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PubMed1990

Different effects of halothane and enflurane on diaphragmatic contractility in vivo.

We examined the effects of halothane and enflurane on diaphragmatic contractility in 12 anesthetized, mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. Animals were randomly assigned to two groups, a halothane group (n = 6) and an enflurane group (n = 6). The Pdi stimulus-frequency relationship was compared at anesthetic levels of 1, 1.5, and 2 MAC (minimum alveolar concentration) in each group. The sequence of changing anesthetic concentration was randomized. In addition, the Pdi-frequency relationship was also compared between 1 MAC of halothane and enflurane in 8 of 12 dogs. In animals anesthetized with enflurane, Pdi significantly decreased with 50- and 100-Hz stimulation in the presence of increasing MAC values, whereas Pdi at 10-Hz stimulation was not affected by the depth of anesthesia. Pdi with 20-Hz stimulation during 2 MAC enflurane also decreased significantly below Pdi levels seen at 1 and 1.5 MAC. By contrast, with halothane there was no difference in Pdi at any of the stimulation frequencies during any of the three levels of anesthesia. There was no statistical difference, however, between Pdi-frequency relationships during 1 MAC of halothane and enflurane in eight animals. From these results, we conclude that halothane does not impair diaphragmatic contractility any more than enflurane does, but enflurane decreases force generation of the diaphragm at high stimulation frequencies in a dose-related fashion. This depressant effect of enflurane occurs mainly through the impairment of neuromuscular transmission and/or membrane excitability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of intraoperative analgesic therapy on end-expired concentrations of halothane associated with spontaneous eye opening in children.

We studied 94 healthy ASA physical status I or II children to determine the end-expired concentration of halothane associated with eye opening on emergence from anesthesia, and to determine if parenteral opioid therapy or regional analgesia significantly altered this concentration. In our study, anesthesia was maintained with halothane in an air-oxygen mixture. After the surgical procedure was completed, the inspired concentration of halothane was adjusted to zero and the end-expired concentrations were permitted to decrease spontaneously. The end-expired concentration at which the child spontaneously opened his or her eyes was recorded. There were no statistically significant differences in the values of the end-expired halothane concentration at eye opening between patients in the control group, who did not receive any supplementation of halothane anesthesia, and patients in the groups that received either morphine supplementation or regional analgesia. These data suggest that analgesia and hypnosis (or loss of consciousness) occur by different mechanisms during halothane anesthesia in children.

Adolescent↗
PubMed1991

Halothane 1.5 MAC, isoflurane 1.5 MAC, and the contractile responses of coronary arteries obtained from human hearts.

Active vasoconstriction of epicardial coronary arteries can cause myocardial ischemia in patients with coronary artery disease. Relief of vasoconstriction can improve blood flow to the heart. The purpose of this study was to determine if 1.5 MAC halothane and 1.5 MAC isoflurane would each attenuate contractions evoked by three putative mediators of coronary constriction in coronary arteries removed from the hearts of human beings. Hearts were obtained in the operating room from five patients undergoing cardiac transplantation and from six brain-dead patients undergoing organ donation procedures. Coronary arteries were dissected free, cut into rings, and studied in organ chambers. Endothelium-dependent relaxations to 10(-6) M bradykinin were examined; they indicated a variable degree of endothelial dysfunction in vessels used in the experiments. Contractile responses to 40 mM KCl were tested and were used as control contractions. Contractions evoked by serotonin, histamine, and prostaglandin F2 alpha were measured and were expressed as a percent of contractile responses evoked by 40 mM KCl. Halothane depressed the agonist-induced contractions. Maximal contractile responses to serotonin were 130% +/- 28% in untreated rings and 63% +/- 10% in rings exposed to halothane (P less than 0.03). Responses to histamine were 183% +/- 46% untreated and 121% +/- 26% during halothane administration (P less than 0.05), and responses to prostaglandin F2 alpha were 227% +/- 42% untreated and 148% +/- 18% with halothane (P less than 0.05). Isoflurane had no effect on contractions. The results demonstrate that 1.5 MAC halothane, but not 1.5 MAC isoflurane, attenuates contractile responses evoked by putative mediators of coronary vasoconstriction in coronary arteries removed from the hearts of human beings.

Adult↗
PubMed1991

Effect of halothane on arrhythmogenic responses induced by sympathomimetic agents in single rat heart cells.

