SEARCH · Search PubMed

Results for “Halothane”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources

PubMed2004

The use of halothane and succinylcholine to identify broilers prone to developing pale, soft, exudative meat.

Within the last several years, the poultry industry has seen a dramatic increase in the occurrence of pale, soft, and exudative (PSE) meat. This problem is known to be associated with a rapid decline in postmortem (PM) muscle pH, which results in inferior protein functionality similar to that found in PSE pork. Many factors such as seasonal changes have been known to influence the occurrence of PSE meat in poultry and swine. Halothane and succinylcholine have been used within the pork industry to identify animals susceptible to stress and prone to developing PSE meat. The mechanism for the triggering of the PSE gene in poultry has not been fully understood. Therefore, a study was conducted to determine the effectiveness of screening broilers with halothane to identify those prone to developing PSE meat. Succinylcholine was used before slaughter to serve as a triggering agent for the PSE condition. At 4 wk of age, broilers from 4 commercial strains (n = 1,000) were subjected to 3% halothane gas and classified as either halothane positive (HAL+) or negative (HAL-) based on muscle rigidity within the legs. Although halothane sensitivity varied slightly among the strains, approximately 14% of the birds overall were classified as HAL+. All HAL- birds (n = 163) and an equal number of HAL-birds (n = 163) in each strain were grown to market age (7 wk) and were commercially processed. At the time of processing, half of the HAL+ and HAL- birds were injected intravenously with succinylcholine and were slaughtered at 0.25 h postinjection. Pectoralis muscle samples were collected at 0.25, 2, 5, and 24 h PM for the evaluation of rigor development (muscle pH) and meat quality (L* value, moisture, drip loss, and cook loss). Halothane sensitivity had no effect on rigor development, muscle color, or water-holding capacity in the 4 broiler strains. Although birds exhibited reactions to the halothane gas, the halothane sensitivity, along with the use of succinylcholine, was not able to identify birds prone to developing PSE meat.

Animals↗

PubMed1997

Quantitative differences in the production and toxicity of CF2=BrCl versus CH2F-O-C(=CF2)(CF3) (compound A): the safety of halothane does not indicate the safety of sevoflurane.

UNLABELLED: Carbon dioxide absorbents degrade both halothane and sevoflurane to toxic unsaturated compounds (CF2=CBrCl and CH2F-O-C[=CF2][CF3] [i.e., Compound A], respectively). Given the long history of safe administration of halothane, comparable toxicities of these degradation products would imply a similar safety of sevoflurane. We therefore examined CF2=CBrCl in the context of four issues relevant to previous studies of the toxicity of Compound A: 1) reactivity of the degradation product in vitro; 2) rate of its production in vitro; 3) its in vivo toxicity; 4) importance of the beta-lyase pathway to the toxicity in vivo. We found the following. 1) CF2=CBrCl is less reactive than Compound A, degrading in human serum albumin at one-fifth the rate of Compound A. 2) Over a 3-h period of "anesthesia," a standard circle system containing Baralyme (Allied Healthcare Products, Inc., St. Louis, MO) produces 30 times as much Compound A from a minimum alveolar anesthetic concentration (MAC) concentration of sevoflurane as CF2=CBrCl from a MAC concentration of halothane; with soda lime, the difference is 60-fold. Correcting for differences in uptake of halothane versus sevoflurane decreases the differences to 20-40 times. 3) For a 3-h administration to rats, the partial pressure of Compound A causing minimal renal injury or necrosis of half the affected tubule cells exceeds the partial pressure of CF2=CBrCl causing minimal injury or necrosis of half the affected tubule cells by a factor of approximately 4-6. Thus, the ratio of production (Item 2 above) to the partial pressure causing injury with CF2=CBrCl is approximately a quarter of that ratio for Compound A. 4) Compounds that block the beta-lyase pathway either do not change (acivicin) or decrease (aminooxyacetic acid; AOAA) renal injury from CF2=CBrCl in rats, whereas these compounds increase (acivicin) or do not change (AOAA) injury from Compound A. We conclude that the safety of halothane cannot be used to support the safety of sevoflurane. IMPLICATIONS: Carbon dioxide absorbents degrade halothane and sevoflurane to unsaturated compounds nephrotoxic to rats. Relative to sevoflurane's degradation product, halothane's degradation product has less toxicity relative to production, less reactivity, and a different mechanism of injury. The clinical absence of halothane nephrotoxicity does not necessarily indicate a similar absence for sevoflurane.

