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PubMedDate not supplied

Effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart.

The effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart were examined. Reperfusion-induced ventricular fibrillation (VF) occurred in all rat hearts, and the duration of VF was 151 +/- 11 (mean +/- SEM) seconds in the control group (no anesthetics administered). Sevoflurane changed neither incidence nor duration of VF at 1, 2, and 3 minimum alveolar concentrations (MAC) of anesthetic. Halothane altered neither the incidence nor duration of VF compared with the control group at 1 MAC; however, at 2 and 3 MAC, halothane significantly reduced the incidence and duration of VF (P < 0.05 at 1, 2, and 3 MAC halothane: respective incidences were 100%, 18%, and 55% and respective durations, 82 +/- 27 seconds, 20 +/- 6 seconds, and 13 +/- 9 seconds). In the isolated rat heart, we found that halothane has antiarrhythmic effects against reperfusion-induced arrhythmia at 2 and 3 MAC. Sevoflurane, however, did not have any antiarrhythmic effects against reperfusion-induced arrhythmia at 1, 2, or 3 MAC.

Animals↗
PubMed1993

Effects of halothane anesthesia on the motility of the sphincter of Oddi and transsphincteric flow in Australian brush-tailed possums.

We evaluated the effect of halothane anesthesia on the motility of the sphincter of Oddi and simultaneous transsphincteric flow in Australian Brush-tailed possums (Trichosurus vulpecula). Halothane levels in the range of 0.25 to 2% were administered and decreased transsphincteric flow in a dose-dependent manner. Sphincter of Oddi basal pressure was higher than normal, but not in a dose-dependent manner. Additionally, halothane anesthesia influenced the sphincter of Oddi motility by decreasing the motility index (mean amplitude multiplied by frequency of contractions). This decrease was dose dependent. These findings indicate that sphincter of Oddi basal pressure is a major component of sphincter of Oddi motility responsible for regulating transsphincteric flow in this species. For studies of the sphincter of Oddi motility in anesthetized Australian Brush-tailed possums, we recommend anesthetic induction with ketamine (50 mg/kg, i.m.) and the inspired halothane level should not exceed 0.75% during the study period, as the effects we have demonstrated were most evident at levels greater than 0.75%. If higher halothane levels are required to maintain satisfactory anesthesia, an alternative anesthetic agent should be considered.

Animals↗
PubMed1993

[Changes in the cell cycle of cultured lymphocytes from patients subjected to halothane anesthesia].

The effect of halothane anesthesia on the proliferative activity of peripheral blood lymphocytes was analyzed. Included in the study were 7 patients. Lymphocyte cultures were prepared by standard methods with blood samples obtained immediately before the operation, after the effect of halothane anesthesia was over and 24 hours later. 5-bromodeoxyuridine in concentration 10 micrograms/ml was used for labelling cells which had passed 1, 2 or more mitotic cycles within the cultivation time. Cell proliferation rate was evaluated by the proportion of metaphases from I, II and III mitotic cycle. Lymphocyte proliferation in the cultures was shown to be inhibited after halothane anesthesia. Inhibition was particularly strong in the first post-halothane sample, but kept on being strong also 24 hours later. The first mitotic cycle was markedly prolonged--to such a degree that subsequent cycles within the 72-hour cultivation period were fully absent. The results were discussed in the light of the overall effect of halothane in the process of its metabolism, its effect on DNA synthesis and eventual implication of additional immunologic mechanisms.

Adult↗
PubMed1996

Adrenoceptor mechanism involved in thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs.

Although thiopental is known to potentiate halothane-epinephrine arrhythmias, the precise mechanism of this potentiation is obscure. The authors investigated the comparative role of alpha 1 and beta adrenergic actions in the thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs. Adult mongrel dogs were anesthetized with halothane alone (1.3%) or thiopental (20 mg kg-1) plus halothane and monitored continuously for systemic arterial pressures and for premature ventricular contractions. The arrhythmogenic doses of phenylephrine and isoproterenol were determined during the two anesthetic methods and the effect of thiopental on the arrhythmogenic action of alpha 1 and beta agonists was examined. Thiopental failed to exert a significant potentiation of arrhythmogenic effect of phenylephrine or isoproterenol, when these agents were administered separately. On the other hand, the potentiation of arrhythmogenicity by thiopental was remarkable in the case of combined administration of both the agonists, that is, thiopental enhanced the synergistic interaction between phenylephrine and isoproterenol for inducing arrhythmias during halothane anesthesia. In addition, the potentiation was more prominent when a low dose of isoproterenol and a high dose of phenylephrine was combined than that when a high dose of isoproterenol and a low dose of phenylephrine was given in combination. The results indicate that thiopental significantly potentiates the arrhythmogenic interaction of alpha 1 and beta adrenergic agonists administered concurrently, although individual potentiation of these agonists is not significant.

