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PubMed1986

Liver function following hypovolemic hypotension in rats anaesthetized with halothane or enflurane.

Rats which had approximately 25-30% of their calculated blood volume removed were exposed to halothane (1%) or enflurane (2%) in 33% oxygen for 30 min. Hepatic function was evaluated by determining, at various time intervals, serum activities of glutamic-oxalacetic and glutamic-pyruvic transaminase, acid phosphatase and gamma-glutamyl-transpeptidase. In this model serum enzyme activities and animal mortality were significantly increased when hypovolemic hypotension was induced during halothane anaesthesia. The same events did not occur in bleeding animals anaesthetized with enflurane. The marked disparity in hepatic dysfunction and mortality between halothane and enflurane-anaesthetized rats during hypovolemic hypotension may be explained by the more pronounced decrease of oxygen available for the liver and production of reductive toxic intermediates in animals exposed to halothane.

Anesthesia↗
PubMed1993

Effects of halothane and isoflurane in the upper airway of dogs during development.

It has been previously found that volatile anesthetics significantly affect the activity of laryngeal receptors. In this study we have investigated the respiratory effects of these volatile anesthetics delivered into the upper airway of newborn and adult dogs. Experiments were performed on 17 5-14-day-old, 3 26-28-day-old and 3 adult dogs, anesthetized and breathing spontaneously through a tracheostomy. In the youngest age group, halothane decreased ventilation (VE) to 37.6 +/- 6.8% of control (mean +/- SE; P < 0.01) due to a decrease in both frequency and tidal volume. Peak inspiratory and expiratory flows, and esophageal pressure (Pes) were depressed also (60.8 +/- 6.5%, 51.6 +/- 7.1% and 66.5 +/- 8.1% of control, respectively; P < 0.01). Superior laryngeal nerve (SLN) section abolished the changes in VE, but residual significant decreases in peak flows and Pes were still present and disappeared only after topical anesthetization of the nasal cavities. Isoflurane had similar but weaker effects on VE (74.2 +/- 2.8% of control; P < 0.01), accompanied by a decrease in peak inspiratory and expiratory flows and Pes. SLN section abolished these changes. In the 26-28 day age group there was only a decrease in peak inspiratory airflow with the halothane challenge; isoflurane did not have any effect. In the adult dogs halothane caused only a marginal decrease in inspiratory time. The depressive effects of halothane and isoflurane should be considered when they are used for induction of anesthesia in newborns.

Age Factors↗
PubMed1981

Halothane-induced nephrotoxicity.

Two cases are reported of combined renal and hepatic failure following exposure to halothane anesthesia. Both patients presented with postoperative fever and rapidly deteriorating liver and kidney function. Both required peritoneal dialysis. Both patients died, and in both cases this was the second exposure to halothane. The pathologic features of the 2 cases were similar in that the liver changes were typical of those seen with halothane hepatitis and the renal lesion was similar to that of methoxyflurane nephritis. This is, to our knowledge, the third report of renal failure occurring after halothane anesthesia. Possible mechanisms regarding its toxicity are discussed.

Aged↗
PubMed1988

Halothane interference at an amperometric oxygen electrode: the development of an oxygen/halothane sensor.

The role of electrode materials in the reduction of halothane and oxygen mixtures at rotating and stationary electrodes is considered. Halothane is found to be electroactive within the available electrode-potential range on silver and on gold. Double potential step experiments are considered in order to isolate the individual halothane and oxygen signals. A double integration, single potential step technique is evaluated for the quantitative simultaneous measurements of oxygen and halothane on gold. The influence of electrode purity is discussed in terms of a reaction mechanism and electrode output error.

Calibration↗
PubMed1987

In vivo 19F-NMR study of halothane distribution in brain.

Halothane distribution and elimination from rabbit brain was studied in vivo using 19F-NMR spectroscopy. Two exponential decay functions for the anesthetic were observed in the clearance curve. They are assigned to halothane in brain held in two distinct chemical environments characterized by different chemical shifts, and half-lives (25 and 320 min). A nonvolatile halothane metabolite with a half-life of several days was found to be present in rabbit brains. The in vivo results were corroborated by ex vivo experiments on excised brain tissue. Halothane was distributed in all of the major cell subfractions, whereas the metabolite was present predominantly in the cytoplasm.

