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PubMed2000

A comparison of the haemodynamic effects of isoflurane and halothane anaesthesia in horses.

The purpose of this study was to compare the haemodynamic effects of equipotent isoflurane and halothane anaesthesia. Six adult horses were investigated on two separate occasions at least 4 weeks apart. On both occasions anaesthesia was induced by ketamine 2.2 mg/kg bwt given 5 min after i.v. administration 100 microg/kg bwt romifidine. Anaesthesia was maintained either by halothane or isoflurane (end-tidal concentrations 0.9-1.0% and 1.3-1.4%, respectively). Horses were ventilated by intermittent positive pressure to maintain PaCO2 between 40-50 mmHg. Haemodynamic variables were measured using catheter-mounted strain gauge transducers in the left and right ventricle, aorta, and right atrium. Cardiac output (CO), velocity time integral (VTI), maximal aortic blood flow velocity (Vmax) and acceleration (dv/dt(max)), left ventricular pre-ejection period (PEP) and ejection time (ET) were measured from aortic blood flow velocity waveforms obtained by transoesophageal Doppler echocardiography. Flow velocity waveforms were recorded from the femoral arteries and veins using low pulse repetition frequency Doppler ultrasound. Time-averaged mean velocity (TAV), velocity of component a (TaVa), velocity of component b (TaVb) and early diastolic deceleration slope (EDDS) were measured. Pulsatility index (PI) and volumetric flow were calculated. Microvascular blood flow was measured in the left and right semimembranosus muscles by laser Doppler flowmetry. Maximal rate of rise of LV pressure (LVdp/dt(max)), CO, Vmax, dv/dt(max), ET, VTI were significantly higher at all time points during isoflurane anaesthesia compared to halothane anaesthesia. Pre-ejection period and diastolic aortic blood pressure were significantly less throughout isoflurane anaesthesia compared to halothane. Isoflurane anaesthesia was associated with significantly lower systemic vascular resistance than halothane anaesthesia. Femoral arterial and venous blood flow were significantly higher and EDDS and PI were significantly lower during isoflurane anaesthesia compared to halothane anaesthesia. In addition during both halothane and isoflurane anaesthesia, femoral arterial flow was higher and EDDS and PI lower in the left (dependent) artery compared to the right (nondependent) artery. This study supports previous work demonstrating improved left ventricular systolic function during isoflurane compared to halothane anaesthesia. This improvement was still evident after premedication with a potent-long acting alpha2-adrenoreceptor agonist, romifidine, and induction of anaesthesia with ketamine. There was also evidence of increased hindlimb blood flow during isoflurane anaesthesia. However, there were differences observed in flow between the left and right hindlimb during maintenance of anaesthesia with each agent, suggesting that there were differences in regional perfusion in anaesthetised horses caused by factors unrelated to agents administered.

Anesthetics, Inhalation↗
PubMed1999

The effects of halothane and sevoflurane on QT dispersion.

QT dispersion is defined as the difference between QT (max) and QT (min) in the 12-lead surface ECG. It has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with arrhythmic events than in those without them. The aim of this study was to examine the effects of halothane and sevoflurane on QT and QTc dispersion during inhalational induction of anaesthesia. The effects on QT and QTc dispersion of halothane and sevoflurane have been investigated during induction of anaesthesia. Forty-six ASA (American Society of Anaesthesiologists) physical status I-II patients, aged 16-50 years, undergoing general anaesthesia were randomly allocated to receive either halothane or sevoflurane. The mean baseline values for QT and QTc dispersion were not significantly different between the two groups (P > 0.05). QT dispersion was increased with halothane compared with baseline values (50 +/- 16 ms vs. 29 +/- 9 ms, P < 0.01) and after sevoflurane compared with baseline (48 +/- 15 vs. 33 +/- 8 ms, P < 0.01). Also, QTc dispersion was increased with halothane compared with baseline values (48 +/- 13 ms vs. 31 +/- 9 ms, P < 0.001) and after sevoflurane compared with baseline (50 +/- 14 vs. 40 +/- 11 ms, P < 0.01). The QTc interval did not change by both sevoflurane (443 +/- 7 vs. 431 +/- 21 ms, P > 0.05) and halothane (419 +/- 33 vs. 431 +/- 19 ms, P > 0.05) compared with baseline. Both halothane and sevoflurane cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion. This may be relevant in the aetiology of arrhythmias in patients during anaesthesia with halothane or sevoflurane.