Anesthetics↗
PubMed1992

Cardiovascular effects of dopexamine HCl in conscious and halothane-anaesthetised horses.

The cardiovascular effects of serial increasing infusions of dopexamine HCl were investigated in six conscious (1, 2, 4, 6, 10 micrograms/kg bodyweight [bwt]/min) and eight (0.5, 1, 5, 10, 20 micrograms/kg bwt/min) halothane-anaesthetised horses. Dopexamine produced dose-dependent increases in heart rate, +dP/dtmax' -dP/dtmax and cardiac output, and a decrease in systemic vascular resistance in conscious and halothane-anaesthetised horses. Mean arterial blood pressure did not change in conscious horses but increased to a maximum value at 10 micrograms/kg bwt/min in halothane-anaesthetised horses. Thereafter, median artery blood flow decreased. Ventricular arrhythmias occurred in two conscious horses during the infusion of 10 micrograms/kg bwt/min dopexamine HCl. No cardiac arrhythmias other than sinus tachycardia were observed in halothane-anaesthetised horses. The administration of propanolol eliminated the haemodynamic response to the infusion of 5 and 10 micrograms/kg bwt/min dopexamine HCl in halothane-anaesthetised horses. The haemodynamic effects of dopexamine HCl offer specific advantages over dopamine and dobutamine for the treatment of low cardiac output states in horses.

Adrenergic beta-Agonists↗
PubMed1997

Comparison of sevoflurane with halothane in pediatric ambulatory anesthesia: an experience in Taiwan.

BACKGROUND: Sevoflurane, with blood/gas partition coefficient of 0.69 and MAC of 1.76 is a fast acting, potent inhalation anesthetic. Its suitability and safety for pediatric ambulatory anesthesia were assessed and compared with that of halothane. METHODS: Thirty two unpremedicated pediatric patients undergoing elective herniorrhaphy on day-surgery basis were randomly allocated to 2 groups of equal number to receive either sevoflurane or halothane anesthesia. Employing mask technique, anesthesia was induced with 60% nitrous oxide and 3 MAC of either sevoflurane or halothane in oxygen. Anesthesia was maintained respectively with 1-1.5 MAC of sevoflurane or halothane. The induction time, emergence time and untoward effects during anesthesia were analyzed and compared. RESULTS: It was shown that both the induction time and emergence time were significantly shorter in patients receiving sevoflurane. None had major complications. CONCLUSIONS: The results strongly suggest that sevoflurane is preferable to halothane for pediatric ambulatory anesthesia.

Ambulatory Surgical Procedures↗
PubMed1977

The role of the canine spleen in cardiovascular homeostasis during halothane anesthesia.

Barbiturate anesthesia is known to increase canine splenic sequestration of red blood cells. In our laboratory, high halothane concentrations have produced a decreased arterial hematocrit in the dog. In order to assess the role of the spleen in this phenomenon, central hematocrit, plasma volume, and ventricular hemodynamics were studied at low and high halothane concentrations before and after splenectomy in the same group of dogs. Although the hematocrit difference was less after splenectomy, it was not abolished. In addition, there was more cardiovascular depression by equivalent or lower halothane doses after splenectomy. It appears that the dog has other areas of red cell sequestration than the spleen accounting for the persistently lower hematocrit with high halothane concentrations after splenectomy. The modifying effect of the canine spleen on the circulatory depression produced by halothane should be taken into account when the drug is used in the dog.

Anesthesia, Inhalation↗
PubMed1997

The arrhythmogenic dose of epinephrine in halothane and isoflurane anesthetized dogs: an assessment of repeatability.