Absorption↗

PubMed1998

The effects of halothane on abnormal automaticity in canine cardiac Purkinje fibers.

UNLABELLED: Abnormal automaticity is the spontaneous beating of cardiac cells with abnormally depolarized resting membrane potentials. The effects of halothane on cardiac arrhythmias caused by abnormal automaticity are controversial, with either antiarrhythmic effects or enhancement of abnormal automaticity reported by different authors. The goal of the present investigation was to clarify the effects of halothane on abnormal automaticity induced by superfusing excised canine Purkinje fibers (PF) with barium chloride. Intracellular microelectrodes recorded action potentials from fibers superfused with buffer solution in a tissue bath. Barium chloride 0.25 mM reduced maximal diastolic potential from -82.1 +/- 5.6 mV to -67.4 +/- 9.4 mV (mean +/- SD, P < 0.05). Fibers developed abnormal automatic rhythms at a rate of 47.1 +/- 5.9 bpm. Halothane, 0.5%-4%, was added to the superfusate. Halothane reduced the rate of firing in a dose-dependent manner, so that abnormal automaticity was abolished by 4% halothane and reduced by lesser concentrations. Serendipitously, during barium superfusion, two additional fibers developed early afterdepolarizations, a cause of triggered arrhythmias in patients with long Q-T syndrome. Halothane abolished early afterdepolarizations in each. In this model of barium toxicity in excised canine PF, halothane antagonized both abnormal automaticity and early afterdepolarizations. IMPLICATIONS: Life-threatening cardiac arrhythmias may occur during anesthesia. An arrhythmia called abnormal automaticity occurs after heart attacks and can be mimicked by adding barium to small segments of heart tissue. Halothane abolished abnormal automaticity in these tissues, which suggests that it or similar agents may benefit patients prone to developing such abnormal rhythms during surgery.

Action Potentials↗

PubMed1998

Enflurane and isoflurane, but not halothane, protect against myocardial reperfusion injury after cardioplegic arrest with HTK solution in the isolated rat heart.

UNLABELLED: To investigate the effects of halothane, enflurane, and isoflurane on myocardial reperfusion injury after ischemic protection by cardioplegic arrest, isolated perfused rat hearts were arrested by infusion of cold HTK cardioplegic solution containing 0.015 mmol/L Ca2+ and underwent 30 min of ischemia and a subsequent 60 min of reperfusion. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial function and cellular injury, respectively. In the treatment groups (each n = 9), anesthetics were given during the first 30 min of reperfusion in a concentration equivalent to 1.5 minimum alveolar anesthetic concentration of the rat. Nine hearts underwent the protocol without anesthetics (controls). Seven hearts underwent ischemia and reperfusion without cardioplegia and anesthetics. In a second series of experiments, halothane was tested after cardioplegic arrest with a modified HTK solution containing 0.15 mmol/L Ca2+ to investigate the influence of calcium content on protective actions against reperfusion injury by halothane. LV developed pressure recovered to 59%+/-5% of baseline in controls. In the experiments with HTK solution, isoflurane and enflurane further improved functional recovery to 84% of baseline (P < 0.05), whereas halothane-treated hearts showed a functional recovery similar to that of controls. CK release was significantly reduced during early reperfusion by isoflurane and enflurane, but not by halothane. After cardioplegic arrest with the Ca2+-adjusted HTK solution, halothane significantly reduced CK release but did not further improve myocardial function. Isoflurane and enflurane given during the early reperfusion period after ischemic protection by cardioplegia offer additional protection against myocardial reperfusion injury. The protective actions of halothane depended on the calcium content of the cardioplegic solution. IMPLICATIONS: Enflurane and isoflurane administered in concentrations equivalent to 1.5 minimum alveolar anesthetic concentration in rats during early reperfusion offer additional protection against myocardial reperfusion injury even after prior cardioplegic protection. Protective effects of halothane solely against cellular injury were observed only when cardioplegia contained a higher calcium concentration.