Adolescent↗
PubMed2000

Membrane and synaptic actions of halothane on rat hippocampal pyramidal neurons and inhibitory interneurons.

A relatively small number of inhibitory interneurons can control the excitability and synchronization of large numbers of pyramidal neurons in hippocampus and other cortical regions. Thus, anesthetic modulation of interneurons could play an important role during anesthesia. The aim of this study was to investigate effects of a general anesthetic, halothane, on membrane and synaptic properties of rat hippocampal interneurons. GABA receptor-mediated IPSCs were recorded with whole-cell patch-clamp techniques in visually identified CA1 pyramidal cells and interneurons located at the border of stratum lacunosum-moleculare and stratum radiatum. Halothane (0.35 mm congruent with 1.2 vol%) depressed evoked IPSC amplitudes recorded from both pyramidal cells and inhibitory interneurons. Also, halothane considerably prolonged the decay time constant of evoked IPSCs in pyramidal cells and interneurons. The frequencies of miniature IPSCs were increased by halothane (two- to threefold) in both types of neuron. On the other hand, halothane effects on resting membrane potentials were variable but minimal in both types of neurons. In current-clamp recordings, halothane depressed EPSP amplitudes and increased IPSP amplitudes recorded from both types of neurons. In addition, halothane increased the failure rate of synaptically evoked action potentials. Taken together, these data provide evidence that halothane increases GABA(A) receptor-mediated synaptic inhibition between synaptically connected interneurons and depresses excitatory transmission, similar to effects observed in pyramidal neurons.

Action Potentials↗
PubMed1975

Porcine malignant hyperthermia: effects of temperature and extracellular calcium concentration on halothane-induced contracture of susceptible skeletal muscle.

Skeletal muscle from malignant hyperthermic (MH) pigs incubated at 37 C in 2.3 mM calcium-Krebs-Ringer solution contracts spontaneously when exposed to halothane. In contrast, halothane did not induce contracture in MH muscle incubated in 2.3 mM calcium-Krebs-Ringer solution at 25 C or in calcium-free Krebs-Ringer's solution at 37 C. Halothane did not induce contracture in normal control muscle in 2.3 mM Krebs-Ringer solution at 25 or 37 C. In the presence of halothane, addition of caffeine produced greater contracture in MH muscle than in normal controls. Halothane-caffeine-induced contractures of MH and control muscles at 25 and 37 C were similar. Elucidation that under certain experimental conditions halothane induces contracture in MH muscle, but not in normal muscle 1) may aid in development of a diagnostic test; 2) establishes further evidence for skeletal muscle as the target tissue for anesthetic-induced MH; 3) suggests that halothane may affect systems that regulate sarcoplasmic calcium concentration below contracture threshold in MH muscle. (Key words: Hyperthermia, malignant; Anesthetics, volatile, halothane; Ions, calcium; Muscle, skeletal, malignant hyperthermia.).

Animals↗
PubMed1992

Halothane relaxes preconstricted small and medium isolated porcine coronary artery segments more than isoflurane.