Repeat determinations of the arrhythmogenic dose of epinephrine (ADE) were made over two 6 h periods on 2 separate days during halothane and isoflurane anesthesia. Each of 6 dogs underwent 4 trials (2 halothane and 2 isoflurane). During each trial, the ADE was determined at baseline, 3 and 6 h. Epinephrine was infused for 3.0 min at increasing dose rates (2.5, 5.0, 10.0 and 20.0 mg/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached. The inter-infusion interval was 20 min. There were no significant differences in the measured cardiovascular parameters (SBP, DBP, MBP, and HR), arterial blood gases, or acid-base status prior to each determination during a single trial. The cardiovascular responses to epinephrine infusion were not significantly different between inhalants or determinations. The range of the ADE determined over both trials during isoflurane anesthesia was 30.12 +/- 12.21 micrograms/kg to 50.83 +/- 9.17 micrograms/kg. The baseline ADE during Day 1 of halothane anesthesia (6.70 +/- 1.36 micrograms/kg) was significantly greater than ADE determinations at 3 (4.65 +/- 0.88 micrograms/kg) and 6 h (4.61 +/- 0.87 micrograms/kg). The reduction in the ADE over time during day 2 of halothane anesthesia was not statistically significant (P = 0.0669). These results suggest that during halothane anesthesia, the ADE is not repeatable over time, and they may influence our interpretation of the results of investigations that measure alterations in the ADE due to pharmacological manipulations without repeated control ADE determinations.

Acid-Base Equilibrium↗
PubMed1997

Effects of halothane and sevoflurane on the electroretinogram of dogs.

OBJECTIVE: To study the effects of halothane and sevoflurane on the electroretinogram of dogs. ANIMALS: 6 clinically normal Beagles. PROCEDURE: Beagles were paralyzed by continuous IV administration of muscle relaxant and were artificially ventilated with a gas mixture of nitrous oxide and oxygen during experiments. Corneal electroretinograms were recorded, using full-field stimuli under several recording conditions before and during 1% halothane or 2% sevoflurane inhalation. RESULTS: The amplitude of the scotopic threshold response (STR) and b-wave was significantly decreased by halothane or sevoflurane inhalation, but the degree of decrease in the STR was much greater. In contrast, the amplitudes of oscillatory potentials were increased. The peak latencies of the 3 components tended to be prolonged by inhalation of the anesthetic. There seemed to be no difference between the effects of halothane and sevoflurane. CONCLUSIONS: Halothane and sevoflurane strongly depressed the STR in Beagles while moderately depressing the b-wave and increasing oscillatory potential amplitudes. Thus, neither is an appropriate anesthetic for use in recording of the STR in dogs.

Anesthetics, Inhalation↗
PubMed1998

Role of potassium channels in halothane-epinephrine arrhythmias.

It has been reported that antiarrhythmic drugs possessing the property of potassium channel blockade were most effective in preventing halothane-epinephrine induced arrhythmias. Recent attention has focused on ATP-sensitive potassium (K(ATP)) channels because of their contribution to the cardiovascular actions of volatile anesthetics. The present study was designed to evaluate whether K(ATP) channels or transient outward potassium channels (Ito) were involved in the mechanism of halothane-epinephrine arrhythmias in rat. Rats were anesthetized with halothane (1.5%), and the lungs were mechanically ventilated. The arrhythmogenic thresholds of epinephrine during halothane anesthesia were determined in 74 rats receiving saline or one of tested agents. The arrhythmogenic dose of epinephrine (ADE) was significantly increased by a K(ATP) channel opener, JTV506 (P < 0.01), and had a tendency to be increased by other K(ATP) channel openers, cromakalim, nicorandil, KRN2391 and Y 26763, but were not affected by a K(ATP) channel blocker, glibenclamide. The Ito blocker, 4-aminopyridine, also significantly increased the ADE. Epinephrine produced second-degree or complete atrioventricular block in 4 out of 7 rats receiving glibenclamide. These results suggest that Ito but not K(ATP) channels might be involved in the mechanism in producing halothane-epinephrine arrhythmias.

Adenosine Triphosphate↗
PubMed1998

Halothane hepatitis.

Halothane, an effective and usually safe anaesthetic agent, is rarely associated with the development of fulminant hepatic failure. Guidelines have been developed to reduce the probability of a patient developing halothane hepatitis. However, cases continue to occur and, in some cases, the guidelines have been ignored. Stricter adherence to the guidelines will reduce, but not totally prevent, further cases from occurring. Once halothane hepatitis has developed, there are no specific treatments and liver replacement may be required. Halothane hepatitis is a paradigm for immune mediated adverse drug reactions. The mechanism appears to be related to development of sensitization to both autoantigens (including CYP2D6) and halothane-altered liver cell determinants.

Anesthetics, Inhalation↗
PubMed1976

Preferential inhibition of DNA synthesis in mouse hemopoietic cells by halothane.