Anesthetics, Inhalation↗

PubMed2000

Halothane does not decrease amiloride-sensitive alveolar fluid clearance in rabbits.

UNLABELLED: Halothane decreases alveolar fluid clearance (AFC), a function required for efficient gas exchange in the rat. Further, halothane decreases amiloride-sensitive Na(+) transport in rat alveolar type II cells, a process responsible for a significant portion of AFC. We tested the hypothesis that halothane would decrease amiloride-sensitive AFC in rabbits. Rabbits anesthetized with 1.8% halothane had 5% albumin in 0.9% NaCl instilled into the right lung with (n = 11) or without (n = 11) 1 mM amiloride present in the instillate. Similarly, animals anesthetized with IV fentanyl and droperidol were administered 5% albumin solution with (n = 11) or without (n = 11) amiloride. At 90 min after instillation, alveolar fluid samples were obtained, and AFC was determined by changes in fluid protein concentration. Rabbits anesthetized with halothane or fentanyl and droperidol in the absence of amiloride had similar AFC values (35% +/- 12% and 35% +/- 7%, respectively, mean +/- SD). Rabbits anesthetized with halothane or fentanyl and droperidol in the presence of amiloride had similar AFC values (20% +/- 10% and 16% +/- 12%, respectively) that were significantly less than the groups not administered amiloride (P < 0.01). Unlike the rat, the ability of the rabbit to clear fluid from the alveolar space through amiloride-sensitive pathways is not decreased by halothane anesthesia. IMPLICATIONS: Unlike the rat, the ability of the rabbit to clear fluid from the alveolar space through amiloride-sensitive pathways is not decreased by halothane anesthesia.

Adjuvants, Anesthesia↗

PubMed2000

Endotoxin augments cerebral hyperemic response to halothane by inducing nitric oxide synthase and cyclooxygenase.

We examined the cerebral hyperemic response to halothane after treatment with bacterial lipopolysaccharide (LPS). To determine the involvement of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2), we tested whether the effect of LPS on halothane-induced hyperemia was altered by pretreatment with the selective iNOS inhibitor, aminoguanidine (100 mg/kg), COX-2 inhibitor, NS-398 (5 mg/kg), or enzyme expression inhibitor, dexamethasone (4 mg/kg). Further, we examined whether the administration of a nitric oxide donor, diethylamine NONOate, would change the cerebral hyperemic response of halothane. Sprague-Dawley rats were anesthetized with 0.5 minimum alveolar anesthetic concentration of halothane and artificially ventilated. Regional cerebrocortical blood flow (rCBF) was assessed by laser-Doppler flowmetry. LPS (1 mg/kg) was administered intracerebroventricularly; artificial cerebrospinal fluid was used in controls. Four hours after LPS infusion, iNOS and COX-2 messenger ribonucleic acid (mRNA) levels (reverse transcription-polymerase chain reaction) and enzyme activities (arginine-citrulline conversion and prostaglandin E(2) enzyme immunoassay) were significantly increased. LPS enhanced halothane-induced 3.9 and 1.6-fold increases in rCBF at 1.0 and 1.5 minimum alveolar concentration, respectively. Co-treatment with NS-398 attenuated, but aminoguanidine or dexamethasone abolished the effect of LPS on halothane-induced rCBF increase. Diethylamine NONOate mimicked the enhanced rCBF response to halothane. These results suggest that LPS augmented halothane-induced cerebrocortical hyperemia by induction of iNOS and COX-2.

Anesthetics, Inhalation↗

PubMed2000

Halothane and sevoflurane decrease norepinephrine-stimulated glucose transport in neonatal cardiomyocyte.

