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PubMed1998

Effects on the intramuscular blood flow and cardiopulmonary function of anaesthetised ponies of changing from halothane to isoflurane maintenance and vice versa.

The effects on intramuscular blood flow and cardiopulmonary parameters of changing from anaesthesia with halothane to isoflurane and vice versa were investigated in six ponies (small horses). Anaesthesia was induced with xylazine, ketamine and diazepam, maintained for one hour with halothane at an end tidal concentration of 1 per cent and then with isoflurane at 1.5 per cent for a further hour (halo/iso). On another occasion the order in which the volatile agents were administered was reversed (iso/halo). After one hour of anaesthesia the mean (sd) arterial blood pressure (MAP) and cardiac output (CO) of the ponies on the two occasions did not differ significantly (iso/halo, MAP 43 [5] mmHg, CO 10.9 [2.4] litre/min; halo/iso, MAP 53 [8] mmHg, CO 8.9 [2.3] litre/min). On changing the anaesthetic, MAP rose similarly in both groups. In the halo/iso group CO remained stable (8.64 [1.4] litre/min after the hour of isoflurane), but in the iso/halo group, CO decreased significantly on the administration of halothane (6.16 [1.3] litre/min after the second hour). When halothane replaced isoflurane, the intramuscular blood flow in both the upper and lower triceps brachii decreased significantly by 23 to 35 per cent, but when isoflurane replaced halothane the changes were not significant. It is concluded that CO and intramuscular blood flow both deteriorated when isoflurane was replaced by halothane. When isoflurane replaced halothane, cardiopulmonary function did not deteriorate further, but any improvement was not statistically significant.

Anesthetics, Inhalation↗
PubMed1976

[Effect of halothane on catecholamine metabolism in the brain stem of rats].

In an experimental study we tried to find out whether halothane, in addition to its effects on vegetative efferents, has also an influence on catecholamine metabolism of the corresponding brain sections. We studied the effects of halothane in the brain stem of rats on dopamine and norepinephrine contents and on the transformation of L-dopa into dopamine and L-norepinephrine. Anaesthesia with 2 vol% halothane reduced dopamine content by 41.4%, norepinephrine content by 17.8%. These findings could be observed even 3 h after narcosis. Electrophysiological studies show that the central nervous sympathetic activity at rest and after central excitation is clearly reduced during anaesthesia with 2 vol% halothane; 70 min after narcosis it returned to normal. Administration of L-dopa led to an increase of dopamine by 43.5% within 45 min. This transformation of L-dopa into dopamine is not affected by concurrent halothane anaesthesia. There is no increase in norepinephrine after administration of L-dopa. Thus, the effect of halothane on catecholamine metabolism in the brain stem affects the precursors of L-dopa. Halothane is said to inhibit transport of the L-dopa precursor L-tyrosine from plasma to brain tissue. Along with such an inhibition goes the depression of the sympathetic activity. In this respect and obviously on the basis of its position within the catecholamine metabolism, dopamine is more important than norepinephrine.

Animals↗
PubMed1976

[The uterotropismus of halothane, chloroform or methoxyflurane in clinical use (author's transl)].

To perform episiotomy, 89 women after childbirth were anaesthetized with either halothane (50 patients), methoxyflurane (24 patients) or chloroform (15 patients). The activity of the uterus was registered tocodynamographically. To examine the alternate influence of narcotics and uterotonica, 57 patients were pre-medicated with sintocinon and methergin i.m. as a prophylaxis. The second group (32 patients) received no premedication to stimulate labor activity, however in 18 cases towards the end of narcosis oxytocin and methergin were given i.v. In addition to these examinations 5 vaginal deliveries were anaesthetised with halothane only. Concerning our own experimental study it can be observed: 1. The relaxative properties of halothane wich suppresses completly the activity of myometrium during the deep stages of anaesthesia are superior to chloroform and methoxyflurane. 2. More rapid relaxation of the uterus with halothane compared with chloroform and methoxyflurane. 3. After the use of halothane a quicker return of the activity of the uterus compared with chloroform and methoxyflurane. 4. The value of a prophylaxis with uterotonica can be demonstrated by a comparatively reduced slowing-down of labour-activity during anaesthesia. 5. In every one of the cases, an interuption of the labour-suppressing, caused by the anaesthesia, can be obtained by injecting intravenously oxytocin or methergin. 6. During vaginal delivery, compared to the post placentar phase, there is no need for higher concentrations of halothane to be used to suppress labour contractions. The discussion deals with the intensity of reduction of the uterus contraction caused by the above mentioned narcotics, the dangers of the atony of the uterus, and the indications and contra-indications of obstetrical anaesthesia with halothane or methoxyflurane.