The combination of catecholamines and halothane has long been recognized as arrhythmogenic. The purpose of this study was to evaluate whether the mechanism of this interaction originates at the single cell level. The incidence of spontaneous contractile waves occurring between stimulated beats (interbeat waves), early aftercontractions, and late aftercontractions was measured in rat myocytes exposed to sympathomimetics with and without halothane. Each of these endpoints in single cells has the potential to produce arrhythmias in multicellular preparations. Interbeat waves and late aftercontractions were observed with isoproterenol (1 X 10(-7) M) and norepinephrine (1-3 X 10(-7) M). The incidence of these phenomena was significantly reduced in the presence of 0.30 mM halothane. Early aftercontractions occurred in the presence of isoproterenol (1 X 10(-7) M), norepinephrine (1-3 X 10(-7) M), and phenylephrine (5-10 X 10(-6) M). There was a statistically significant decrease in the incidence of early aftercontractions in the presence of 0.30 mM halothane. These results indicate that the mechanism behind the clinically observed increased arrhythmogenicity of catecholamines with halothane does not arise at the level of single ventricular cells because halothane inhibited sympathomimetic-induced arrhythmogenic activity in this model. The probable mechanisms rather include altered impulse propagation, which might lead to phenomena such as reentry.

Animals↗
PubMed1991

Breathing pattern and occlusion pressure waveform in humans anesthetized with halothane or sevoflurane.

To examine the ventilatory effects of sevoflurane, breathing pattern, airway occlusion pressure waveform, and the mechanical variables of the respiratory system were determined in seven subjects anesthetized with sevoflurane and in an additional seven subjects anesthetized with halothane. All patients breathed 1 MAC of anesthetic using oxygen as the carrier gas, and the measurements were performed in the absence of surgical stimulation. The durations of inspiration and expiration were significantly longer during sevoflurane than during halothane administration. Tidal volumes were larger in the sevoflurane group than in the halothane group. Occlusion pressure waveforms were also markedly different between the two groups. Occlusion pressure during the initial 300-400 ms tended to be less in the sevoflurane-anesthetized than in the halothane-anesthetized subjects. There was no evidence of an active Hering-Breuer reflex with either anesthetic. Mechanical variables of the respiratory system were essentially identical between the two anesthetics. We conclude that (a) the ventilatory effects of halothane and sevoflurane are different, (b) the difference in the respiratory timing and depth of breathing originates from the action of the anesthetics on the central respiratory neural network, and (c) the different shape of the tracheal occlusion pressure may be largely due to the different effects of halothane and sevoflurane on the muscles of the rib cage.

Airway Resistance↗
PubMed1992

Halothane- and enflurane-induced inhibition of phasic responses to carbachol in isolated guinea pig trachea.

Volatile anesthetics produce bronchodilatation by a combination of effects on the autonomic nervous system as well as direct effects on the airway smooth muscle. We sought to further explain the direct effects on airway smooth muscle by studying the effect of volatile anesthetics on the phasic and tonic components of the contractile response. The effects of 1.2%, 2.3%, and 4.3% halothane and 1.6%, 3.2%, 4.9%, and 8.7% enflurane on the phasic and tonic components of the contractile response to 10 microM carbachol and 40 mM KCl in isolated guinea pig trachea were determined using steady-state and kinetic analyses. No direct effect of either anesthetic on resting tension was observed. The peak tensions of the phasic responses to 10 microM carbachol were significantly inhibited by all concentrations of halothane and enflurane. The inhibition by enflurane was concentration-dependent and eliminated the phasic response at 8.7%. The peak tensions of the tonic responses to 10 microM carbachol were unaffected. The peak tensions of the responses to 40 mM KCl were unaffected by halothane but were significantly inhibited by 4.9% enflurane. The decay rate of the phasic response was unaffected by the anesthetics. The onset rate of the tonic response was significantly inhibited only by 8.7% enflurane, whereas halothane was without effect. The EC50 concentration for carbachol, as determined by cumulative concentration response curves, was increased by both 8.7% enflurane and 4.3% halothane. The results support the hypothesis that halothane and enflurane inhibit that portion of the contractile response to carbachol dependent on the release of intracellular Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Halothane myocardial depression: interactions with the adenylate cyclase system.