UNLABELLED: Catecholamine regulates myocardial glucose use. However, the effect of inhaled anesthetics on myocardial glucose transport stimulated by catecholamine is unclear. We studied the effect of halothane and sevoflurane on uptake of 2-deoxyglucose stimulated by norepinephrine in neonatal cardiomyocytes and the mechanism that modulates glucose transport. We studied the effects of halothane and sevoflurane on norepinephrine (NE)-stimulated glucose uptake and the effects of halothane and sevoflurane on glucose uptake stimulated by W7 (a calcium releasing agent), phorbol 12 myristate-13-acetate (a protein kinase C agonist), and LiCl. Sevoflurane decreased NE-stimulated glucose uptake from 63.7 +/- 7.0 to 41.2 +/- 3.7 pmol h(-1) mg protein(-1), and halothane also attenuated NE-stimulated glucose uptake to 37.8 +/- 5.7 pmol h(-1) mg protein(-1). W7 at 10 micromol/L increased glucose uptake from 16.4 +/- 1.4 to 41.2 +/- 3. 4 pmol h(-1) mg protein(-1). The stimulation was inhibited in the presence of 0.8 mmol/L sevoflurane and 0.58 mmol/L halothane to 23.9 +/- 3.7 and 25.6 +/- 3.6 pmol h(-1) mg protein(-1), respectively. Halothane and sevoflurane did not significantly affect the glucose uptake stimulated by 1 nmol/L insulin, 10 micromol/L PMA, or 10 mmol/L LiCl. We conclude that halothane and sevoflurane decrease NE-stimulated glucose uptake through decrease in intracellular calcium in cardiomyocytes. IMPLICATIONS: The effect of inhaled anesthetics on myocardial glucose uptake during administration of catecholamine is unclear. The myocardial glucose uptake is stimulated not only by catecholamine, but also by insulin, protein kinase C, and increase of intracellular calcium. We examined the effects of halothane and sevoflurane on glucose uptake.

Adrenergic alpha-Agonists↗

PubMed1976

Halothane depresses mucociliary flow in the trachea.

Tracheal mucociliary flow rates in dogs were measured with a radioactive droplet technique during thiopental anesthesia, and subseqently during halothane anesthesia. Body temperature and inspired gas temperature and humidity were held constant. Ventilation was controlled with 25 per cent oxygen in nitrogen to produce PaCO2 30 torr. Mucociliary flow rate remained constant when halothane concentration was held constant at 1.2 MAC halothane. Mucociliary flow rates at 0.6 MAC halothane were comparable to those after thiopental, 25 mg/kg. Increases in concentration from 0.6 to 1.2 to 1.8 to 2.4 MAC halothane progressively depressed mucociliary flow. Flow at 2.4 MAC halothane was 27 per cent of the control (thiopental) value. Flow returned to previous values as end-tidal halothane concentration was reduced. The depression produced by halothane may represent impairment of an important pulmonary defense mechanism.

Animals↗

PubMed1976

Studies of the dual effects of halothane on the lipolysis of human fat cells.

Halothane has dual effects on lipolysis of human adipose tissue: at low tissue concentrations a stimulatory effect is found, while at higher tissue concentrations lipolysis is inhibited. The lipolytic resonse of human adipose tissue was studied in vitro with or without halothane, the phosphodiesterase inhibitor theophylline, the lipase activator dibutyryl cAMP(dbcAMP), the alpha-receptor antagonist phentolamine, the nonselective beta-receptor antagonist propranolol, and the selective beta1-receptor antagonist practolol. In the absence of beta-receptor antagonists low concentrations of halothane stimulated lipolysis, This effect was blunted by beta-receptor antagonists, indicating that halothane at low tissue concentrations may directly stimulate the beta-receptors. The inhibitory effect of higher tissue concentrations of halothane was not the result of increased alpha-receptor activity since addition of phentolamine did not inhibit this effect. High concentrations of theophylline or dbcAMP increased lipolysis in specimens exposed to halothane, but the lipolytic rate was still less than that found in specimens not exposed to halothane. The data thus indicate that the inhibitory effect of halothane is exerted at a step beyond the formation and degradation of cAMP.

Adipose Tissue↗

PubMed1976

Effects of halothane on DNA synthesis and the presynthetic phase (G 1) in dividing fibroblasts.

The effects of halothane on deoxyribonucleic acid (DNA) synthesis and events preceding DNA synthesis have been examined in Chinese hamster fibroblasts in culture.DNA synthesis was studied by the uptake of 3H-thymidine during short periods of incubation that minimized effects on cells in the presynthetic phase (G1). Halothane produced slight but significant dose-related depression of 3H-thymidine uptake (20 per cent depression with 2 per cent halothane). In a separate series of experiments, synchronized cultures were exposed to 1-3 per cent halothane in G 1 phase for three or five hours. Halothane caused a postponement of onset of DNA synthesis (S phase), indicating a delay in G 1. This delay roughly equalled the duration of exposure to 3 per cent halothane but was less with 2 per cent halothane. The delay was only about one hour with 1 per cent halothane.