Adult↗
PubMed1990

The echocardiographic assessment of left ventricular performance during sevoflurane and halothane anesthesia.

The cardiovascular effects of sevoflurane were studied and compared with those of halothane in 30 healthy patients. The patients were assigned to receive 1 MAC sevoflurane (n = 10), 2 MAC sevoflurane (n = 10) or 1 MAC halothane (n = 10) in N(2)O 2 l.min(-1) and O(2) 4 l.min(-1). The changes in left ventricular diastolic and systolic dimension (Dd and Ds), fractional shortening (FS), mean velocity of circumferential fiber shortening (mVcf), left ventricular diastolic and systolic volume (Vd and Vs), stroke volume (SV), ejection fraction (EF) and cardiac index (CI) were evaluated by echocardiography. Sevoflurane produced significant dose-dependent decreases in FS, mVcf, EF and SV, but no significant changes in Dd and Vd. Therefore, the decrease in SV was due mainly to the increase in left ventricular residual volume (Vs). One MAC halothane produced a more significant decrease in FS, mVcf, EF and SV, when compared to values obtained at 1 MAC sevoflourane ( P < 0.01). CI was more significantly decreased with 1 MAC halothane than with 1 MAC and 2 MAC sevoflurane ( P < 0.01). This was brought about by a slight decrease in HR with halothane and a slight increase in HR with sevoflurane, in addition to a smaller decrease in SV with sevoflurane than with halothane. This study suggests that sevoflurane may better preserve cardiac function as a pump in healthy patients, when compared to halothane.

Journal Article↗
PubMed2002

Histochemical and immunohistochemical changes in rat hepatocytes after halothane exposure.

PURPOSE: Histochemical and immunohistochemical changes were observed in hepatocytes to study the developing and recovery processes of halothane-induced hepatic injury from 0 to 7 days after halothane exposure. METHODS: A total of 330 7-week-old male Sprague-Dawley rats, with or without phenobarbital preteatment, were exposed to halothane in 100%, 21%, 10% oxygen or oxygen alone for 2 h. RESULTS: In the phenobarbital group, degenerated hepatocytes were observed immediately after exposure to 10% oxygen, both with and without halothane: glycogen and ribosomal ribonucleic acid (rRNA) disappeared immediately and 6 h after exposure, respectively, and necrosis developed in zones 3 to 2 at 6 h after exposure. From 12 h to day 1, the necrosis was more marked and more widely observed in the cells with halothane than those without halothane. However, all tissues returned to normal by day 7. CONCLUSION: Disappearance of glycogen at 0 h and rRNA at 6 h after exposure to halothane under 10% oxygen is considered to be one of the factors inducing necrosis around the central vein. Recovery of the hepatolobular structure was attributed to the rearrangement of the remaining hepatocytes in the portal vein area.

Journal Article↗
PubMed1987

Postanesthetic respiratory depression in humans: a comparison of sevoflurane, isoflurane and halothane.