To compare the putative vasodilatory effects of isoflurane versus halothane on porcine coronary arteries, we studied the capacity of isoflurane and halothane to relax K(+)-constricted (30 mM) small (0.5-1.0 mm outside diameter [OD]) and medium (1.0-1.5 mm OD) porcine coronary arteries with use of in vitro tension recording. We also examined the effect of the dihydropyridine calcium channel agonist BAY K8644 on previously constricted epicardial porcine coronary artery segments in the presence of halothane or isoflurane. Our purpose was to determine (a) whether anesthetic effect on coronary arteries varied with arterial diameter, and (b) whether halothane and isoflurane inhibited BAY K8644-induced contraction of coronary vessels. Small and medium porcine coronary artery segments were constricted with K+ (30 mM) and the resulting contraction was allowed to stabilize. This was followed by exposure to 0.5%, 1.0%, 2.0%, and 3.0% isoflurane or halothane and the resultant tension was again measured. Potassium-induced contractions were significantly relaxed by halothane in small coronary artery segments at 0.5%, 1.0%, 2.0%, and 3.0% and in medium coronary artery segments at 1.0%, 2.0%, and 3.0%. Potassium-induced contractions were significantly reduced by isoflurane only at 3.0% in both small and medium coronary artery segments. Halothane caused significantly more relaxation of both small and medium porcine coronary arteries previously constricted with K+ (30 mM) than did isoflurane. There were no significant differences in coronary artery response to isoflurane or halothane with respect to coronary artery diameter. These experiments indicate that in porcine coronary arteries greater than 0.5 mm OD, studied in vitro after K(+)-induced contraction, isoflurane was not a potent coronary vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1981

Chronic halothane modification of eeg-like activity recorded from somatosensory cortex and deep nuclei in freely behaving rats.

Chronic exposure to the anesthetic agent halothane has been implicated in morphological and biochemical alterations of central nervous system tissue. In the present experiments, analysis of electroencephalographic (EEG) recordings has been used to examine effects on brain electrical activity. EEGs were recorded from freely behaving rats with stereotaxically implanted permanent semimicroelectrodes. Recordings were taken from the somatosensory cortex (SC), nucleus parafasciculus thalami (PF), mesencephalic central gray (CG), and the ventromedial hypothalamus (VMH) before (control) and after 28 and 56 days of chronic intermittent halothane administration (0.5%, 3 hr/day, 5 days/week). On each recording day (0, 28 and 56), EEGs were obtained prior to halothane exposure and following exposure to 0.25%, 0.5% and 1.5% halothane. In halothane-naive rats (day 0), the EEG dominant frequency (DF) showed a dose-response pattern consisting of an initial increase with 0.25% (significant only for the PF) followed by suppression at 0.5% and a marked significant decrease in all regions at 1.5%. On day 28, the pre-drug DF recorded from three of four regions showed a slowing trend. Additionally, with 1.5% halothane, only the SC DF was significantly decreased. Following 56 days of intermittent exposure, the pre-drug EEG frequencies were significantly decreased in all regions as compared to naive values. Subsequent administration of 0.25% halothane produced a significant increase in all regional DFs which was also obtained with 0.5% and with 1.5% for the CG and VMH. The high DF values from the PF, CG and VMH at 0.5% and from the CG and VMH at 1.5% represent statistically significant increases over naive 1.5% values. Chronic halothane exposure is thus shown to progressively alter EEG activity and the EEG pattern of dose-responsiveness in four brain regions.

Anesthetics, Inhalation↗
PubMed2005

Effects of vitamin C on liver enzymes and biochemical parameters in rats anesthetized with halothane.

Halothane is an important human and veterinary anesthetic, which produces free radicals during biotransformation. Occasionally, these free radicals may cause hepatic injury, especially in case of multiple halothane exposures over short periods. Vitamin C may protect cellular lipids and lipoproteins against oxidative damage by the free radicals. This study investigated the effects of vitamin C on liver enzymes and other biochemical parameters in rats anesthetized with halothane. One group of rats was used as a control, and saline (0.9% NaCl) was injected intraperitoneally into these animals as a placebo. The second group of rats was used as an anesthesia control group and was only anesthetized by halothane for 2 h. The third group was anesthetized by halothane and injected vitamin C intraperitoneally. Activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase enzymes were significantly increased (p < 0.05, p < 0.01, p < 0.05, respectively) by halothane anesthesia, but decreased (p < 0.05, p < 0.05, p < 0.05, respectively) with administration of vitamin C. Concentrations of triglycerides, cholesterol, total bilirubin and creatinine were statistically affected (p < 0.05, p < 0.01, p < 0.05, and p < 0.01, respectively) by injection of vitamin C. Values of erythrocyte counts, packet cell volumes, hemoglobin concentration, leukocyte counts, rates of neutrophils and lymphocytes were significantly affected (p < 0.01, p < 0.05, p < 0.05, p < 0.01, p < 0.001 and p < 0.01, respectively) by halothane anesthesia. The values of erythrocyte counts, leukocyte counts, neutrophil and lymphocyte rates were significantly decreased (p < 0.05, p < 0.05, p < 0.05, p < 0.01 and p < 0.01, respectively) with administration of vitamin C. Based upon these results, vitamin C may play an important role in the prevention of hepatic cellular injury inflicted by halothane anesthesia.

