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PubMed2006

Mg2+ dependence of Ca2+ release from the sarcoplasmic reticulum induced by sevoflurane or halothane in skeletal muscle from humans susceptible to malignant hyperthermia.

BACKGROUND: In normal resting muscle, cytosolic Mg(2+) exerts a potent inhibitory influence on the sarcoplasmic reticulum (SR) Ca(2+) release channel (ryanodine receptor, RyR1). Impaired Mg(2+)-regulation of RyR1 has been proposed as a causal factor in malignant hyperthermia (MH). The aim of this study was to compare the effects of cytosolic Mg(2+) on SR Ca(2+) release induced by halothane or sevoflurane in normal (MHN) and MH susceptible (MHS) human skeletal muscle fibres. METHODS: Samples of vastus medialis muscle were obtained from patients under investigation for MH susceptibility. Single fibres were mechanically skinned and perfused with solutions mimicking the intracellular milieu. Changes in [Ca(2+)](i) were detected using fura-2 fluorescence after application of equimolar halothane or sevoflurane. RESULTS: In MHN fibres, concentrations of sevoflurane or halothane as high as 10 mM typically failed to induce SR Ca(2+) release at physiological free [Mg(2+)] (1 mM). However, when [Mg(2+)] was decreased to 0.4 mM, SR Ca(2+) release occurred in 51% (16/33) and 6% (2/33) of MHN fibres after the addition of 1 mM halothane or 1 mM sevoflurane, respectively. Further decreases in [Mg(2+)] increased the proportion of responsive fibres. In the presence of 0.1 mM [Mg(2+)], Ca(2+) release occurred in all fibres (33/33) after the introduction of 1 mM halothane or 1 mM sevoflurane. In MHS fibres, 1 mM halothane or 1 mM sevoflurane-induced Ca(2+) release in 54% (7/13) or 15% (2/13) of fibres, respectively, at 1 mM Mg(2+). A decrease in [Mg(2+)] to 0.2 mM Mg(2+) was sufficient to render 100% of MHS fibres (13/13) responsive to 1 mM halothane or 1 mM sevoflurane. CONCLUSIONS: In both MHS and MHN fibres (i) halothane is a more potent activator of SR Ca(2+) release than sevoflurane and (ii) as with halothane, the efficacy of sevoflurane-induced SR Ca(2+) release exhibits a marked dependence on cytosolic [Mg(2+)]. The marked potentiation of SR Ca(2+) release after a moderate reduction in cytosolic [Mg(2+)] suggests that conditions which cause hypomagnesaemia will increase the probability and possibly severity of an MH event. Conversely, maintenance of a normal or slightly increased cytosolic [Mg(2+)] may reduce the probability of MH.

Anesthetics, Inhalation↗
PubMed2000

Effects of halothane on respiratory mechanics and lung histopathology in normal rats.

It is generally accepted that halothane reduces airway and tissue resistance in lungs with preexisting airway tone. However, under conditions of resting airway tone, pulmonary resistance remains unaltered. In this study, we have determined the effects of halothane on respiratory system, pulmonary and chest wall resistive, elastic and viscoelastic mechanical properties, and related the results to findings from lung histology in intact normal rats. Sixteen adult male Wistar rats were allocated randomly to one of two groups (n = 8 in each group): control or halothane group. In the control group, animals were sedated with diazepam 5 mg i.p. and anaesthetized with pentobarbital 20 mg kg-1 i.p. In the halothane group, the anaesthetic was administered at an end-tidal concentration of I MAC throughout the study. Rats were paralysed and underwent mechanical ventilation. Halothane decreased airway resistance but increased the tissue component of resistance (caused by viscoelastic elements and lung inhomogeneity). Static and dynamic elastance also increased with halothane anaesthesia. Pulmonary resistance remained unchanged. Lung histopathology demonstrated airway dilatation and a greater degree of lung collapse and hyperinflation in the halothane group. We conclude that halothane anaesthesia acts both on airway and lung tissue. In airway tissue, dilatation occurs but the lung periphery stiffens. Consequently, these opposing effects result in no overall apparent change in mechanical properties, although changes are observed during halothane anaesthesia in normal animal and subjects.

