 48 hours after anesthesia. This goat had been anesthetized with halothane and had the longest duration of anesthesia. No clinically important abnormalities were seen on histologic examination of liver specimens. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that use of halothane or isoflurane for anesthesia in young healthy goats is unlikely to cause hepatic injury.

Alkaline Phosphatase↗
PubMed2006

Effects of halothane sensitivity on mobility status and blood metabolites of HAL-1843-normal pigs after rigorous handling.

The objective of this study was to determine if HAL-1843-normal pigs that respond abnormally to halothane anesthesia were more likely to become nonambulatory (NA) when subjected to rigorous handling than pigs that exhibit a normal response to halothane. After a 1,100-km transport, pigs exhibiting low (HS-L; n = 33), intermediate (HS-I; n = 10), and high (HS-H; n = 47) sensitivity to halothane were moved through a 36.6-m long aisle that was 2.1 m wide at each end and 0.6 m wide in the middle 18.3 m. Ten groups of 8 pigs were briskly moved down the aisle and back 4 times, receiving a minimum of 1 electrical prod per pass (8 prods/pig). Before testing, rectal temperature was measured, open-mouth breathing and skin discoloration were visually evaluated, and a blood sample was collected from each pig. After the test, the pigs were returned to their pens, and the same measurements were taken immediately posttest and 1 h posttest (no blood at 1 h posttest). Pigs that were HS-H were more prone to becoming NA compared with HS-L pigs (P < 0.02). Regardless of halothane status, a greater number of pigs exhibited open-mouth breathing and skin discolorations immediately posttest than at the pretest or 1 h posttest times (P < 0.05). No differences were observed in blood metabolites between the different halothane sensitivity categories. However, pigs that became NA had elevated blood levels of creatine phosphokinase, lactate, glycerol, nonesterified fatty acids, ammonia, and urea nitrogen before testing (P < 0.05). Collectively, these data suggest HS-H pigs are more susceptible to becoming NA than HS-L. The elevated pretest blood metabolites of NA pigs suggest that they were in a hypermetabolic state that predisposed them to becoming NA.

Anesthetics, Inhalation↗
PubMed2004

Is isoflurane safer than halothane in equine anaesthesia? Results from a prospective multicentre randomised controlled trial.

REASONS FOR PERFORMING STUDY: Approximately 1 in 100 horses suffer unexpectedly from anaesthetic-related death. Identification and use of the safest anaesthetic drugs should support this aim. Experimental evidence has suggested that isoflurane should be a safer maintenance agent in equine anaesthesia than halothane. HYPOTHESIS: The death rate would be reduced in horses being maintained with isoflurane compared to halothane. METHODS: A multicentre randomised controlled trial was undertaken to compare the effects of isoflurane and halothane for maintenance of equine anaesthesia for all types of operation. Data were analysed from 8242 horses in which anaesthesia was maintained with either halothane or isoflurane using mixed effects logistic regression models. RESULTS: No overall benefit of either drug was detected. However, although not part of the primary hypothesis, data showed that the overall death rate was significantly reduced in horses age 2-5 years with isoflurane and that death from cardiac arrest was also reduced with isoflurane, particularly in high risk cases. CONCLUSIONS AND POTENTIAL RELEVANCE: Halothane remains an acceptable anaesthetic for maintenance of anaesthesia in horses, but isoflurane may be safer in the young horse and in high risk cases.

Age Factors↗
PubMed1985

Dose effects of halothane on sensory evoked responses obtained from the cortex, reticular formation and central gray.

Sensory evoked field potentials were recorded from the mesencephalic reticular formation (MRF), central gray (CG) and somatosensory cortex (SCX), following incremental doses of halothane in freely-moving rats. Halothane concentrations of 0.25%, 0.5% 1.0% and 2.0% were used. In general, the responses from each structure were affected in dose response manner. The averaged acoustic evoked responses (AAER) exhibit more sensitivity to halothane than the averaged visual evoked responses (AVER). The evoked response and its components obtained from each structure were affected differently by halothane mainly following the initial two halothane doses, (0.25% and 0.5%); mainly increase in amplitude was observed in the recording obtained from the MRF, decrease in the CG, and mixed (increase and/or decrease) in SCX. The degree of the depression of the sensory evoked responses was directly correlated to the level of anesthesia as assessed by sural nerve stimulation.

Animals↗
PubMed1996

Halothane inhibits T cell proliferation and interleukin-2 receptor expression in rats.