Administration, Inhalation↗
PubMed1991

Alpha-adrenoceptor stimulation in the presence of halothane: effects on impulse propagation in cardiac Purkinje fibers;.

Halothane effects on action potential characteristics and conduction were determined in canine Purkinje fibers, before and during alpha-adrenergic stimulation. Halothane significantly decreased effective refractory period and action potential duration in Purkinje fibers. alpha-Adrenergic stimulation restored effective refractory period and action potential duration in Purkinje fibers exposed to halothane via an alpha 1-adrenoceptor mediated effect antagonized by prazosin. Halothane significantly slowed propagation of impulses initiated at a basic cycle length of 500 ms, and conduction of premature impulses, in Purkinje fibers. In the presence of halothane, alpha-adrenergic stimulation had no additional effects on normal impulse propagation; however, alpha-adrenergic stimulation significantly slowed the conduction of premature impulses in Purkinje fibers exposed to halothane. These data refute a previous report that alpha-adrenergic stimulation enhances halothane's negative dromotropic effect in Purkinje fibers paced at a basic drive cycle length. alpha-Adrenergic prolongation of the conduction times of premature stimuli in Purkinje fibers exposed to halothane is a new finding.

Action Potentials↗
PubMed1990

[Effects of halothane on membrane potential, Ca2+ current and intracellular cAMP content in single guinea pig ventricular myocytes].

In order to assess directly the actions of halothane on myocardium, especially on the Ca2+ channel we studied effects of halothane on electrophysiological and biochemical properties in single ventricular myocytes isolated enzymatically from guinea pig hearts. Membrane potentials and the slow inward Ca2+ current (ICa) were recorded with a suction microelectrode technique and a whole cell voltage clamp technique. The plateau duration of the action potential, maintained by ICa, and ICa was depressed by 2% halothane (to 58% and 29% of control respectively). To define the site on which halothane acts in the cell membrane, we measured cyclic adenosine monophosphate (cAMP) content of single ventricular myocytes using radioimmunoassay. One percent (1%) and 2% halothane directly produced a dose-dependent decrease in myocardial cAMP content (79% and 65% of control respectively). In conclusion, the present results suggest that the decrease of ICa by halothane participates in the observed depression of the action potential plateau phase and demonstrate that halothane depression of ICa is in part due to an inactivation of phosphorylation dependent gate in the Ca2+ channel resulting from the decrease in cAMP content by halothane.

Animals↗
PubMed1989

Growth of allogeneic sarcoma in mice subjected to halothane anesthesia and/or surgical stress.