Airway Resistance↗
PubMed1995

Effects of halothane on calcium(2+)-activated tension of the contractile proteins and calcium(2+) uptake and release by the sarcoplasmic reticulum in skinned human myocardial fibers.

Based on studies using skinned myocardial fibers from animals, it has been postulated that one of the major mechanisms by which halothane depresses myocardial contractility is by decreasing the Ca2+ content of the sarcoplasmic reticulum (SR). In this study we examined, in skinned human myocardial fibers, the effects of halothane on Ca(2+)-activated tension development of the contractile proteins and Ca2+ uptake and release by the SR. Left ventricular muscle samples obtained from patients undergoing aortocoronary bypass operations were mechanically skinned and immersed in test solutions equilibrated with N2 and halothane preceded and followed by immersion in control solution (no halothane). To study Ca(2+)-activated tension development of the contractile proteins, free Ca2+ concentrations in the bathing solutions were buffered by EGTA. To study Ca2+ uptake and release by the SR, Ca2+ was loaded into the SR and released with caffeine and the resulting tension transients were measured. Halothane (1%-3%) depressed maximum Ca(2+)-activated tensions (pCa = -log[Ca2+](M) = 3.8) by 5% for each 1% increase in concentration. Tensions generated by submaximum Ca2+ concentrations expressed as a percentage of maximum tension were not significantly decreased by halothane except at 3%. Halothane decreased Ca2+ uptake (IC50 = 1.7%), and increased (by approximately 50%) Ca2+ release by the SR. We conclude that decreased activation of the contractile proteins and Ca2+ uptake by the SR can both contribute to the myocardial depression produced by halothane. Of these, decreased Ca2+ uptake by the SR is probably a major mechanism for halothane depression of myocardium.

Animals↗
PubMed1996

The dose-dependent effects of halothane on right ventricular contraction pattern and regional inotropy in swine.

The right ventricle (RV) is comprised of two embryologically distinct units, the inflow and outflow tracts, which normally contract sequentially and differ in the magnitude of increased inotropy during sympathetic nervous stimulation. The present study examined the dose-response effects of halothane on the RV contraction pattern and regional contractility in seven open-chest pigs instrumented for measurement of inflow and outflow tract pressures and segment lengths. The RV contraction pattern was evaluated by comparing the phase of inflow and outflow tract shortening, and regional contractility was determined by calculation of preload recruitable stroke work (PRSW) slope. Using this methodology, an inflow-outflow tract contraction phase difference of -27 degrees (inflow tract shortened earlier) was evident at baseline, but was abolished by 1.0 and 1.5 minimum alveolar anesthetic concentration (MAC) halothane; PRSW slope of both the inflow and outflow tracts, however, demonstrated similar dose-related change. To determine whether alterations in cardiac sympathovagal balance played a role in the RV response to halothane, an additional four animals were studied after pretreatment with hexamethonium, propranolol, and atropine. In these animals, there was no difference in the regional contraction phase either at baseline or during halothane administration, and dose-related depression of PRSW by halothane was again similar in both regions. However, when halothane effects on regional PRSW in animals with autonomic blockade were compared to those of neurally intact animals, a 20% greater depression of outflow tract PRSW by 0.5 MAC halothane was evident. This study demonstrates that halothane abolishes the normal sequential pattern of RV contraction without exerting markedly variant negative inotropic effects within different regions of the RV, and provides evidence to suggest that alterations in cardiac sympathovagal balance may contribute to the effect of halothane on RV contraction dynamics.

Anesthetics, Inhalation↗
PubMed1996

Comparison of emergence and recovery characteristics of sevoflurane, desflurane, and halothane in pediatric ambulatory patients.