Animals↗

PubMed1979

Cerebral energy levels during trimethaphan-induced hypotension in the rat: effects of light versus deep halothane anesthesia.

Hypotension may be expected to produce less perturbation of metabolism in the brain when cerebral metabolic rate is lowered by deep anesthesia. Male Wistar rats having unilateral carotidartery ligation were exposed to mean arterial pressure (MAP) of 40 torr for 22 min by an intravenous infusion of trimethaphan during anesthesia with halothane, 0.6 or 2 per cent, in oxygen. Cortical tissue metabolite levels on the side of the ligated carotid artery were more abnormal in rats receiving halothane, 0.6 per cent, than in those receiving halothane, 2 per cent. Values at halothane, 0.6 per cent, were adenosine triphosphate (ATP), 1.71 +/- 0.05 (+/-SEM) mumol/g, phosphocreatine (PCr) 1.97 +/- 0.07 mumol/g. and lactate 16.5 +/- 5.1 mumol/g; corresponding values at halothane, 2 per cent, were ATP 2.27 +/- 0.02, PCr 4.02 +/- 0.23, and lactate 4.75 +/- 0.9 mumol/g. ATP and PCr values were significiantly lower (P less than 0.05) and the lactate value was significantly higher with halothane, 0.6 per cent, than with halothane 2 per cent. Cerebral oxygen consumption decreased 47 per cent in rats anesthetized with halothane, 2 per cent. Preservation of cortical metabolite levels in deeply anesthetized animals suggests a protective effect of cerebral metabolic depression.

Adenosine Triphosphate↗

PubMed1981

Halothane reversibly inhibits human neutrophil bacterial killing.

The effect of halothane, at clinically relevant concentrations on the ability of human polymorphonuclear leukocytes (PMNL) to kill the most frequently isolated gram-negative organisms responsible for human bacteremias, Escherichia coli and Klebsiella pneumoniae, was studied. Exposure of PMNL to 0.75 per cent halothane is air significantly inhibited the killing of E. coli (from 81 per cent to 65 per cent) but not K. pneumoniae. At 1.0 per cent halothane there was no killing of E. coli and the killing of K. Pneumoniae was reduced from 98 per cent to 82 per cent. With 1.5 per cent halothane, the killing of K. pneumoniae by PMNL was further reduced to 65 per cent. This inhibition of bacterial killing could be reversed after exposure of halothane-treated PMNL to air. The mechanism of inhibition may be due in part to a deleterious effect of halothane on the oxidative microbicidal activity of human PMNL. Although halothane reversibly inhibits the ability of PMNL to kill bacteremic culture isolates, the degree of susceptibility of bacteria to halothane-treated PMNL may vary.

Bacteriological Techniques↗

PubMed1982

Cardiovascular and regional blood flow changes during halothane anesthesia in the aged rat.

The authors investigated the cardiovascular and regional hemodynamic changes that occur in the aged rat under unanesthetized control conditions and during the induction of halothane anesthesia. Regional blood flow changes were measured in young (4-month-old) and aged (27-29-month-old) F-344 rats using radioactive microspheres under unanesthetized conditions and during three levels of halothane anesthesia. Blood halothane levels were measured at each anesthetic level. The inspired concentrations of halothane were adjusted in young vs. aged rats so that each group was tested at the same depth of anesthesia. Results indicate that aged rats had significantly lower blood pressures than young rats in an unanesthetized state and at all levels of halothane anesthesia. Tissue blood flow was similar between young and aged rats in skeletal muscle and skin, while blood flow to renal and small intestinal tissues was consistently higher in young rats. Heart blood flow was initially 100 per cent higher in young rats but decreased to similar levels as aged at the highest levels of halothane anesthesia used. Cerebral blood flow was similar initially in young vs. aged, but increased in young rats with deeper levels of halothane anesthesia while decreasing in aged rats. These results indicate significant regional hemodynamic differences in young compared to aged rats under unanesthetized conditions as well as in response to halothane anesthesia.