The postanesthetic respiratory depression with sevoflurane, isoflurane and halothane was studied in twenty-one patients. They were divided into three groups of seven patients each. One group underwent sevoflurane anesthesia, another group isoflurane and the third group halothane. Following extubation, the decrease in blood concentration of the anesthetic agent was most rapid with sevoflurane and slowest with halothane. Twenty minutes following extubation, resting ventilation and ventilatory response to carbon dioxide returned to the preanesthetic state with sevoflurane and isoflurane anesthesia. With halothane anesthesia, however, the depressive respiratory effects of halothane remained; depressed ventilatory response to carbon dioxide, decreased tidal volume and increased respiratory frequency. Although halothane has been reported to have the least depressive respiratory effect of the three, its elimination was slowest. Thus the respiratory effects of halothane persisted up to and past the twenty minute mark, far longer than with sevoflurane or isoflurane.

Journal Article↗
PubMed1989

Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs.

We investigated the relative effects of 0.5, 1.0, 1.5, 2.0 MAC halothane and enflurane, and concurrent noxious stimulus on hepatic blood flow and oxygen consumption in 14 mongrel dogs randomly divided into groups of seven each. Hepatic arterial and portal venous blood flow (HABF and PVBF, respectively) were measured continuously using ultrasonic transit time flow meter. Mean arterial blood pressure (MAP), cardiac index (CI), hepatic oxygen supply, and hepatic oxygen consumption (HVO2) were measured. Halothane significantly deceased HABF, but not PVBF in a dose dependent manner. Enflurane did not affect HABF and PVBF significantly. MAP and CI decreased in both groups, with halothane producing more marked decreases than enflurane. HVO2 did not change with enflurane, but did with halothane, producing significant differences, with halothane being greater at 1.5, 2.0 MAC. A noxious stimulus only caused minor change in blood flow. The results suggest that liver blood flow and oxygen consumption are affected differently by halothane and enflurane and that halothane has a stronger tendency to cause an imbalance between liver oxygen supply and consumption than dose enflurane.

Journal Article↗
PubMed1996

Variability of energy metabolism and nuclear T3-receptors within the skeletal muscle tissue of pigs different with respect to the halothane gene.

Energy metabolism of skeletal muscle tissue of pigs growing from approximately 12 to 18 kg (12 homozygous halothane negative, HH; 16 heterozygotes, Hh; 17 homozygous halothane susceptible, hh) was measured in vivo using 31P nuclear magnetic resonance (NMR) spectroscopy. Data for intracellular pH, phosphocreatine (PCr), phosphomonoesters (PME), and ATP were analyzed by canonical discriminant analysis, an artificial neural network approach, and analysis of variance. Within the hh pigs, two subpopulations could be distinguished before the application of halothane treatment. Some of the hh pigs had a high PME concentration in the biceps femoris muscle (hh(pme+)), whereas others had a low concentration (hh(pme-)) (2.18 +/- .12 for hh(pme+) vs 1.68 +/- .12 mM for hh(pme-), P < .004). The hh(pme+) pigs were statistically different from HH pigs for pH (P < .03), PME (P < .004), and PCr (P < .008) before halothane treatment. The hh(pme-) pigs were not different from the Hh and HH pigs with respect to PME when measured before halothane treatment (P > .05). However, intracellular pH (P < .03) and PCr (P < .008) of the hh(pme-) pigs were different from those of HH pigs (7.15 vs 7.19 for pH and 38.7 vs 35.1 for PCr, respectively). When combining intracellular pH, PME, and PCr within a canonical discriminant analysis, all were measured before halothane treatment, Hh pigs were found to be different from HH pigs (Mahalanobis distance different from zero, P < .02). In a second experiment, growth rate, depth of longissimus muscle, and maximal binding capacity of nuclear T3-receptors of skeletal muscle tissue were different (P < .05, P < .002, and P < .02, respectively) among pigs selected from the same genetic lines. Of the variability in depth of the longissimus muscle, 22% was explained by variability in maximal binding capacity of nuclear T3-receptors. These results, if confirmed with a large number of pigs, might open new possibilities for selection procedures for leanness because, with respect to halothane susceptibility, a shift between genotypic and phenotypic variability was observed.

Adenosine Triphosphate↗
PubMed1991

Biological monitoring of the occupational exposure to halothane (fluothane) in operating room personnel.