This study compares the emergence and recovery characteristics of sevoflurane, desflurane, and halothane in children undergoing adenoidectomy with bilateral myringotomy and the insertion of tubes. Eighty children 1-7 yr of age were studied. Thirty minutes prior to the induction of anesthesia, all patients received 0.5 mg/kg midazolam orally. Patients were randomly assigned to one of four groups: Group 1, sevoflurane induction and maintenance (S:S); Group 2, halothane induction and sevoflurane maintenance (H:S); Group 3, halothane induction and maintenance (H:H); or Group 4, halothane induction and desflurane maintenance (H:D). Tracheal intubation was facilitated with the use of a single dose of 0.2 mg/kg mivacurium. A Mapelson D circuit was used, and all patients received N2O:O2 60:40 for induction and maintenance at standardized appropriate fresh gas flow. Ventilation was controlled to maintain normocapnia. End-tidal concentration of anesthetics was maintained at approximately 1.3 minimum alveolar anesthetic concentration (MAC) (halothane: 0.56; sevoflurane: 2.6; desflurane: 8.3) until the end of surgery when all anesthetics were discontinued. Emergence (extubation), recovery (Steward score 6), and discharge times were compared among patients in the four groups using analysis of variance and Newman-Keuls tests P < 0.05 was considered significant. There were no significant differences among the four groups with respect to age, weight, duration of surgery, or duration of anesthesia. Emergence and recovery from anesthesia were significantly faster in the desflurane group (Group 4) compared with the sevoflurane and halothane groups (Groups 1, 2, and 3) (5 +/- 1.6 min vs 11 +/- 3.7, 11 +/- 4.0, 10 +/- 4.0 min and 11 +/- 3.9 min vs 17 +/- 5.5, 19 +/- 7.1, 21 +/- 8.5 min, respectively). There was a significantly greater incidence of postoperative agitation and excitement in patients who received desflurane (55%) versus sevoflurane (10%) and halothane (25%). There were no significant differences among the four groups with respect to the time to meet home discharge criteria (134 +/- 36.9, 129 +/- 53.3, 117 +/- 64.6, 137 +/- 22.6 in Groups 1, 2, 3, and 4, respectively), in the time to drink oral fluids (139 +/- 31.6, 136 +/- 53.8, 123 +/- 65.0, 142 +/- 29.4 min, respectively), or in the incidence of postoperative vomiting. It is concluded that, although desflurane resulted in the fastest early emergence from anesthesia, it was associated with a greater incidence of postoperative agitation. Sevoflurane resulted in similar emergence and recovery compared with halothane. Desflurane and sevoflurane did not result in faster discharge times than halothane in this patient population.

Adenoidectomy↗
PubMed2000

A comparison of the incidence of the oculocardiac and oculorespiratory reflexes during sevoflurane or halothane anesthesia for strabismus surgery in children.

UNLABELLED: We examined changes in the cardiorespiratory system of small children during surgical correction of strabismus with a laryngeal mask airway and spontaneous respiration with sevoflurane or halothane inhaled anesthesia. Fifty-one children, 1-7 yr old, having outpatient strabismus correction were randomized to sevoflurane (S) or halothane (H) in 66% nitrous oxide at 1.3 minimum alveolar concentration. Children breathed spontaneously through a laryngeal mask airway and were not pretreated with anticholinergics. The oculocardiac reflex (OCR), defined as a 20% decrease in heart rate (HR) from baseline, dysrhythmias, or sinoatrial arrest concomitant with ocular muscle traction occurred less frequently with sevoflurane than with halothane (S 38%, H79%, P = 0.009). The baseline HR was higher with sevoflurane (S 114 +/- 13 bpm, H 101 +/- 15 bpm, P = 0.002). The lowest HR occurred with halothane (S 95 +/- 22 bpm, H 73 +/- 19 bpm, P = 0.001). The incidence of dysrhythmias was higher in the halothane group (S 4%, H 42%, P = 0.004). Reductions in minute ventilation and PETCO(2) accompanied OCRs. Airway irritability was present with halothane only (S 0, H 3). Eleven children, of whom the majority had received halothane, required measures to correct SpO(2) < 95% or PETCO(2) > 60 mm Hg during maintenance anesthesia (S 11%, H 32%). Sevoflurane may be a more suitable anesthetic than halothane for operations involving traction on the ocular muscles with spontaneous respiration in children because of reduced incidence of OCR, airway irritability, and ventilatory disturbances. IMPLICATIONS: Some children experience a sudden slowing of the heart and impaired breathing when the surgeon pulls on the eye muscles during squint operations under anesthesia. Sevoflurane, a recently developed anesthetic vapor, may reduce this problem when compared with the established vapor halothane.