The present study was designed to clarify mechanisms involved in suppression of cell-mediated immunity reported in patients undergoing major surgery with general anesthesia by determining the effects of halothane anesthesia with and without surgery on the growth of Sarcoma I (Sa I), a tumor allogeneic to BALB/c mice. Mice were given subcutaneous injections of 5 X 10(6) tumor cells from A/Jax mice and then immediately exposed to 0.5%-1.0% halothane for 1 hr without surgery (n = 7) or with surgery (midline laparotomy; n = 12). In control groups mice were also injected with tumor cells but were not exposed to prolonged halothane anesthesia. Some of them received only Sa I (n = 6), while the rest (n = 7) were also laparotomized. The rejection time of Sa I in mice exposed to halothane anesthesia was significantly longer (15.4 +/- 1.25 days) than in untreated controls (12.0 +/- 0.68 days) (P less than 0.05). In the mice exposed to halothane tumor growth was also greater. Surgical stress per se did not significantly affect growth or rejection time of Sa I (11.0 +/- 0.66 vs 12.0 +/- 0.68 days). Similarly, the combination of surgical stress with halothane anesthesia did not affect the immunosuppression associated with halothane alone (12.9 +/- 1.3 vs 15.4 +/- 1.25; P less than 0.05). The results indicate that halothane anesthesia per se may be associated with impairment of cell-mediated immunity under experimental conditions.

Anesthesia, Inhalation↗
PubMedDate not supplied

Current concept of halothane hepatitis (review).

Clinically, halothane is still a useful volatile anesthetic, but since many cases of liver disorders considered attributable to halothane have been reported up to date, a number of studies have been made on the etiology and mechanism of halothane hepatitis. There are at least two possible mechanisms of halothane hepatitis; the first is the direct toxic reaction associated with free radical that is related to reductive pathway enhanced by hypoxia, and the other is the immune--mediated reaction in which the antigen is associated with the oxidative and/or reductive route. However, the etiology and mechanism of halothane hepatitis have yet to be elucidated, and clinically there is no obvious evidence that halothane can induce hepatic disorders. We have concluded at present that the use of halothane should be avoided in patients with liver disorders, in patients under long-term administration of drugs that may induce enzymes involved in halothane metabolism, in patients with high allergic sensitivity, and in patients undergoing operations in which liver circulation is reduced.

Adult↗
PubMed1988

Nitrous oxide: cardiovascular effects in infants and small children during halothane and isoflurane anesthesia.

Two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular function in 31 unmedicated infants and small children. In 15 patients, the cardiovascular effects of equipotent levels of halothane were compared with and without N2O. In 16 patients, the cardiovascular effects of isoflurane with and without N2O were compared. Prior to anesthesia induction, cardiovascular measurements of heart rate (HR), mean blood pressure (MBP), and two-dimensional and pulsed Doppler echocardiography were recorded. The echocardiographic measurements were used to determine cardiac output (CO), stroke volume (SV), ejection fraction (EF), and left ventricular end-diastolic and end-systolic volume (LVEDV and LVESV). Twenty minutes after mask inhalation induction with halothane or isoflurane with N2O and O2 (3:2 liters/min), cardiovascular measurements were repeated with end-expired halothane or isoflurane maintained at 0.9 MAC. A third set of cardiovascular data was collected 10 minutes after the discontinuation of N2O, with inspired isoflurane or halothane levels in O2 (5 liters/min) increased to maintain 1.5 MAC end-expired levels. Ventilation was controlled throughout the study period and the study was completed before intubation and the start of elective surgery. Heart rate and MBP decreased to similar degrees below awake levels in both patient groups during N2O with halothane or isoflurane. When N2O was discontinued and end-expired levels of halothane or isoflurane increased, MBP remained at levels observed during N2O-O2 with halothane or isoflurane. Heart rate increased during isoflurane in O2. Cardiac output decreased significantly and similarly below awake levels during both halothane of isoflurane with and without N2O.

Blood Pressure↗
PubMed1987

Characterization of a halothane-induced humoral immune response in rabbits.

An animal model of halothane-induced liver injury has been developed in the rabbit to study the production of humoral immunity towards a biotransformation intermediate of halothane. Rabbits exposed many times to halothane in a 75% O2/25% N2 atmosphere produce an antibody that cross-reacts with the trifluoroacetyl moiety of trifluoroacetylated rabbit serum albumin (TFA-RSA). The generation of this halothane-induced immunogen is dependent upon high oxygen tension as shown by the minimal anti-TFA antibody response seen in rabbits exposed to halothane in a 14% O2/86% N2 atmosphere. In addition, halothane exposure of rabbits specifically immunized with the metabolite-carrier complex, TFA-RSA, induces a secondary antibody response toward the immunogen. In rabbits, either immunized with TFA-RSA or not, multiple halothane exposures induce populations of antibodies with varying specificities. Evidence suggests that predominance of the metabolic intermediate, the ensuing immunogen, and the subsequent antibody response depends upon the oxygen tension during successive exposures to halothane. These successive exposures could potentially generate many different immunogens resulting in varied antibody specificities.