The concentration of halothane (fluothane) in the ambient atmosphere was determined in five operating theaters of two hospitals in Italy. The concentrations of halothane in the ambient air exceeded the NIOSH recommended time-weighted average exposure levels (median value: 10.38 mg/m3). Halothane was detected in the urine of 58 exposed subjects (anesthetists, surgeons, and nurses). A significant correlation was found between the halothane concentration in urine produced during the shift (Cu, micrograms/L) and halothane environmental concentration (CI, mg/m3) (Cu = 0.242 x CI + 3.51) (N = 58; r = 0.92; p less than 0.0001). The results show that the urinary halothane concentration can be used as an appropriate biological exposure index. The biological values proposed are: 92 micrograms/L, corresponding to a 50 ppm of environmental exposure; 6.5 micrograms/L, corresponding to 2 ppm of environmental exposure and 3.9 micrograms/L, corresponding to a 0.5 ppm of environmental exposure.

Adult↗
PubMed1989

Halothane-induced hepatic microsomal lipid peroxidation in guinea pigs and rats.

Halothane-induced hepatic microsomal lipid peroxidation in guinea pigs and rats was examined with respect to the mixed function oxidase system, anaerobic dehalogenation activity of halothane, and the antioxidant system. The levels of cytochrome P-450 and NADPH-cytochrome P-450 reductase were significantly higher in guinea pigs than in rats. There was no difference between the two animals in anaerobic dehalogenation activity of halothane per cytochrome P-450 in microsomes. Microsomal alpha-tocopherol was significantly lower in guinea pigs than in rats, and was increased by multiple exposure to halothane in guinea pigs but remained lower than in rats. Microsomal alpha-tocopherol was decreased in rats by multiple exposure. The concentration of reduced glutathione and ascorbic acid was decreased significantly by multiple exposure to halothane in guinea pigs but not in rats. These results suggest that the higher level of halothane-induced hepatic microsomal lipid peroxidation in guinea pigs is due to the large production of radical metabolites resulting from the large amounts of cytochrome P-450, the high activity of NADPH-cytochrome P-450 reductase, and the low concentration of microsomal alpha-tocopherol.

Animals↗
PubMed1990

Isoniazid potentiation of a guinea pig model of halothane-associated hepatotoxicity.

Isoniazid (INH) is a selective inducer of cytochrome P-450 isozymes that are involved in the biotransformation of organohalogen anesthetics. It has been used to produce a rat model of halothane-associated hepatotoxicity that was linked to enhanced oxidative biotransformation of the anesthetic. Guinea pigs were pretreated with INH in order to potentiate halothane-induced hepatic necrosis and to study the oxidative pathway as a hepatotoxic mechanism in this species. The animals received either 12.5, 25.0 or 50.0 mg kg-1 INH i.p. for 7 days. Following halothane exposure, there were dose-dependent increases in plasma levels of the oxidative halothane metabolite, trifluoroacetic acid. These increases were associated with increases in 48 h plasma alanine aminotransferase (ALT) levels. When combined with halothane exposure, the two higher doses of INH killed the animals before planned termination. These deaths were not attributable to hepatic failure. Dividing the 25 mg kg-1 INH dose into twice daily injections of 12.5 mg kg-1 reduced deaths. INH pretreatment control animals exhibited occasional non-dose-dependent increases in ALT as well as the occurrence of fatty vacuolization of hepatocytes at the highest dose. Even though INH pretreatment enhanced oxidative halothane biotransformation and subsequent hepatotoxicity, sensitivity of guinea pigs to the deleterious actions of INH would contraindicate its use as a cytochrome P-450 induction agent.

Alanine Transaminase↗
PubMed1986

Porcine malignant hyperthermia: cell injury enhances halothane sensitivity of biopsies.