Anesthesia, Inhalation↗
PubMed1975

Halothane and the beating response and ATP turnover rate of heart cells in tissue culture.

The effects of halothane on the beating response of rat heart cells in tissue culture were studied using an optical-electronic monitoring device. A dose-response curve was obtained over a concentration range to as much as 5 vol per cent halothane. The clinical dosage of 1 vol per cent halothane decreased the inotropic response of 4-10-day-old cells to 59 plus or minus 10 per cent of the original beating strength; no significant decrease in beating strength was seen in 25-30-day-old cells. One volume per cent halothane caused no significant change in the chronotropic response of the heart cells. Higher concentrations of halothane caused significant negative chronotropic and negative inotropic responses in a dose-related manner. When glycolysis was inhibited by 2-deoxyglucose in the growth medium, the cells became dependent on fatty-acid oxidation and oxidative phorphorylation for energy and showed increased sensitivity to halothane; for example, the chronotropic response to 5-8-day old cells treated with 2-deoxyglucose was decreased approximately 70 per cent by exposure to 3 vol per cent halothane, whereas 4-10-day-old cells maintained on a complete growth medium showed only a 40 per cent decrease. Increasing concentrations of halothane decreased the rate of ATP turnover. This supports evidence suggesting that halothane blocks electron transport in the NADH-coenzyme Q reductase level. The model described provides a means for determining anesthetic potency in a mammalian system in terms of functional as well as metabolic responses. It also provides a means for study of metabolic effects of anesthetics and other drugs.

Adenosine Triphosphate↗
PubMed1976

Synergism between halothane and nitrous oxide in the production of nuclear abnormalities in the dividing fibroblast.

When Chinese hamster fibroblasts divide in the presence of halothane there is an increased incidence of cells with abnormal nuclei, both in mitosis and in interphase. The authors compared the effects of halothane and nitrous oxide separately and in combination. Nitrous oxide, 75 percent, alone had no significant effect compared with controls, less than 1.4 per cent of cells showing abnormalities, while halothane alone had a dose-dependent effect on both phases of the cell cycle. Halothane, 1 per cent, caused abnormalities in 7 per cent (SEM +/- 0.32) of cells in interphase and in 12 per cent (SEM +/- 0.95) of cells in mitosis, but the combination of 0.75 per cent halothane with 75 percent nitrous oxide produced 15 per cent (SEM +/- 0.68) abnormal cells in interphase and 22 per cent (SEM +/- 0.51) abnormal mitoses. Similar highly significant differences were obtained throughout the dose-response curves to as much as 4 per cent halothane in air and 2.35 per cent halothane in 75 per cent nitrous oxide. This appears to demonstrate synergism between halothane and nitrous oxide in the production of this particular side effect. In contrast, the effects of halothane and nitrous oxide on growth rate were additive.

Anesthesia, Inhalation↗
PubMed1979

An animal model of halothane hepatotoxicity: roles of enzyme induction and hypoxia.

Exposure of phenobarbital-pretreated male Sprague-Dawley rats to halothane, 1 per cent, for two hours under conditions of hypoxia (FIO2 0.14) resulted in extensive centrilobular necrosis within 24 hours. Accompanying the morphologic damage were an increase in serum glutamic pyruvic transminase (SGPT) and a decrease in hepatic microsomal cytochrmoe P-450. Glutathione levels in the liver were unchanged. Phenobarbital-pretreated rats anesthetized with halothane, 1 per cent, at FIO2 0.21 had only minor morphologic changes at 24 hours. Hepatic injury was not apparent in any non-phenobarbital-induced rat or in any induced animal exposed to ether at FIO2 0.10 or to halothane at FIO2 0.99. There was a 2.6-fold increase in the 24-hour urinary excretion of fluoride in those rats in which extensive centrilobular necrosis developed. The in-vivo covalent binding to lipids of 14C from 14C-halothane also was increased markedly when 14C-halothane was administered intraperitoneally to phenobarbital-induced rats maintained hypoxic (FIO2 0.14) for two hours. These results support the authors' hypothesis that halothane is metabolized to hepatotoxic intermediates by a reductive or non-oxygen-dependent cytochrome P-450-dependent pathway. This animal model of halothane-induced hepatotoxicity may be clinically relevant. A decrease in hepatic blood flow during halothane anesthesia may decrease the PO2 available to hepatocytes and thus direct the metabolism of halothane along its reductive, hepatotoxic pathway.