In order to determine the effects of halothane on rat cell-mediated immune function, rats were exposed to 1% halothane for up to 5 hours. Immediately, 24 hours or 48 hours following anesthesia, rat lymphocytes from the spleen were analyzed for their ability to respond to the mitogens phytohemagglutinin (PHA), pokeweed mitogen (PWM), concanavalin A (ConA) and lipopolysaccharide (LPS). In addition, percentages of lymphocyte subpopulations in the spleen were assessed as well as ability of the lymphocytes to express specific receptors. Extended periods of halothane anesthesia (5 hours) suppressed the ability of the lymphocytes to respond to the mitogen PHA immediately following anesthesia. Twenty-four hours later, proliferative responses to the mitogens PHA, PWM and ConA were significantly reduced. However, by 48 hours following treatment, proliferative responses were normal. Halothane did not alter proliferative responses to the mitogen LPS. Prolonged anesthesia (5 hours) also increased the percentage of T and CD8+ (cytotoxic) lymphocytes in the spleen, although for less than 24 hours. The ability of T lymphocytes to express both the CD8 and CD25 (IL-2) receptors in response to PHA were suppressed. These results suggest that halothane suppresses rat T cell function, perhaps through suppression of IL-2 receptor expression.

Animals↗
PubMed2004

Halothane induced hepatitis: case report.

Halothane as a cause of hepatitis is rare and may be overlooked when evaluating a patient with sudden onset jaundice. A 34-year-old lady, a nurse, presented to the liver clinic with sudden onset non-pruritic jaundice. Viral and collagen serological tests were all normal, malaria and sickling tests were negative, but transaminases were elevated. She reported inadvertent exposure to halothane in surgical theatre where she works. She improved on conservative management, then had a re-exposure to halothane after three weeks and developed a similar clinical picture, which improved on conservative management. In an area endemic of malaria, hepatitis and haemolysing conditions like sickle cell anaemia, the diagnosis of halothane hepatitis requires high index of suspicion. The mechanism of halothane-induced hepatic damage in this patient is very likely idiosyncratic. This is because of the modest dose at first exposure and more severe clinical picture at re-exposure.

Adult↗
PubMed1999

Cardiovascular effects of epidurally administered oxymorphone and an oxymorphone-bupivacaine combination in halothane-anesthetized dogs.

OBJECTIVE: To evaluate cardiovascular effects of epidurally administered oxymorphone (OXY) and an OXY-bupivacaine combination (O/B) in halothane-anesthetized dogs. ANIMALS: 6 dogs. PROCEDURE: In a randomized crossover design study, dogs were anesthetized with halothane and given OXY, O/B, and saline solution (SAL). Eucapnia and end-tidal halothane concentration of 1.2% were established. Heart rate (HR), systemic and pulmonary arterial pressures, central venous pressure (CVP), and cardiac output were measured at baseline and 5, 15, 30, 45, 60, and 75 minutes after treatment. At 90 minutes, glycopyrrolate was administered IV, and measurements were repeated at 95 minutes. Cardiac index (CI), stroke volume, stroke index, systemic vascular resistance (SVR), and left ventricular work were calculated. End-tidal halothane concentration was decreased to 0.8% from 17 to 45 minutes and to 0.5% from 47 to 95 minutes for OXY and O/B, whereas for SAL, it was maintained at 1.5 and 1.2%, respectively. Samples were obtained at 0, 2, 5, 15, 30, 45, 60, and 95 minutes for measurement of serum opiate concentration and comparison with values after IM administration of OXY. RESULTS: HR decreased, but CVP and SVR increased in response to OXY and O/B. These changes were reversed after IV administration of glycopyrrolate, resulting in significant increase in CI, compared with that in response to SAL. Serum opiate concentration increased markedly and peaked within 15 minutes after OXY and O/B administration but did not differ from values after IM administration. CONCLUSIONS: Epidural administration of OXY results in rapid systemic uptake and decreased HR. Glycopyrrolate administration improves HR, resulting in improved CI at equipotent halothane concentrations.

Analgesia, Epidural↗
PubMed1998

[Discordance and cosegregation of swine halothane susceptibility and 1843 C-T mutation of their RYR1 locus responsible for the ryanodine receptor].