Aging↗

PubMed1982

Halothane depresses the response of carotid body chemoreceptors to hypoxia and hypercapnia in the cat.

Halothane is known to inhibit the ventilatory responses to hypoxia and hypercapnia. In order to determine whether this inhibition was mediated by peripheral chemoreceptors, the authors measured the effect of halothane on the response of carotid body chemoreceptors to these stimuli. Cats were decerebrated under brief halothane anesthesia, paralyzed, and ventilated. Chemoreceptor activity was recorded from single- or few-fiber preparations of carotid sinus nerve, and the inspiratory drive was recorded from the whole phrenic nerve. Steady-state responses were measured at three levels of CO2 tension (19-92 mmHg) during hyperoxia, and at four levels of O2 tension (35-450 mmHg) at a fixed PaCO2. Both responses were measured before, during, and after 0.5-1.0 per cent halothane was inspired. The halothane inhalation was maintained for at least 30 min before the responses were obtained. Halothane reduced the slope of chemoreceptor response to hypercapnia to about 48 per cent of the control slope. The response to hypoxia was reduced to about 58 pr cent of the control response. The increase in firing after intravenous nicotine (100 micrograms), summed for 20 s, was reduced to 25 per cent of the prehalothane control values; that after NaCN (25 micrograms) was reduced to 17 per cent of the control value. The effect of halothane was prompt (half complete in 1-2 min) and reversible. This finding explains some of the inhibition of the ventilatory responses to hypoxia and hypercapnia caused by halothane.

Animals↗

PubMed1982

Effect of halothane and N2O on the oxidative activity of human neutrophils.

The effect of clinically used concentrations of halothane and N2O on the microbicidal oxidative function of human neutrophils was investigated. Neutrophil oxidative activity was assessed utilizing the method of luminol dependent chemiluminescence (LDCL) by particulate (opsonized zymosn) and nonparticulate (phorbol myristate acetate, [PMA]) stimulated cells. In vivo exposure of neutrophils to 2 and 3% halothane resulted in a 13 and 40% inhibition, respectively of the air-exposed LDCL response with zymosan-activated neutrophils; 1% halothane had no effect. Similar results were seen with PMA-stimulated neutrophils. N2O 80% did not inhibit the LDCL response, and also did not show an additive inhibition when combined with halothane. Although th halothane inhibition of LDCL was reversible (equal to control, no anesthetic, LDCL responses following exposure to air), neutrophils treated with N2O plus halothane and then exposed to air for 30 min showed a significantly higher LDCL response over the control experiments. The inhibition of zymosan- or PMA-stimulated neutrophil LDCL by halothane suggests either a membrane perturbation or a direct inactivation of oxidative enzyme(s) by the anesthetic. This impairment of oxidative activity may partly explain the reduced bacterial killing by neutrophils seen after exposure to halothane.

Adult↗

PubMed1983

Epinephrine-halothane interactions in children.

Cutaneous infiltration of dilute solutions of epinephrine for hemostasis during halothane anesthesia can result in ventricular dysrhythmias. Our clinical experience, published reports, and a study comparing piglets with adult swine suggest that children may be less susceptible than adults to dysrhythmias under these conditions. We therefore undertook a prospective survey of heart rate and rhythm in halothane-anesthesized children who received subcutaneous epinephrine for hemostasis. Mass spectrometry was used to quantify end-tidal halothane and to avoid hypercarbia. In 83 children anesthesized with halothane, we continuously recorded ECG, heart rate (HR), end-tidal halothane (ETHalo), and carbon dioxide (ETCO2). The surgeons injected 0.4--15.7 micrograms/kg of epinephrine (in saline or 1% lidocaine) to provide hemostasis at a variety of sites. No child developed a ventricular dysrhythmia. One child had self-limited premature atrial contractions (PAC). Sixty-three children had some increase in heart rate after epinephrine injection, while seven increased their HR 15% or more above pre-injection levels. No relation between any increase in HR and epinephrine dosage, ETHalo, ETCO2, physical status, or age was found by multiple linear regression; however, HR was increased significantly in patients receiving epinephrine in head and neck sites other than the palate. The authors conclude that children tolerate higher doses of subcutaneous epinephrine than adults during halothane anesthesia. The arrhythmogenic dose of epinephrine in children receiving halothane has yet to be determined, but at least 10 micrograms/kg of epinephrine infiltration may be used safely in normocarbic and hypocarbic pediatric patients without congenital heart disease. The presence of PAC and tachycardia emphasize the need for continuous ECG monitoring and caution during halothane anesthesia with epinephrine injection.