Alanine Transaminase↗
PubMed1981

Low-level binding of halothane metabolites to rat liver histones in vivo.

Binding of halothane metabolites to rat liver histones was investigated after in vivo administration of 14C-halothane. Animals were injected with either a mixture of triiodothyronine, glucagon and heparin (TGH) to stimulate liver growth or with saline as a control. Twenty-four hours later, animals were administered 14C-halothane and maintained at 8--10 per cent O2 for 6 hours. Detergent washed nuclei from liver homogenates were subfractionated to allow quantitative measurements of 14C-halothane binding to histones. Although our studies suggest that much of the previously reported binding of halothane metabolites to major cell fractions was a result of redistribution of endoplasmic reticulum components during isolation procedures, carefully controlled experiments demonstrated that the radioactivity associated with histones could not be due to residual microsomal lipid. Of the initial 132 mumol of 14C-halothane administered, 1.1 mumol remained as nonvolatile metabolites in the liver homogenate and 25 pmol were associated with purified histones. This corresponds to approximately one halothane moiety per 15,000 histone molecules. No significant binding to liver cell RNA or DNA was observed. With this low level of histone modification and lack of convincing evidence of halothane metabolite binding to hepatic DNA or RNA, it is unlikely that significant alteration of the genome occurs after exposure to halothane.

Alkylating Agents↗
PubMed1984

Liver circulation and function during isoflurane and halothane anesthesia.

Hepatic arterial blood flow (HABF) and portal blood flow (PBF) were measured in 18 dogs while awake and during isoflurane and halothane anesthesia. Surgical preparation 1 week before the measurements consisted of a left thoracotomy, placement of a left atrial catheter, and insertion of another catheter into the distal aorta via the left femoral artery. Cardiac output and liver blood flow were determined using microspheres at three stages: stage 1-awake state; stage 2-after 45 min of 1 MAC of isoflurane (eight dogs) or halothane (10 dogs) anesthesia; and stage 3-after 45 min of 2 MAC of inhalation anesthesia. Half-life and fractional clearance for indocyanine green (ICG) were determined 1 day before the experiment (awake state), and at the end of stages 2 and 3. Mean arterial pressure (MAP) and cardiac index (CI), as well as PBF, decreased during isoflurane and halothane anesthesia. HABF increased significantly during isoflurane anesthesia, remained unchanged during 1 MAC of halothane anesthesia, and significantly decreased during 2 MAC of halothane anesthesia. Apparently, hepatic oxygen supply was maintained much better during isoflurane than during halothane anesthesia. PBF correlated with CI during halothane (r = 0.97) and, to a certain extent, with MAP during isoflurane (r = 0.66). HABF correlated with CI and MAP during halothane (r = 0.74 and 0.71, respectively) but did not correlate with systemic hemodynamic variables during isoflurane. ICG half-life significantly increased during 1 and 2 MAC of halothane anesthesia. The degree of increase did not correlate with the level of anesthesia or the decrease in total hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Chemistry of halothane-enflurane mixtures applied to anesthesia.

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

Anesthesia, Inhalation↗
PubMed1986

Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs. I. Verapamil and halothane.

In order to assess the interaction between halothane and verapamil on the cardiovascular system, mongrel dogs were instrumented so that the following measurements could be made awake and under the influence of the drugs: aortic, left ventricular, and left atrial blood pressures; myocardial segment length shortening; heart rate and rhythm; and coronary, carotid, and renal blood flows. The effect of two infusion doses of verapamil (3 micrograms X kg-1 X min-1 and 6 micrograms X kg-1 X min-1 after 200 micrograms X kg-1 bolus) were examined awake. On a different day in the same dogs, two concentrations of halothane (1.2-low and 2.4-high % end-tidal) and the effect of the two infusion doses of verapamil during low and high halothane were studied. Thirty minutes of either infusion dose of verapamil produced only heart rate and electrocardiographic P-R interval increases in conscious dogs. Halothane produced dose-related decreases in mean aortic pressure, left ventricular maximum rate of tension development (dP/dt), and segment length shortening and increases in heart rate and left atrial pressure. Carotid blood flow was increased by low halothane concentrations and returned to control with high halothane concentrations. There were no significant changes in coronary or renal blood flow produced by halothane. Verapamil infusion during low halothane concentration produced minimal effects. However, both the 3 and 6 micrograms X kg-1 X min-1 verapamil doses further depressed hearts already depressed by the high concentrations of halothane and decreased renal and carotid blood flows.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Endotracheal↗
PubMed1986