The involvement of the adenylate cyclase system in myocardial depression by halothane was investigated in an isolated, electrically stimulated, rat left atrial preparation. The twitch tension dose-response curve to the muscarinic agent, carbachol, was unaltered by 0.27 mM (0.8%) halothane. Pertussis toxin irreversibly blocks the inhibition of adenylate cyclase by muscarinic agonists. Atria from animals pretreated with pertussis toxin were insensitive to the negative inotropic effect of carbachol, but the depression in twitch tension by halothane was unaltered. Halothane shifted the dose-response curve to isoproterenol downward and to the right. However, the depression in twitch tension by 0.27 mM halothane was similar in preparations incubated with the nonhydrolyzable cAMP analogue, dibutyryl-cAMP, compared to control atria stimulated with isoproterenol. We conclude that halothane attenuates the response to beta-adrenergic stimulation in myocardial tissue, and alterations in adenylate cyclase activity do not contribute significantly to this process.

Adenylate Cyclase Toxin↗
PubMed1993

Halothane inhibits the intraalveolar recruitment of neutrophils, lymphocytes, and macrophages in response to influenza virus infection in mice.

The effect of halothane anesthesia on the influenza A specific immune response and the pathogenesis of infection was evaluated in mice. Three-wk-old CD-1 mice were anesthetized with either 2% halothane for 2 h or ketamine (100 mg/kg intraperitoneally) and subsequently inoculated intranasally with a sublethal dose of influenza type A/PR/8/34 virus. Bronchoalveolar lavage was performed on animals from each group at 4 h postinoculation and daily thereafter for 14 days. Total and differential white blood cell counts were measured in the lavage fluid and the lungs were examined histologically for evidence of injury. Infected mice anesthetized with halothane had lower daily cell counts in the lung than animals anesthetized with ketamine and a marked change in cell type distribution. On Days 4 and 11 postinoculation, there were significantly (P < 0.05) more white blood cells in the lavage fluid of animals anesthetized with ketamine than halothane (mean/mL, 738,000 +/- SEM, 128,000 vs 196,000 +/- 51,400, respectively, and 1,020,000 +/- 227,000 vs 117,000 +/- 34,600, respectively). Differential counts were significantly higher (P < 0.05) in the ketamine group compared to the halothane for neutrophils on Day 4 (452,000 +/- 77,900 vs 72,000 +/- 46,000, respectively) and on Day 11 for lymphocytes (340,000 +/- 59,000 vs 33,000 +/- 17,000, respectively) and macrophages (480,000 +/- 120,000 vs 130,000 +/- 61,000). Infected mice that were given ketamine were qualitatively "sicker" than the halothane-treated group as evidenced by the appearance of ruffled fur, tachypnea, and cachexia. Animals anesthetized with ketamine demonstrated a greater degree of pulmonary histopathology including diffuse infiltration of macrophages, neutrophils, hemorrhage, and fibrin deposition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Nitric oxide synthase inhibitor does not reduce minimum alveolar anesthetic concentration of halothane in rats.

Nitric oxide (NO) synthase inhibitor (N omega-nitro-L-arginine methyl ester [L-NAME]) has been reported to reduce minimum alveolar anesthetic concentration (MAC) of halothane when administered intravenously (i.v.) and to reduce thermal hyperalgesia, or produce antinociception in the formalin test, when administered intracerebroventricularly (ICV) or intrathecally (IT). This study attempts to identify the site(s) in the central nervous system (CNS) where L-NAME acts to reduce the halothane MAC. For this purpose, we examined the effects of i.v., ICV, and IT administration of L-NAME on the halothane MAC in rats. In contrast to an earlier study, we did not observe any decrease in the halothane MAC after i.v. (10-30 mg/kg) administration of L-NAME. ICV (100 micrograms) and IT (100 micrograms and 1 mg) administration of L-NAME also did not alter the halothane MAC. These findings indicate that the L-arginine-NO pathway is not involved in the mechanism of action of halothane to suppress mechanical nociceptive response or in the nociceptive neural mechanism of mechanical stimulation.

Amino Acid Oxidoreductases↗
PubMed1994

The difference of isoflurane and halothane in ventriculoarterial coupling in dogs.