Animals↗
PubMed1986

Delayed enhancement of acetaminophen hepatotoxicity by general anesthesia using diethyl ether or halothane.

Acetaminophen (Tylenol) is a widely used analgesic/antipyretic drug which is enzymatically bioactivated, or toxified, by the cytochromes P-450 to a hepatotoxic reactive intermediary metabolite. Brief general anesthesia with diethyl ether has been shown to inhibit both the toxifying cytochromes P-450 and enzymatic glucuronidation, the latter constituting up to 60% of acetaminophen elimination via a nontoxifying pathway. Thus ether potentially could produce a temporally differentiated inhibition of bioactivating and "detoxifying" pathways, resulting in an enhancement of acetaminophen hepatotoxicity if the balance favored bioactivation. To evaluate this possibility, separate groups of male NIH strain mice were treated with acetaminophen at different times after 5 min of anesthesia with ether. Ether produced a 40-fold enhancement in acetaminophen hepatotoxicity as determined by plasma glutamic-pyruvic transaminase (GPT) concentrations. This toxicologic enhancement was observed only if acetaminophen administration was delayed, with a maximal enhancement when acetaminophen was given 6 hr after ether, and no effect with a delay of 16 hr. Similar studies in male CD-1 mice were carried out using halothane (Fluothane) as the general anesthetic given either over 5 min or over 1 hr. While halothane given over 5 min had no effect, a 1 hr anesthetic duration produced a 10-fold increase in acetaminophen hepatotoxicity as determined by peak GPT concentration, with no observed hepatotoxicity in the halothane controls. Toxicologic enhancement occurred only with delayed administration of acetaminophen; however, the maximal enhancement observed with a 6-hr delay was still evident with a 12-hr delay. Conversely, inhibition of acetaminophen hepatotoxicity was observed if acetaminophen was given either 2 hr or 18 hr after halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1992

Formation and identification of protein adducts to cytosolic proteins in guinea pig liver slices exposed to halothane.

The anesthetic halothane can be bioactivated to the reactive intermediate, trifluoroacetyl chloride, which can covalently bind to liver protein. The product of this reaction is trifluoroacetyl-N-epsilon-lysine which can act as a foreign epitope in altering both protein immunogenicity and antigenicity. An in vitro liver slice system was used to study the formation of protein adducts following exposure to halothane. Liver slices (30-35 mg wet weight, 250-300 microns thick) from adult male Hartley guinea pigs (600-800 g) were exposed to [14C]halothane (0.6-0.9 microCi, 1.0-1.7 mM) in 95% O2/5% CO2 for 1, 6 and 12 h. The slices were homogenized and subcellular fractions prepared. Proteins were resolved by electrophoresis and bound radioactivity was detected by scintillation counting and autoradiography. Greater than 80% of detectable radioactivity to whole liver cell protein was localized in the 20-30-kDa range and increased in a linear fashion over the 12-h incubation period. Covalent binding was localized to two proteins of 27 kDa and 26 kDa present in the cytosolic compartment. Purification followed by N-terminal amino acid sequence analysis of the 27-kDa protein has identified it to be homologous with glutathione-S-transferase b. This cytosolic protein appears to be the major target for trifluoroacetylation in liver slices exposed to halothane.

Amino Acid Sequence↗
PubMed1995

Isoflurane acts as an inhibitor of oxidative dehalogenation while acting as an accelerator of reductive dehalogenation of halothane in guinea pig liver microsomes.

The effects of isoflurane, 1-chloro-2,2,2-trifluoroethyl difluoromethyl ether, on the oxidative metabolism of halothane to produce trifluoroacetic acid (TFA) and on the reductive metabolism of halothane to produce chlorodifluoroethylene (CDE) and chlorotrifluoroethane (CTE) in liver microsomes of guinea pig were examined. Isoflurane enhanced the production of CDE and CTE and inhibited the production of TFA. Isoflurane enhanced cytochrome P450 reduction and formation of an intermediate complex with cytochrome P450 without enhancement of NADPH-cytochrome P450 reductase (EC 1.6.2.4) activity. We conclude that isoflurane interacts with cytochrome P450 to prevent the formation of the halothane-cytochrome P450 complex, causing inhibition of the oxidative dehalogenation. This interaction of isoflurane enhances the reduction of cytochrome P450 and the formation of a reductive intermediate-cytochrome P450 complex under anaerobic conditions causing reductive dehalogenation of halothane.