Mode of action of halothane on histamine-induced airway constriction in dogs with reactive airways.

To determine if clinical concentrations of halothane have direct relaxant effects on airway smooth muscle, the authors compared dose-response curves to histamine in the control state (thiopental) and during halothane anesthesia (1.0 and 1.5 MAC), in six basenji-greyhound (BG) dogs untreated and pretreated with atropine aerosols (10 mg X ml-1). Pulmonary resistance (RL) and dynamic compliance (Cdyn) were continuously monitored. Baseline airway tone was not significantly different during thiopental, halothane (1.0 MAC and 1.5 MAC), and after atropine aerosol administration. During thiopental anesthesia, histamine produced dose-related increases in RL and decreases in Cdyn. Both halothane and atropine significantly attenuated the bronchoconstriction induced by histamine 1 mg X ml-1. There was no significant differences in the extent of antagonism of histamine-related bronchoconstriction between halothane (1.0 MAC and 1.5 MAC) and the atropine aerosol. Moreover, in four dogs halothane anesthesia in the presence of atropine offered no additional protection compared with atropine alone. Because the protection afforded by halothane was not greater than that of atropine pretreatment alone, and the addition of halothane to atropine failed to increase the protection, it is concluded that block of vagal reflexes was the major action of halothane responsible for the attenuation of histamine-induced bronchoconstriction.

Aerosols↗
PubMed1987

Effects of halothane on myocardial high-energy phosphate metabolism and intracellular pH utilizing 31P NMR spectroscopy.

Utilizing 31phosphorus nuclear magnetic resonance (NMR) spectroscopy, the authors tested the two hypotheses that the negative inotropic action of halothane is the result of: 1) myocardial intracellular acidosis, and 2) a decrease in myocardial high-energy phosphates. In isolated, paced, Langendorff-perfused rabbit hearts, halothane (1.5 vol %) dissolved in the coronary perfusate produced a 48 +/- 2% decrease (P less than 0.01) in left ventricular developed pressure. In contrast, halothane administration had no significant effect on myocardial intracellular pH (7.18 +/- 0.04 at control vs 7.21 +/- 0.02 during halothane). Halothane exposure decreased (P less than 0.01) the forward rate constant of the creatine kinase reaction by 32 +/- 6%, as measured using saturation transfer NMR, suggesting a decline in the rate of high-energy phosphate metabolism. This was further indicated by a concomitant decrease (P less than 0.05) in myocardial oxygen consumption (20 +/- 5%). During the halothane-induced reduction in left ventricular developed pressure, only small decreases in the myocardial steady state concentrations of phosphocreatine (7 +/- 1%; P less than 0.01) and beta ATP (12 +/- 4%; P less than 0.05), and an increase in Pi (18 +/- 6%; P less than 0.05) were observed. However, similar changes in steady-state high-energy phosphate metabolites were also measured in time-control hearts not exposed to halothane. These results indicate that the negative inotropic action of halothane is not mediated by myocardial intracellular acidosis. Moreover, these findings do not support the concept that the negative inotropic action of halothane is the result of a reduction in myocardial high-energy phosphates.

Adenosine Triphosphate↗
PubMed1987

Hepatic oxygen supply during halothane or isoflurane anesthesia in guinea pigs.