Effective arterial elastance (Ea) and left ventricular end-systolic elastance (Ees) are used as indices of cardiac afterload and cardiac contractility, respectively. We compared the effects of two volatile anesthetics, halothane and isoflurane, on ventriculoarterial coupling using an index of Ea/Ees in 20 mongrel dogs. Ees was obtained using a single-beat estimation technique. Ea was estimated as the ratio of the mean arterial pressure to stroke volume. Basal anesthesia consisted of pentobarbital and alpha-chloralose. Dogs were further anesthetized either with halothane 1 minimum alveolar anesthetic concentration (MAC) and 2 MAC (n = 10) or with isoflurane 1 MAC and 2 MAC (n = 10). Halothane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 35.5% +/- 4.9%, 18.3% +/- 12.6%, and 39.7% +/- 10.8%, respectively. Isoflurane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 37.9% +/- 4.0%, 38.7% +/- 6.4%, and 43.0% +/- 6.0%, respectively. The decreases in cardiac output and Ees were not significantly different between halothane and isoflurane. Halothane increased Ea/Ees from 0.83 +/- 0.05 to 1.22 +/- 0.13, whereas isoflurane maintained the Ees/Es at a constant level. Our results suggest that mechanical efficiency is well maintained during isoflurane anesthesia because it has an equivalent effect on left ventricular contractility and arterial properties, whereas halothane can impair mechanical efficiency by depressing left ventricular contractility more than the arterial system.

Animals↗
PubMed2003

Anesthetic sensitivities to propofol and halothane in mice lacking the R-type (Cav2.3) Ca2+ channel.

UNLABELLED: Because inhibition of voltage-dependent Ca(2+) channels can be a mechanism underlying general anesthesia, we examined sensitivities to propofol and halothane in mice lacking the R-type (Ca(v)2.3) channel widely expressed in neurons. Sleep time after propofol injection (26 mg/kg IV) and halothane MAC(RR) and MAC (50% effective concentrations for the loss of the righting reflex and for the tail pinch/withdrawal response, respectively) were determined. Significantly shorter propofol-induced sleep time (291.6 +/- 16.8 s versus 344.4 +/- 12.1 s) and larger halothane MAC(RR) (1.11% +/- 0.04% versus 0.98% +/- 0.03%) were observed in Ca(v)2.3 channel knockouts (Ca(v)2.3(-/-)) than in wild-type (Ca(v)2.3(+/+)) litter mates. To investigate the basis of the decreased anesthetic sensitivities in vivo, field excitatory postsynaptic potentials and population spikes (PSs) were recorded from Schaffer collateral CA1 synapses in hippocampal slices. Propofol (10-30 micro M) inhibited PSs by potentiating gamma-aminobutyric acid-ergic inhibition, and this potentiation was markedly smaller at 30 micro M in Ca(v)2.3(-/-) mice, possibly accounting for the decreased propofol sensitivity in vivo. Halothane (1.4%-2.2%) inhibited field excitatory postsynaptic potentials similarly in both genotypes, whereas 1%-2% halothane depressed PSs more in Ca(v)2.3(-/-) mice, suggesting the postsynaptic role of the R-type channel in the propagation of excitation and other mechanisms underlying the increased halothane MAC(RR) in Ca(v)2.3(-/-) mice. IMPLICATIONS: Because inhibition of neuronal Ca(2+) currents can be a mechanism underlying general anesthesia, we examined anesthetic sensitivities in mice lacking the R-type (Ca(v)2.3) Ca(2+) channels both in vivo and in hippocampal slices. Decreased sensitivities in mutant mice imply a possibility that agents blocking this channel may increase the requirements of anesthetics/hypnotics.

Anesthetics, Inhalation↗
PubMed2003

Neither spinal gamma-aminobutyric acid-A nor strychnine-sensitive glycine receptor systems are the sole mediators of halothane depression of spinal dorsal horn sensory neurons.