A possible relationship between muscle cell injury or deterioration and enhanced halothane sensitivity was studied by monitoring mechanical responses of skeletal muscles from normal pigs and pigs susceptible to malignant hyperthermia (MH). Increased time postbiopsy and decreased maximum control tetanic tension both correlated significantly with enhanced sensitivity to halothane. In both normal and MH-susceptible (MHS) muscles, greater halothane sensitivity was observed in cut cell than in intact cell bundles and in low tetanic tension as compared to high tension preparations. Subsequent to halothane exposure, twitches of high tension (greater than or equal 1.75 kg . cm-2) intact bundles of both normal and MHS muscles were potentiated. Tetani of normal intact bundles were not altered, whereas those of MHS bundles were depressed after halothane exposure. Control twitch-to-tetanus ratios (twitch ratios) were higher in MHS (0.23) than in normal (0.12) intact bundles. According to discriminant analysis, the best distinction between normal and MHS muscles, either cut or intact, was obtained by comparing halothane-induced changes in tetanic tension and control twitch ratios.

Animals↗
PubMed1989

Malignant hyperthermia: effects of halothane on the surface membrane.

We studied the electrical properties of intact muscle fibers from normal and malignant hyperthermia-susceptible (MHS) pigs. Resting membrane potentials, action potentials, and current-voltage relationships were measured with and without the presence of halothane. There were no changes in the resting potentials or the specific membrane conductances at any concentration of halothane in either the normal or MHS fibers. The current-voltage relationships of normal and MHS fibers did not differ. Contractures were observed in MHS muscle when the concentration of halothane was greater than or equal to 0.8%. These halothane-induced contractures were not associated with depolarization of the surface membrane. Contractures were not observed in normal muscle even at concentrations of 6.0% halothane. In contrast, halothane altered the shape of the action potentials of both MHS and normal fibers. However, these changes were significantly greater in MHS fibers, occurred at much lower concentrations, and were partially prevented by preincubation in 10 microM dantrolene.

Action Potentials↗
PubMed2000

Effect of halothane on the oligomerization of the sarcoplasmic reticulum Ca(2+)-ATPase.

The exact molecular mechanism of inhalational anesthetics remains obscure. Since the enzyme activity of the sarcoplasmic reticulum Ca(2+)-ATPase from skeletal muscle fibres is modified by halothane and because protein-protein interactions play an important role in the regulation of Ca(2+)-regulatory proteins, we investigated the effect of this volatile drug on the oligomerization of the fast-twitch Ca(2+)-ATPase. Using electrophoretic separation following incubation with halothane, increases in relative molecular mass were determined by immunoblotting with a monoclonal antibody to the SERCA1 isoform of the Ca(2+)-ATPase. Distinct drug-induced decreases in electrophoretic mobility indicated oligomerization of the native Ca(2+)-pump by halothane, comparable to crosslinking-mediated formation of homo-tetramers. Determination of the effect of halothane on enzyme activity suggested that halothane-mediated protein aggregation triggers a partial inhibition of Ca(2+)-pump units. Thus, halothane appears to exert its action via specific peptide binding sites and not indirectly by lipid perturbation. These findings support the protein theory of anesthetic action.

Anesthetics↗
PubMed1994

Lack of prophylactic or therapeutic efficacy of 5-HT2A receptor antagonists in halothane-induced porcine malignant hyperthermia.

During halothane-induced malignant hyperthermia (MH), plasma levels of serotonin (5-hydroxytryptamine, 5-HT) increase in pigs. Administration of 5-HT agonists which stimulate the 5-HT2A subreceptor triggers MH in susceptible pigs. A possible link between MH induced by 5-HT2A receptor agonists and halothane could be an increase of second messengers such as phosphoinositides (inositol polyphosphates), which have recently been implicated in the abnormal regulation of skeletal muscle calcium release in MH. If so, antagonists of 5-HT2A receptors which are linked to phosphoinositide turnover should be capable of preventing, retarding or attenuating halothane-induced MH. This possibility was investigated in the present study in MH susceptible pigs, using dantrolene for comparison, Development of MH triggered by a halothane challenge (inhalation of 3% halothane for 15 min) was completely prevented by dantrolene, 3.5 mg/i.v., whereas the 5-HT2A receptor antagonists ritanserin (0.5-10 mg/kg i.v.) or ketanserin (0.5-10 mg/kg i.v.) exerted no prophylactic effect. In pigs in which dantrolene, ritanserin or ketanserin where given in combination with hyperventilation after development of MH, dantrolene exerted therapeutic efficacy, whereas neither ritanserin nor ketanserin were effective treatments. The data indicate that 5-HT is not critically involved in the mechanisms of halothane-induced MH, at least under the conditions of the present experimental study.