Anesthetics, Inhalation↗
PubMed1984

Fiber types and metabolic characteristics in muscles of wild boars, normal and halothane sensitive Swedish landrace pigs.

Muscle fiber characteristics, glycogen content and enzyme activities were studied in muscles of six Swedish landrace pigs, six wild boars and in three halothane sensitive landrace pigs. The wild boars have a higher proportion of type I and IIA fibers compared with Swedish landrace pigs. Fiber composition is similar in landrace pigs and halothane sensitive landrace pigs. The wild boars revealed the highest citrate synthase (CS) and 3-OH-acyl-CoA dehydrogenase (HAD) activities and the lowest glycogen content compared with the other two groups. Lower CS and HAD activities were observed in the halothane sensitive pigs compared with the other pigs. The data show that wild boars have a higher and halothane sensitive landrace pigs a lower aerobic capacity in skeletal muscles compared with Swedish landrace pigs.

Animal Population Groups↗
PubMed1992

The effect of halothane on cultured fibroblasts and neuroblastoma cells.

Halothane exposure over the cultured cells (100 and 1,000 ppm) caused a disruption of the pattern of actin distribution in both fibroblasts and neuroblastoma cells. Neuroblastoma cells exposed to halothane also lost microspikes; however, neurite elongation was not affected by halothane. The present study suggests that halothane induces the functional disruption of actin, resulting in an interference of normal neural development in vivo.

Actins↗
PubMed1993

Halothane acts on many potassium channels, including a minimal potassium channel.

There has been considerable controversy over whether general anesthetics act directly on membrane proteins, and if so, whether there are uniquely sensitive protein targets upon which they act. Here, we examine the actions of halothane on a diverse collection of voltage-gated potassium channels expressed in Xenopus oocytes, and find that they are all sensitive at clinically relevant concentrations. To investigate further the molecular basis of this commonality, human and rat minimal potassium (minK) channels, which have exceedingly short amino acid sequences, were examined. Current through these channels is reversibly reduced to 68% of control values by 0.5% (0.34 mM) halothane. A double deletion mutant of the 130-amino acid minK protein, in which 30 amino acids of the N-terminus, thought to be extracellular, and 37 amino acids of the putative intracellular C-terminus are deleted (resulting in a protein in which more than half of both the extracellular and intracellular domains have been removed) responds to low halothane concentrations similarly to the parent channel. While alternative explanations are possible, this result is consistent with a model whereby halothane interacts with the channel protein from within the lipid bilayer.

Animals↗
PubMed1988

Effects of Sarcocystis miescheriana infection on carcass quality and on the water-binding capacity of the meat of halothane-tested fattening pigs.

Ten halothane-positive pigs (stress sensitive, group A) and ten halothane-negative pigs (stress insensitive, Group C) with a mean body weight of 36 kg were each inoculated orally with 50,000 sporocysts of Sarcocystis miescheriana. Twelve halthane-positive pigs (Group B) and ten halothane-negative pigs (Group D) served as non-infected controls. Thirteen weeks post infection (p.i.) the lean: fat ratios of the pigs of the infected groups A and C were lower (A, 1:0.41 +/- 0.09; C, 1:0.50 +/- 0.10) than those of the pigs of the non-infected groups B and D (B, 1:0.50 +/- 0.08; D, 1:0.55 +/- 0.08). The back-fat thickness, the fat thickness 'A' and the fat thickness 'B' were thinner in infected pigs than in non-infected pigs. The difference in Lendenstärkespeckquotient (Loin Fat Thickness Quotient) (LSQ) between infected and non-infected pigs was not statistically significant. The values of the water-holding capacity were lower in infected pigs than in non-infected pigs, the difference being statistically significant only in the halothane-negative groups (C, 0.45 +/- 0.02; D, 0.48 +/- 0.04). The water-absorbing capacity was significantly higher in the infected groups (A, 5.92 +/- 3.99%; B, 2.26 +/- 1.08%; C, 8.96 +/- 2.90%; D, 4.97 +/- 2.51%). In conclusion, it can be said that there was a slight tendency towards a better carcass quality and a better water-binding capacity in infected pigs, although this was combined with reduced growth rates.