Animals↗
PubMed1986

Interaction of halothane and verapamil in isolated papillary muscle.

The combined depressant effects of verapamil and halothane on myocardial contractility were studied using isolated papillary muscle from the rabbit. Verapamil alone (0.5 microM) significantly decreased peak developed tension (PDT) by 15 +/- 2%, time to peak tension (TPT) by 10 +/- 1%, and maximum rate of increase of tension (+dT/dt) by 5 +/- 1%, but not maximum rate of decrease of tension (-dT/dt). Halothane alone (0.8%) significantly decreased PDT by 56 +/- 2%, TPT by 11 +/- 2%, +dT/dt by 53 +/- 2%, and -dT/dt by 56 +/- 2%. During the exposure period, the combination of verapamil and halothane together produced a simple additive effect (no significant interaction effect by two-way analysis of variance), with PDT decreased by 68 +/- 2%, TPT by 20 +/- 3%, +dT/dt by 62 +/- 2%, and -dT/dt by 65 +/- 2%. The reversibility of halothane-induced depression was also studied. Peak developed tension showed complete reversibility 30 min after discontinuing halothane. In the presence of verapamil, however, the reversibility of halothane-induced depression was not complete, and significant residual depression of PDT (19 +/- 3%) was observed. We conclude that the acute depressant effect of verapamil plus halothane in isolated papillary muscle is additive, but reversibility of halothane-induced depression may be impaired or prolonged in the presence of verapamil.

Animals↗
PubMed1985

Guinea-pig model of halothane-associated hepatotoxicity in the absence of enzyme induction and hypoxia.

Halothane anesthesia (1%) administered in 21% oxygen for 4 hr to an outbred strain of guinea pig in the absence of enzyme induction resulted in liver damage in 40 of the 65 animals studied. Necrosis was either confluent around the central veins or in scattered foci throughout the lobules. Damage was present on the second and third days after anesthesia. By day 7 the livers had recovered, evidenced by lack of histological changes and normal serum alanine aminotransferase activity. Administration of halothane in 14 or 80% inspired oxygen did not alter the extent or incidence of liver damage. Major end-metabolites of halothane biotransformation (2-chloro-1,1-difluoroethylene, 2-chloro-1,1,1-trifluoroethane, inorganic fluoride and trifluoroacetic acid) were identified at each oxygen concentration. The metabolic inhibitor SKF-525A significantly decreased the amounts of the volatile metabolites 2-chloro-1,1,1-trifluoroethane and 2-chloro-1,1-difluoroethylene. SKF-525A also decreased the incidence and severity of hepatic damage. Both halothane (1%) and isoflurane (1.1%) anesthesia caused similar reductions in mean arterial blood pressure. However, in contrast to halothane, isoflurane was not hepatotoxic. The results indicate that liver necrosis is unlikely to be caused by anesthesia per se, but rather by hepatotoxic metabolites of halothane. This model offers the opportunity to study the pathogenesis of halothane hepatotoxicity after the administration of halothane alone.

Animals↗
PubMed1985

[Depressant effects of inhalational anesthetic halothane on autonomic nervous activities].