The effect of prolonged light halothane anesthesia (0.8%) on the proliferation rate of different mouse tissues was investigated, using [5-125I]5-iodo-2-deoxyuridine uptake into DNA as the test parameter. It was found that DNA synthesis in spleen, femoral bone marrow, and, occasionally, the small intestine was significantly depressed after exposure for 24 hr to halothane in vivo. The time course of DNA synthesis inhibition was then investigated by utilizing a shorter (6-hr) exposure time. This period was found to be insufficient to cause DNA synthesis inhibition in any of test tissues. Because anesthesia was found to be associated with hypothermia at normal room temperatures, it was established that the inhibition of DNA synthesis was not due to cooling of the mice under anesthesia by demonstrating that inhibition in sensitive tissues occurred at warmer temperatures as well. To examine the specificity of this finding, the DNA synthesis rate of cells in other normal tissues, e.g., skin and muscle, and in s.c.-growing tumor cells of a mouse mammary carcinoma, L1210 leukemia, and a first transplant AKR lymphoma were examined. In none were responses noted with 24 hr of halothane exposure. However, halothane was found to inhibit DNA synthesis in regenerating marrow. Finally, it was found that after significant exposure to halothane, complete recovery was seen in the spleen after 24 hr, whereas femur DNA synthesis was still depressed by 20% at the same time.

Animals↗
PubMed1998

Halothane requirement--a comparison between laryngeal mask airway insertion and endotracheal tube intubation in pediatric patients.

BACKGROUND: The present study was to determine the effective concentration of halothane for insertion of laryngeal mask airway (LMA) and for intubation of endotracheal tube (ETT) in pediatric patients. METHODS: Forty-eight ASA class 1 patients, aged from 10 months to 6 years, scheduled for minor elective surgery were randomly assigned to two groups i.e., LMA and ETT. The concentration of halothane effective in fifty percent of patients (EC50) was determined by the up-and-down method (with 0.5% as a step size). After the predetermined concentration of halothane delivered from a calibrated vaporizer was established and maintained for 20 min, LMA insertion or ETT intubation was attempted without the patient being curarized. The response of patient to LMA or ETT was reported either as "movement" or "non-movement". The effective concentration and associated 95% confidence limits were determined in each group. RESULTS: An effective concentration of halothane for LMA insertion was 1.5 +/- 0.4% (95% confidence limits 1.4-1.7%), whereas that for ETT intubation was 2.3 +/- 0.5% (95% confidence limits 2.1-2.5%). The difference between these two values was statistically significant (p < 0.01). Airway reflexes after LMA insertion were minimal. CONCLUSIONS: The insertion of LMA could be performed at a significantly less halothane concentration in comparison with ETT intubation in children.

Anesthetics, Inhalation↗
PubMed1999

Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs.

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.

Adrenergic alpha-Agonists↗
PubMed1991

Enzyme inhibition by analgesic and hypnotic agents on anaerobic dehalogenation of halothane.

Enzyme inhibition on anaerobic dehalogenation of halothane by various analgesic or hypnotic agents was investigated in vitro using rat liver microsomal fraction. The production rate of chloro-difluoro-ethylene (CDE) and chloro-trifluoro-ethane (CTE), anaerobic metabolites of halothane, was measured when various concentrations of analgesic or hypnotic agents (fentanyl, morphine, pentazocine, buprenorphine, ketamine, diazepam, chlorpromazine and hydroxyzine) were supplemented. Inhibitor constant (Ki) of each agent was calculated and compared with each other. The activity of NADPH-cytochrome c reductase (fp(2)) and NADH-ferricyanide reductase (fp(1)) was measured when each agent was added. The values of inhibitor constants (Ki) for CDE and CTE formation were in the following order from large to small values; morphine (656 microM and 2570 microM), chlorpromazine (49.7 microM and 68.1 microM), ketamine (24.9 microM and 64.4 microM), fentanyl (23.9 microM and 34.6 microM), hydroxyzine (19.2 microM and 50.8 microM), diazepam (17.0 microM and 13.9 microM), buprenorphine (11.2 microM and 22.4 microM), and pentazocine (1.96 microM and 6.67 microM) respectively. Pentazocine inhibited the formation of CDE 300 fold greater than morphine. The activity of fp(2) and fp(1) did not change by the addition of these analgesic or hypnotic agents. These results indicate that various analgesic or hypnotic agents, which are commonly used with halothane in clinical anesthesia, suppress the anaerobic dehalogenation of halothane in vitro. They also imply that the suppression of production of halothane metabolites is the result of direct enzyme inhibition on cytochrome P-450, since these agents did not affect the activity of fp(2) and fp(1) which are flavoproteins existing in the microsomal electron transport system.