The present study was designed to determine changes in hepatic oxygen supply in guinea pigs during halothane or isoflurane anesthesia. Twenty-seven guinea pigs were randomly divided into three equal groups: control (no anesthesia) group, and animals anesthetized with halothane or isoflurane to decrease mean arterial pressure (MAP) by 50%. Hepatic arterial blood flow (HABF) and portal blood flow (PBF), as well as arterial and portal venous blood oxygen content, were determined in awake animals (stage I, baseline values), and during anesthesia (stage II). HABF was found to be extremely low (0.04 ml.min-1.g-1) during both stages of observation in the control (no anesthesia) group, as well as during stage I (awake) in animals treated with halothane or isoflurane. Equal degrees of arterial hypotension during halothane and isoflurane anesthesia were accompanied by decreased HABF during halothane (37%), but no significant change in HABF during isoflurane anesthesia. PBF decreased significantly in both experimental groups; however, the decrease was more prominent during halothane than during isoflurane anesthesia (57% vs. 23%). The observed hepatic circulatory changes led to a 65% decrease in hepatic oxygen delivery during halothane, but only a 34% decrease during isoflurane anesthesia. The present study does not exclude the possibility that liver damage in the guinea pig model is related to the reductive metabolism of halothane or any other mechanism. However, the extremely low HABF and a prominent reduction in both HABF and PBF during halothane anesthesia may be responsible for hepatic damage observed in the guinea pig model.

Anesthesia, Inhalation↗
PubMed1988

Comparison of the in vitro myocardial depressant effects of isoflurane and halothane anesthesia.

The myocardial depressant effects of isoflurane and halothane were compared using feline right ventricular papillary muscles bathed in Krebs-bicarbonate solution. In experiment 1 muscles were stimulated by field electrodes (0.2 Hz) to obtain control measurements of developed tension (dt) and maximal rate of tension development (dF/dt) prior to exposing the papillary muscles to four concentrations of either isoflurane (4.0%, 2.0%, 1.0%, 0.5%) or halothane (2.0%, 1.0%, 0.5%, 0.25%). Repeat measurements of dt and dF/dt were recorded after 20 min at each concentration. Isoflurane and halothane both caused dose-dependent depression of dt and dF/dt, but at 0.5%, 1.0%, and 2.0%, halothane was significantly more depressant than isoflurane (P less than 0.01 for dt and dF/dt). Quadratic equations were fitted to the dose-response data by least squares analysis (R2 greater than .985 for both anesthetics), and the isoflurane and halothane concentrations that decreased dt to 90%, 70%, 50%, and 30% of control were determined to compare the relative myocardial depressant potency of isoflurane and halothane by linear regression analysis. This potency relationship is described by the equation: isoflurane concentration = -0.005 + 1.445 (halothane concentration). In experiment 2 papillary muscle responses at two similar cardiodepressant concentrations of isoflurane (1.25% and 2.0%) or halothane (0.80% and 1.35%) were compared at stimulus frequencies of 0.05, 0.1, 0.2, 0.4, 0.8, 1.0, and 2.0 Hz. The concentrations of isoflurane and halothane were selected from the data obtained in experiment 1 and represent the anesthetic concentrations that diminish muscle function to approximately 70% and 50% of control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Pulmonary resistance during halothane anesthesia is not determined only by airway caliber.

Studies of the effect of halothane on airway smooth muscle have used pulmonary resistance as an index of airway caliber. However, pulmonary resistance (RL) is the sum of airway resistance (Raw), which changes with airway caliber, and of tissue resistance (Rti), which depends on the pressure-volume hysteresis of the lung. To separate the effects of halothane on airway caliber from its possible effects on tissue pressure-volume hysteresis in the unstimulated lung and during bronchoconstriction, the authors measured both components of RL before and during vagus nerve stimulation in 12 dogs before and during halothane administration. Rti was always the major component of RL, constituting 77 +/- 14% (mean +/- SD) of RL before vagus nerve stimulation and 64 +/- 21% of RL during stimulation in the absence of halothane. Vagus nerve stimulation caused approximately equal increases in both Rti and Raw. Halothane attenuated the response of both Rti and Raw to vagus nerve stimulation in a dose-dependent fashion. At 1 MAC, the Rti response was 44 +/- 13% of its value before halothane administration and the Raw response was 32 +/- 12% of its value before halothane administration; these responses were not significantly different. The authors conclude that changes in RL during halothane administration are caused not only by changes in airway caliber, as previously assumed, but also reflect a significant effect of halothane on lung tissue pressure-volume hysteresis.

Airway Resistance↗