UNLABELLED: Inhaled anesthetics depress the response of spinal dorsal horn low-threshold (LT) neurons to peripheral receptive field stimulation. Part of that depression may be mediated by anesthetic interactions with gamma-aminobutyric acid type A (GABA(A)) and strychnine-sensitive glycine inhibitory neurotransmitter systems. In this electrophysiological study, we attempted to antagonize halothane depression of LT neurons by administering bicuculline (a competitive GABA(A) antagonist) and/or strychnine (a competitive glycine antagonist) systemically, alone or in combination, to decerebrate, spinal cord-transected rats. We observed that both bicuculline and strychnine, alone or in combination, significantly but only partially reversed halothane depression of LT neuronal responses to receptive field stimulation. The inability of bicuculline and strychnine, alone or in combination, to completely reverse halothane depression suggests that although GABA(A) and glycine systems are involved in the observed halothane depression, additional mechanisms of action are also required for halothane depression of LT spinal sensory neurons. IMPLICATIONS: The results of this study support the hypothesis that halothane depression of spinal sensory neurons is mediated, but not completely, by the anesthetic effects on gamma-aminobutyric acid type A and strychnine-sensitive glycine neurotransmitter systems.

Action Potentials↗
PubMed2005

Identification of the central imidazoline receptor subtype involved in modulation of halothane-epinephrine arrhythmias in rats.

We previously reported that imidazoline receptors in the central nervous system are involved in modulation of halothane-epinephrine arrhythmias. These receptors have been subclassified as I1 and I2 subtypes, but it is not known which receptor subtype is involved in halothane-epinephrine-induced arrhythmias. We designed the present study to clarify the involvement of central imidazoline receptor subtype in the modulation of halothane-epinephrine-induced arrhythmias. Rats were anesthetized with halothane and monitored continuously for systemic arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of epinephrine was defined as the smallest dose that produces three or more premature ventricular contractions within a 15-s period. Intracisternal moxonidine dose-dependently inhibited the epinephrine-induced arrhythmias during halothane anesthesia. Intracisternal efaroxan, a selective I1 antagonist with little affinity for I2 subtype, but not rauwolscine, an alpha2 antagonist without affinity for imidazoline receptors, blocked the antiarrhythmic effect of moxonidine. Intracisternal BU 224 and 2-BFI, selective I2 ligands, also inhibited the epinephrine-induced arrhythmias dose-dependently; however, these effects were abolished by efaroxan. We conclude that central I1, but not I2, receptors play an important role in inhibition of halothane-epinephrine arrhythmia.

Animals↗
PubMed2006

The dose-response relationship and regional distribution of lactate after intramuscular injection of halothane and caffeine in malignant hyperthermia-susceptible pigs.

We hypothesized that IM halothane and caffeine injection increases local lactate concentration dose-dependently in malignant hyperthermia-susceptible (MHS) and nonsusceptible (MHN) pigs and that the hypermetabolic reaction measured by regional distribution of lactate and carbon dioxide is limited to a small muscle volume. Microdialysis probes were placed in the hindlimbs of 7 MHS and 7 MHN pigs and perfused with Ringer's solution. After equilibration, boluses of increasing halothane and caffeine concentrations were injected. For the second hypothesis regarding regional distribution, microdialysis probes were positioned in 7 MHS and 6 MHN pigs at the injection site for halothane and caffeine and at a distance of 10 mm and 25 mm. Lactate was measured in the dialysate by spectrophotometry. In addition, PCO2 was measured in the halothane experiments. Halothane and caffeine increased IM lactate dose-dependently in MHS pigs significantly more than in MHN pigs. Lactate and PCO2 were increased only at the injection site but not at 10 mm and 25 mm distance. MH susceptibility leads to a leftward shift of the dose-response curve for IM lactate after local injection of halothane and caffeine. The increase of lactate and carbon dioxide levels after local MH trigger injection is limited to a small area around the probe.

Anesthetics, Inhalation↗
PubMed2006

The effect of sevoflurane on ciliary motility in rat cultured tracheal epithelial cells: a comparison with isoflurane and halothane.

Halothane and isoflurane potently depress airway ciliary motility. We compared the effect of sevoflurane on ciliary beat frequency (CBF) with that of halothane and isoflurane using purified and cultured rat tracheal epithelial cells. Rat tracheal epithelial cells were isolated from adult male Sprague-Dawley rats to establish an air-liquid interface culture. Apical surfaces of the cells were exposed to a fresh gas containing humidified and warmed (25 degrees C) air (vehicle) with or without sevoflurane (0%-4%), halothane (0%-2%), or isoflurane (0%-2%). The images of motile cilia were videotaped and CBF was analyzed using a computer. Baseline CBF (= 100%) and CBF 30 min after the exposure were measured. CBF 30 min after vehicle exposure was 101% +/- 4% (mean +/- sd). Exposures to 0.25%-2% sevoflurane did not change CBF significantly, although exposures to 0.25%-2% halothane or isoflurane decreased CBF dose-dependently. CBFs 30 min after exposures to 2% of sevoflurane, halothane, and isoflurane were 97% +/- 9%, 56% +/- 14%, and 47% +/- 6%, respectively (n = 5 each). Sevoflurane 4% reduced CBF significantly but slightly (84% +/- 2%, n = 5). These results show that sevoflurane has a direct cilioinhibitory action but its action is much weaker than that of halothane and isoflurane in isolated rat tracheal epithelial cells.