Journal Article↗
PubMed1993

Effect of halothane on intercellular adhesion molecule-1 (ICAM-1) in melanoma cells.

There have only been a few reports relating to the effect of inhalational anesthetics on the tumor cell morphology in cancer patients undergoing surgery. We hypothesized that some anesthetic agents might influence the spread of unresectable cancer cells and might additionally worsen the condition of the patient due to depressed host immune surveillance. We therefore evaluated the influence of halothane on tumor cell adhesion, which is closely linked to tumor cell metastasis. Human melanoma cells from SK-MEL-37 cell-line were exposed to 4% halothane for 3, 6, 12 or 24 hours, respectively. Furthermore, after 24 hours halothane exposure, they were incubated in a 5% CO2 atmosphere for 12 or 24 hours. The cells were then analyzed using a fluorescence flowcytometer and intercellular adhesion molecule-1 (ICAM-1) expression in SK-MEL-37 cells was quantified as the intensity of fluorescence of ICAM-1 expressed in 10,000 cells. ICAM-1 expression in cells exposed to halothane for 3, 6, 12 or 24 hours was lower than that of non-exposed cells and returned to control level after further incubation in 5% CO2 atmosphere for either 12 or 24 hours. We conclude that halothane might affect the progression of tumor cell metastasis in vitro.

Journal Article↗
PubMed1987

Stabilization of the reduced halocarbon-cytochrome P-450 complex of halothane by N-alkanes.

Under anaerobic conditions, various halogenated compounds, when metabolized by cytochrome P-450, form complexes which are spectrally detectable. Previous studies have shown that halothane forms such a complex with cytochrome P-450, and the result is a strong absorption at 470 nm. Stabilization of this proposed intermediate carbanion complex has never been demonstrated in a biological system. Data are presented which show that several organic solvents (C5-C7N-alkanes) will stabilize the complex formed between halothane and cytochrome P-450. Stabilization allowed the decay of the complex to be studied, and it is demonstrated that the product of decay was chlorodifluoroethylene, which substantiates the hypothesis that the complex is a two electron-reduced carbanion. Carbon tetrachloride and benzyl bromide, which also produce spectrally visible intermediate complexes, were not stabilized by this treatment. Stabilization of the halothane complex in a biological system may facilitate studies to identify precisely the halothane-cytochrome P-450 complex and to clarify the mechanisms of halothane reduction by cytochrome P-450.

Alkanes↗
PubMed1998

Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart.

A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts perfused at a constant flow (10 ml min-1, PO2 80 kPa) and paced at 350 beat min-1, we determined left ventricular developed pressure (LVDP) and release of creatine kinase (CKR) as indices of myocardial performance and cellular injury, respectively. Seven control hearts underwent 30 min of no-flow ischaemia and 1 h of reperfusion. In the treatment groups, halothane, enflurane, isoflurane, sevoflurane or desflurane (each group n = 6) was added to the perfusion medium for the first 30 min of reperfusion at a concentration corresponding to 1.5 MAC in the rat. In the control group, cellular injury occurred at early reperfusion (peak CKR 283 (SEM 57) iu litre-1 at 10 min of reperfusion). Peak CKR to the coronary venous effluent was attenuated by all anaesthetics (halothane group 156 (45), enflurane group 134 (20), sevoflurane group 132 (20), desflurane group 159 (25) iu litre-1; each P < 0.05). Isoflurane did not differ from controls (303 (53) iu litre-1; P = 0.5). In the sevoflurane group, there was a delayed peak CKR after discontinuation of the anaesthetic at 30 min of reperfusion (260 (34) iu litre-1). Functional recovery was improved by all anaesthetics, but was seen much earlier with desflurane (LVDP 28 (3)% of baseline at 5 min reperfusion compared with halothane (6 (1)%), enflurane (11 (3)%), isoflurane (9 (6)%), sevoflurane (10 (2)%) and controls (3 (1)% of baseline)). At 30 min of reperfusion, recovery of LVDP was improved to a similar extent by all anaesthetics (halothane 30 (9)%, enflurane 36 (9)%, isoflurane 33 (5)%, sevoflurane 30 (5)%, desflurane 36 (4)% of baseline values) compared with controls (13 (5)%; each P < 0.05). All inhalation anaesthetics protected against myocardial reperfusion injury, but showed differences in attenuation of cellular injury and functional recovery. These differences may suggest different protective mechanisms.

Anesthetics, Inhalation↗