Adolescent↗

PubMed1983

The effect of halothane anesthesia on myocardial necrosis, hemodynamic performance, and regional myocardial blood flow in dogs following coronary artery occlusion.

The effect of halothane anesthesia on myocardial necrosis resulting from coronary artery ligation was examined in 28 anesthetized mongrel dogs. In 18 dogs, the left anterior descending coronary artery (LAD) was ligated immediately proximal to the first apical diagonal branch, and 1 h later the dogs were assigned randomly either to receive halothane, 0.5-1.0% inspired in room air for 12 h (n = 10) or to awaken without further intervention (control, n = 8). Infarct size was measured by staining the myocardium with triphenyl tetrazolium chloride 24 h after LAD ligation. Infarct size in halothane-treated dogs was 17.8 +/- 2.0% of the left ventricle, compared with 27.3 +/- 3.3% in control dogs (P less than 0.05). Myocardial salvage was present transmurally but was greatest in epicardial regions. In 10 additional dogs, hemodynamic variables (heart rate, arterial pressure, left ventricular end-diastolic pressure, peak left ventricular dP/dt, tension-time index, and rate-pressure product) were measured or calculated, and radionuclide-labeled microspheres were injected for measurement of cardiac output and regional myocardial blood flow (RMBF). Thirty minutes after LAD ligation and after initial hemodynamic measurements and microsphere injection, these dogs were assigned randomly to receive either halothane, 1.0%, inspired in room air (n = 5) or no intervention (control, n = 5). After 15 min of halothane inhalation (45 min after LAD ligation in control dogs), measurements were repeated. Halothane inhalation reduced heart rate, arterial pressure, and indexes of left ventricular contractile and pump performance. During halothane treatment, RMBF declined in normal myocardium but not in ischemic regions, while neither normal nor ischemic zone RMBF changed in control dogs. Systemic vascular resistance was unchanged in either group. Thus, halothane was associated with a 35% smaller myocardial infarct, transmural myocardial salvage, reduced heart rate, reduced left ventricular contractile and pump performance, reduced RMBF to nonischemic regions, and unchanged RMBF in the ischemic myocardium.

Anesthesia, Inhalation↗

PubMed1983

Halothane inhibits metabolism of enflurane in Fischer 344 rats.

The authors investigated the effect of prior administration of halothane upon the metabolism of enflurane. Twenty-four, one-year-old male, Fischer 344 rats were assigned randomly to four anesthetic exposure groups. Groups 1 and 2 were controls exposed only to halothane and enflurane, respectively. Group 3 was exposed for 1 h to 0.3% halothane, followed by 2 h of 1% enflurane. Group 4 was exposed for 1 h to 1% halothane and then to 2 h of 1% enflurane. Blood samples were taken prior to, immediately following, and 1, 24, and 48 h after anesthetic exposure. Serum was assayed for inorganic fluoride (F-), SGOT and SGPT. Twenty-four-hour urinary collections were assayed for F excretion. Group 1 rats exposed to halothane alone had the lowest peak mean serum F- (5.0 microM). Group 2 rats exposed to enflurane alone had the highest serum F concentration 4 h after anesthesia (18.7 microM). Peak serum F in Group 3 rats (9.5 microM) was significantly lower than in Group 2 rats (enflurane control). In Group 4 rats, serum F- was not significantly different from Group 1 rats (halothane control) at any time. In the first 24 h after anesthetic exposure, urinary F- excretion in Groups 2 and 3 was significantly higher than in Groups 1 and 4. This study demonstrated that prior exposure to halothane reduced the metabolism of enflurane; previous work suggested that this was due to an interaction of halothane with hepatic cytochrome P-450.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