To evaluate the effects of halothane on central nervous function, preganglionic sympathetic and vagal tones (ST, VT), ganglionic transmission and somato-sympathetic reflex potential (SSRP) were studied under different concentrations of halothane in 17 cats and 6 dogs. Compound action potentials of the cervical sympathetic trunk and the vagus nerve were recorded simultaneously and analyzed quantitatively. Relative ganglion-blocking potencies of halothane, enflurane and methoxyflurane were examined by recording evoked potentials from the postganglionic nerve of the stellate ganglion. SSRP was recorded from the cervical sympathetic trunk followed by stimulation of the ipsilateral radial nerve. Mean arterial pressure was kept constant at 100 mmHg to eliminate barostatic response. Halothane affected sympathetic and parasympathetic outflows and moderately blocked ganglionic transmission compared with other inhalational anesthetics and markedly diminished SSRP. ST and VT levels were almost equally depressed and attenuated to about 70, 60, 50 and 30% of the control level (N2O 75% in oxygen) with additional halothane concentrations of 0.5, 1.0, 1.5 and 2.0 MAC, respectively. The magnitude of SSRP was decreased to 68, 34, 24 and 13% with the similar concentrations of halothane, respectively. Halothane moderately depressed ganglionic transmission to about 70% and enflurane markedly decreased it to about 20% at anesthetic depth of 2 MAC, respectively. Methoxyflurane, however, did not depress ganglionic transmission at anesthetic depth of 4 MAC. It was demonstrated that halothane markedly depressed the sympathetic and vagal outflows from the nervous system without changing the balance between the central sympathetic and vagal tones, and decreased ganglionic transmission and somato-sympathetic reflex.

Animals↗
PubMed1983

Effect of calcium on halothane-depressed beating in heart cells in culture.

Heart cells in culture need no external stimulation to contract; they beat rhythmically at a rate and intensity dependent on culture conditions. These cells respond to the general anesthetic 2-bromo-2-chloro-1,1,1-trifluorethane (halothane), with a loss of beating intensity and a lessening of beating rate. Increased calcium concentrations in growth medium reversed the halothane-depressed beating intensity of heart cells in culture; however, increased calcium concentrations had no effect on the halothane-depressed beating rate. Calcium uptake and release took place in two phases, fast and slow. Only the fast calcium uptake was affected by halothane. Like halothane-depressed beating intensity, the halothane-depressed fast calcium uptake also can be reversed by increased calcium in the growth medium of beating heart cells in culture. Data in this manuscript support the theory that general anesthetics dissolve in membranes and thus disrupt membrane function. The anesthetic halothane appears to affect myocardial beating intensity through its ability to disrupt fast calcium uptake. Halothane also depresses the cardiac beating rate, but the data collected do not relate beating rate with calcium metabolism.

Animals↗
PubMed1983

The mechanism of halothane-induced myocardial depression. Altered diastolic mechanics versus impaired contractility.

Although halothane has been shown to depress left ventricular function, it remains a common alternative to narcotic anesthesia in cardiac operations. To clarify the mechanism by which this functional depression occurs (direct decrease in contractility versus altered diastolic compliance), we studied seven dogs in the closed-chest state following instrumentation with ultrasonic dimension transducers to measure left ventricular anteroposterior diameter and micromanometers to measure transmural left ventricular pressure. Ventricular volumes were varied with transient vena caval occlusions in the awake state and following general anesthesia with halothane at 1% and 2% end-tidal concentrations. Ventricular contractility was assessed by the slope of the end-systolic pressure-diameter relationship (EES). Following normalization of end-diastolic diameters with a Lagrangian strain definition (E), diastolic compliance was assessed by fitting end-diastolic pressure-strain data to the exponential: P = alpha (e beta E -1), where alpha and beta are nonlinear elastic coefficients. Halothane was found to produce a significant, dose-dependent decrease in EES from 10.6 +/- 0.6 control to 6.7 +/- 0.4 at 1% halothane and 4.2 +/- 0.5 at 2% halothane (p less than 0.05, control versus both 1% and 2% halothane). Furthermore, halothane at the concentrations studied did not significantly alter alpha and beta nor significantly shift the exponential end-diastolic pressure-strain curve from control. These data indicate that halothane produces a direct, severe depression of left ventricular contractility without primarily altering the diastolic mechanical properties of the myocardium.

Animals↗