Animals↗
PubMed1979

Effects of halothane on caffeine-induced tension transients in functionally skinned myocardial fibers.

The effects of halothane on caffeine-induced tension transients in functionally skinned myocardial fibers were investigated. Fiber bundles from mechanically disrupted rabbit right ventricular papillary muscles were mounted on a tension transducer. The fiber preparation was loaded with Ca2+; Ca2+ was then released by the use of caffeine (25 mM); and the area of the resulting tension transient was measured. Each preparation was sequentially transferred from control to test to control solution. The control solutions were equilibrated with 100% N2, and the test solutions with a mixture of N2 and various halothane concentrations. The preparation was exposed to halothane during the Ca2+ uptake or the release phase only, or during both Ca2+ uptake and release phases. The areas of the test tension transients were compared with those of the two control tension transients. It was found that halothane depressed the caffeine-induced tension transient either during the uptake phase or the combined-uptake-and-release phase but not during the release phase. The halothane-induced depression was dose-dependent, reversible, and comparable to the depression observed in intact isolated papillary muscles. We conclude that halothane could induce myocardial depression by inhibiting Ca2+ uptake by the sarcoplasmic reticulum.

Animals↗
PubMed1981

Halothane accumulation in rat brain and liver.

Halothane concentrations (microgram/g wet weight) was measured in rat brain and liver following exposure to various concentrations of halothane in air. Because of the difficulty of determining the amount of a volatile compound in brain, we analyzed tissue fixed by two different methods. The apparent concentration of halothane in brain was higher following direct decapitation into liquid nitrogen, than after decapitation, removal of fresh tissue, and then freezing. However, the relative effects of altering the inspired concentration were essentially the same in each case. Thus, absolute quantitative accuracy remains a point for discussion; however, we can reach several conclusions regarding the relative accumulation of halothane in brain tissue following various conditions of exposure. Resultant tissue concentrations of halothane were not linearly related to ambient concentrations. Above an inspired concentrations of 1.0%, an increase to 1.5% inspired concentration caused little further increase in the halothane concentration in brain, although the liver concentration increased in proportion to the dose increase. Below an inspired concentration of 0.5%, tissue concentrations were less expected, probably as a result of metabolic degradation occurring at a rate that becomes more noticeable at lower inspired concentrations. Body size was shown to be an important variable affecting the time required for each tissue to reach equilibrium at a given inspired concentration. These data indicate that tissue concentrations at low exposure levels may be less than proportional at dose and that concentrations in small laboratory animals may be expected to exceed values in humans under equivalent conditions of exposure.

Animals↗
PubMed1981

Effect of halothane on myocardial infarct size in rats.

The effect of halothane on myocardial infarction caused by ligation of the left descending coronary artery was studied in rats. The extent of infarction was quantified 48 hours after ligation of the artery by planimetric measurement of left ventricular slices stained with nitrobluetetrazolium. Animals exposed to halothane one per cent for three hours after the coronary ligation were compared with a control group which received halothane for only 5-7 minutes during surgery. It was found that halothane caused a small increase in infarction size (31.3 +/- 1.5 per cent of the left ventricle compared to 25.7 +/- 2.3 per cent, p less than 0.05). This effect was accompanied by a decrease in systolic blood pressure (91 +/- 2 mmHg compared to 113 +/- 3 mmHg, p less than 0.001). Heart rate did not change significantly. Analysis of our results in comparison to previously reported data on the effect of halothane on myocardial ischaemia in different experimental conditions shows that halothane may produce beneficial as well as detrimental effect on ischaemic injury to the myocardium. The latter can result when the drug causes marked hypotension in the absence of a significant decrease in heart rate.

Animals↗