Anesthetics, Inhalation↗
PubMed2006

The differential effects of halothane and isoflurane on windup of dorsal horn neurons selected in unanesthetized decerebrated rats.

Halothane and isoflurane, in the peri-minimum alveolar anesthetic concentration (MAC) range, exert differential effects on spinal nociceptive neurons, whereby halothane further depresses their responses from 0.8 to 1.2 MAC, whereas isoflurane does not. We presently investigated if these anesthetics differentially affect windup, the progressive increase in neuronal responses to repetitive noxious stimuli, over a broad concentration range from 0 to 1.2 MAC. In decerebrated rats, single-unit recordings were made from dorsal horn neurons exhibiting windup to 20 1-Hz C-fiber strength electrical stimuli. Halothane and isoflurane (0, 0.4, 0.8, and 1.2 MAC) were tested in a counterbalanced crossover protocol. Increasing halothane and isoflurane from 0 to 1.2 MAC progressively suppressed the response to the first stimulus, as well as summed responses to all stimuli (to 34% +/- 8% and 50% +/- 8%, respectively; P < 0.05). Absolute windup (summed response minus 20x the first response) was suppressed by both anesthetics from 0 to 0.8 MAC, with further depression by halothane but not isoflurane at 1.2 MAC. Responses of neurons isolated at 0 MAC were partially, but never totally, depressed at 0.8 MAC. The dose-dependent suppression of windup is consistent with reduced temporal summation of pain. Further depression at 1.2 MAC halothane, but not isoflurane, suggests different sites of immobilizing action for these two anesthetics. Immobility seems to not be mediated by severe anesthetic depression of a subpopulation of nociceptive neurons.

Anesthetics, Inhalation↗
PubMed1982

Structural changes in dividing sea-urchin eggs induced by the volatile anaesthetic halothane.

Fertilized Lytechinus eggs exposed to the volatile anaesthetic halothane before metaphase do not undergo cytoplasmic cleavage. This effect has been correlated with the failure of the contractile ring to assemble. Comparative studies on mitotic apparatuses isolated from control and halothane-treated cells show that halothane significantly impairs both spindle and aster growth as early as metaphase. When transferred to control solutions, halothane-treated cells initiate furrowing activity in association with either the first or second mitotic division, depending on the duration of the exposure to anaesthetic and the concentration employed. In contrast to these effects, halothane has no effect on any aspect of the cleavage process if applied later than metaphase. In this case, furrows develop even in the presence of halothane, deepen progressively, and complete cell division. These observations confirm and extend previous studies on echinoderm eggs exposed to volatile anaesthetics, and support the view that anaesthetic agents indirectly prevent cell cleavage by inhibiting the growth of mitotic apparatus.

Animals↗
PubMed1994

Synergistic interaction between class I antiarrhythmic drugs and halothane in depressant effects on ventricular activation in a canine myocardial infarction model.

Previous studies have showed that halothane has depressed ventricular activation in a canine myocardial infarction model. It is also well known that class I antiarrhythmic drugs depress ventricular activation in the infarcted myocardium. In the present study, we examined whether some electrophysiologic interactions between halothane and two class I antiarrhythmic drugs, lidocaine and procainamide, occur in a canine myocardial infarction model. Halothane, lidocaine and procainamide prolonged the activation time in the infarcted zone, and the combination of halothane and either lidocaine or procainamide markedly prolonged the activation time or blocked the delayed activation in the infarcted zone. Although the mechanism of the interaction is not clear, the present results suggest a synergistic interaction between halothane and class I antiarrhythmic drugs. Therefore, care should be taken that doses of class I antiarrhythmic drugs during halothane anesthesia will not be an overdose.

Animals↗