Absorption↗
PubMed1987

Modulation of the reductive metabolism of halothane by microsomal cytochrome b5 in rat liver.

To study the modulation of the reductive metabolism of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) by microsomal cytochrome b5, formation of 2-chloro-1,1,1-trifluoroethane (CTE) and 2-chloro-1,1-difluoroethylene (CDE), major reduced metabolites of halothane, was analyzed in vivo and in vitro. Rats were pretreated with both malotilate (diisopropyl-1,3-dithiol-2-ylidenemalonate) and sodium phenobarbital (malotilate-treated rats) or only with sodium phenobarbital (control rats). The microsomes of malotilate-treated rats had significantly more cytochrome b5 than the controls, whereas the cytochrome P-450 content was not different between the two groups. At the end of 2-h exposure to 1% halothane in 14% oxygen, the ratio of CDE to CTE in arterial blood was significantly higher in malotilate-treated rats than in the controls. Under anaerobic conditions, the formation of CDE and the ratio of CDE to CTE were significantly greater in microsomal preparations of malotilate-treated rats than those of the controls. In a reconstituted system containing cytochrome P-450PB purified from rabbit liver, addition of cytochrome b5 to the system enhanced the formation of CDE and increased the ratio of CDE to CTE. These results suggested that cytochrome b5 enhances the formation ratio of CDE to CTE by stimulating the supply of a second electron to cytochrome P-450, which might reduce radical reactions in the reductive metabolism of halothane.

Anaerobiosis↗
PubMed1991

Naloxone modifies the inotropic decrease induced by halothane on isolated left atria.

1. The present study evaluates the interaction between naloxone and halothane on the left atria. 2. Halothane produced significant decrease in auricular inotropism at concentrations ranging from 0.3 to 2.5 v/v%. 3. Naloxone modified the concentration response curve to halothane. The antagonism between both drugs is consistent with a competitive antagonism since the curve obtained had a slope which did not differ significantly from -1. 4. These results suggest that the negative inotropic effects induced by halothane could be mediated by opioid receptors.

Animals↗
PubMed1994

Influence of halothane and methoxyflurane on regional brain and spinal cord concentrations of methionine-enkephalin in the rat.

Rats were exposed to either oxygen (controls), 1.5% halothane in oxygen, or methoxyflurane (0.5%) in oxygen over a period of 2 h, then sacrificed at the end of exposure (2-h group), 4 h after removal from environmental chamber (4-h group), or at 24 h following anesthetic exposure (24-h group). Pituitary (excluding the neural lobe, Pit), brain, and spinal cord areas were isolated and processed with Met-enkephalin tissue concentrations determined. In halothane-exposed animals, Met-enkephalin concentrations in pit and across CNS areas studied were significantly lower at 2 h following anesthetic exposure than in control animals. Concentrations of Met-enkephalin in many areas of CNS and Pit of 4-h group approached control levels. Concentrations of Met-enkephalin in all areas studied except spinal cord returned to basal levels by 24 h following halothane exposure. Exposure to methoxyflurane resulted in less dramatic changes in Met-enkephalin concentrations across CNS regions examined. Exposure to methoxyflurane resulted in significant decreases in Met-enkephalin levels in olfactory bulb, thalamus, and hippocampus only. Met-Enkephalin levels did not change significantly in other areas of the central nervous system following methoxyflurane exposure. These results indicate that halothane and methoxyflurane may have differential effects on the endogenous opioid system.

Animals↗
PubMed1989

The actions of halothane on spontaneous activity, action potential shape and synaptic connections of the giant serotonin-containing neurone of Lymnaea stagnalis (L.).