In two Siberian swine populations, the halothane test and PCR were used to determine the halothane susceptibility of the animals and to reveal a point mutation in their RYR1 gene, respectively. No correlations were found between the halothane susceptibility of an animal and the presence or absence of a point mutation at its RYR1 locus. However, the population changes in halothane susceptibility and the frequency of the mutation proved to be unidirectional. In the studied swine populations, the halothane-susceptible animals had no hyperthermia and the frequencies of their Hal and RYR1 genes changed similarly. These phenomena along with the phylogenesis of malignant hyperthermia and the porcine stress syndromes (PSS) in different breeds are discussed. In the populations studied, PSS is suggested to be under the polygenic control.

Anesthetics, Inhalation↗
PubMed1999

[The study of the anesthetic action of halothane on the rat spinal cord by fos immunoreactivity].

This study was performed to examine the anesthetic action of halothane on the spinal cord of rats by using fos immunoreactivity, a marker for neuronal activity following noxious stimulation. Sprague-Dawley rats were injected with 150 microliters of 5% formalin subcutaneously into the left hindpaw. Control group (n = 5) received 100% oxygen for 3 hours after injection. 1 MAC group (n = 5) and 1.5 MAC group (n = 5) of rats were anesthetized with 1 MAC or 1.5 MAC halothane, respectively, for 3 hours after injection. The number of fos immunoreactive cells was counted in the lumbar spinal cord of each rat. All rats showed escape reactions against noxious stimulation in the control group. In the 1 MAC and 1.5 MAC groups, two of five rats showed response to noxious stimulation and the another three showed no response, respectively. There was profound relation between the responding rats and the expression of fos immunoreactivity in the spinal dorsal horn. The number of fos immunoreactive cells decreased in the cord of rats that showed no response to noxious stimulation by halothane 1 or 1.5 MAC. These findings suggest that halothane has analgesic action on spinal nociceptive neurons in the rats on the condition that its reactions to noxious stimulation are suppressed by halothane of any concentration.

Anesthesia, Inhalation↗
PubMed1999

Hemodynamic effects of ionized calcium in horses anesthetized with halothane or isoflurane.

OBJECTIVES: To evaluate the effects of halothane and isoflurane on cardiovascular function and serum total and ionized calcium concentrations in horses, and to determine whether administration of calcium gluconate would attenuate these effects. ANIMALS: 6 clinically normal adult Thoroughbreds. PROCEDURE: Catheters were inserted for measurement of arterial blood pressures, pulmonary arterial blood pressures, right ventricular pressure (for determination of myocardial contractility), right atrial pressure, and cardiac output and for collection of arterial blood samples. Anesthesia was then induced with xylazine hydrochloride and ketamine hydrochloride and maintained with halothane or isoflurane. An i.v. infusion of calcium gluconate was begun 75 minutes after anesthetic induction; dosage of calcium gluconate was 0.1 mg/kg of body weight/min for the first 15 minutes, 0.2 mg/kg/min for the next 15 minutes, and 0.4 mg/kg/min for an additional 15 minutes. Data were collected before, during, and after administration of calcium gluconate. RESULTS: Halothane and isoflurane decreased myocardial contractility, cardiac index, and mean arterial pressure, but halothane caused greater depression than isoflurane. Calcium gluconate attenuated the anesthetic-induced depression in cardiac index, stroke index, and maximal rate of increase in right ventricular pressure when horses were anesthetized with isoflurane. When horses were anesthetized with halothane, a higher dosage of calcium gluconate was required to attenuate the depression in stroke index and maximal rate of increase in right ventricular pressure; cardiac index was not changed with calcium administration. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of calcium gluconate may support myocardial function in horses anesthetized with isoflurane.

Anesthesia, Inhalation↗
PubMed2000

[Halothane anesthesia decreases the level of interstitial striatal dopamine of awake freely moving rats in an in vivo microdialysis study].

We investigated the effect of halothane on the level of interstitial dopamine of in vivo awake, free moving rats brain striatum using microdialysis techniques. Rats were implanted a microdialysis probe to right striatum of the brain and administered 1.5% of halothane (approximately 1.2 MAC) for 1 or 2 hours, and dialysates from the probe were determined every 20 minutes. Halothane anesthesia reduced the amount of dopamine derived from dialysate, and after discontinuation of halothane and at emergence from anesthesia, the level of dopamine was increased. The levels of metabolites of dopamine during anesthesia were increased lineally in a time dependent manner. We hypothesized that halothane might increase the rate of re-uptake of dopamine at nerve endings and decreased level of interstitial dopamine is compensated by dopamine releases during anesthesia.

Anesthesia, Inhalation↗