1. Cerebral giant cells (CGCs) in the isolated central nervous system (CNS) of the pond snail Lymnaea stagnalis (L.) exhibit bursting activity when superfused with anaesthetic concentrations of halothane. 2. Calcium-dependent components of the CGC action potential appear more sensitive to halothane than do other ionic mechanisms. 3. Higher concentrations of halothane block the chemical synaptic connection between CGC and buccal motoneurone B1, but have no effect on the strong electrotonic coupling between the CGCs. 4. The mechanisms underlying CGC bursting and synaptic block in the presence of halothane are discussed.

Action Potentials↗
PubMed1988

The effect of arterial pressure alterations during halothane anesthesia on residual flow and infarct size with transient regional ischemia of the dog.

The present study was designed to determine if infarct size under halothane anesthesia could be reduced by increasing the pressure gradient across the collateral vascular bed, thereby increasing flow within the occluded vascular bed. Forty-nine mongrel dogs were anesthetized with halothane under identical physiologic conditions with the exception of systemic arterial blood pressure. The control group of 18 animals anesthetized with halothane was compared to two experimental groups. In one group of 15 dogs, the mean systemic pressure was raised 25% above control with phenylephrine (BP25). In the second group of 15 dogs, systemic pressure was raised 50% above control (BP50). Adjacent marginal branches of the left circumflex coronary artery were ligated for 90 minutes followed by 90 minutes of reflow. The area of the occluded vascular bed was similar in all groups, but the area of infarction as a percentage of the occluded vascular bed was reduced from 47.7 +/- 4.7% to 25.4 +/- 4.3% in the BP25 group (P < or = .05 v control) and to 33.1 +/- 5.0% in the BP50 group. Flow measurements using microspheres showed a larger zone of ischemic tissue receiving adequate residual flow in the BP25 and BP50 groups compared to the control. It is concluded that infarct size during halothane anesthesia in the dog can be reduced by increasing systemic blood pressure with phenylephrine.

Analysis of Variance↗
PubMed1990

Volatile anesthetics and regional myocardial perfusion in chronically instrumented dogs: halothane versus isoflurane in a single-vessel disease model with enhanced collateral development.

The influence of halothane and isoflurane on regional myocardial blood flow was investigated in chronically instrumented dogs with a well developed coronary collateral circulation. Dogs were implanted with an Ameroid constrictor on the left anterior descending (LAD) coronary artery to produce slowly progressive coronary artery occlusion and collateral development. Contractile function in the collateral-dependent region was ascertained periodically during brief balloon cuff occlusion or during atrial pacing to characterize the degree of ongoing collateral development. Following documentation of enhanced collateral perfusion by the lack of contractile dysfunction during brief balloon cuff occlusion or atrial pacing at 50 days postimplantation, dogs were anesthetized (inhalation induction) with halothane (1.5% or 2.5%; n = 7) or isoflurane (2.0% or 3.0%; n = 8) using equihypotensive inspired concentrations of either agent. Radioactive microspheres were administered to measure regional myocardial perfusion during the conscious state and at stable hemodynamic states during both low and high concentrations of each volatile anesthetic. Myocardial blood flow during anesthesia was also determined following the adjustment of arterial pressure and heart rate to conscious levels by administration of phenylephrine and atrial pacing, respectively. Over the course of collateral development, balloon cuff-induced contractile dysfunction and pacing-induced contractile dysfunction in the collateral-dependent zone were reduced, indicating extensive collateral development. Halothane and isoflurane decreased global and regional indices of contractility and arterial pressure in a dose-dependent manner, but only isoflurane reduced coronary vascular resistance. Both anesthetics decreased myocardial perfusion within normal and collateral-dependent regions; however, flow was restored to levels found in the conscious state coincidental with control of arterial pressure and heart rate. Neither anesthetic alone, nor with concomitant control of arterial pressure and heart rate, produced a maldistribution of blood flow transmurally or between normal and collateral-dependent zones. The results suggest that both halothane and isoflurane, although decreasing major determinants of myocardial oxygen demand, do not unfavorably alter the regional distribution of coronary blood flow in a single-vessel disease model with enhanced collateral development.

Anesthesia, Inhalation↗