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PubMed1985

Immunochemical evidence of trifluoroacetylated cytochrome P-450 in the liver of halothane-treated rats.

Four hours after the administration of halothane to phenobarbital-pretreated rats, subcellular fractions of liver were isolated and the proteins in the fractions were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, transferred to nitrocellulose sheets, and immunochemically stained with anti-trifluoroacetylated antibodies. The microsomal fraction contained the highest level of trifluoroacetylated adducts. Its major trifluoroacetylated component was immunochemically identified as a phenobarbital-inducible form of cytochrome P-450 (54 kDa), whereas the other observed trifluoroacetylated protein fraction (59 kDa) was not identified. The plasma membrane fraction also contained a 54-kDa trifluoroacetylated adduct, which was immunochemically related to the 54-kDa cytochrome P-450. Microsomes from untreated rats that were administered halothane contained only the 59-kDa trifluoroacetylated protein fraction. The specificity of the immunochemical staining for the bound oxidative metabolite of halothane was confirmed by the finding that rats treated with deuterated halothane had considerably less stained liver proteins than did those treated with halothane. These results suggest that the CF3COX oxidative metabolite of halothane is so reactive that it binds predominantly to the cytochrome P-450 that produced it.

Acetylation↗
PubMed1985

Arterial to end-tidal CO2 tension and alveolar dead space in halothane- or isoflurane-anesthetized ponies.

The correlation between end-tidal partial pressure of CO2 (PETCO2) and arterial (PaCO2) was determined for spontaneously breathing ponies under halothane or isoflurane anesthesia. The PETCO2 was useful as a trend indicator of PaCO2 during the first 60 minutes of halothane or isoflurane anesthesia when PaCO2 values were less than 60 to 70 mm of Hg. Halothane anesthesia lasting greater than 90 minutes was associated with PaCO2 values in excess of 60 to 70 mm of Hg, a large arterial- to end-tidal PCO2 difference (PaCO2-PETCO2) and a significant increase in alveolar dead space. These effects were not seen during the same period of isoflurane anesthesia. Arterial blood gas analysis is therefore recommended during halothane anesthesia when the PETCO2 is greater than 60 to 70 mm of Hg. A decrease in alveolar capillary perfusion relative to alveolar ventilation is the most likely cause for the increase in alveolar dead space during halothane anesthesia. Based on these findings, isoflurane may be superior to halothane for prolonged anesthesia of spontaneously breathing horses.

Anesthesia, General↗
PubMed1985

Reduction in halothane MAC: comparison of morphine and alfentanil.

The anesthetic potency and effectiveness of alfentanil and morphine were established by determining the effects of increasing drug doses on the alveolar anesthetic requirement of halothane to maintain a constant anesthetic (MAC) level. Six selected doses of alfentanil and four of morphine were administered to groups of mechanically ventilated rats anesthetized with halothane. Alfentanil was given as a loading dose followed by an intravenous infusion of 0.01-100 micrograms X kg-1 X min-1, and morphine was administered as a subcutaneous dose of 4-20 mg/kg. The reduction in halothane requirement after morphine was biphasic, with a rapid linear increase occurring up to an 8 mg/kg subcutaneous dose, followed by a further, slower reduction in halothane requirement after doses of 8-20 mg/kg. At a 20 mg/kg dose, the halothane MAC was reduced approximately 84%. With alfentanil, a curvilinear reduction in halothane MAC occurred up to an alfentanil dose of 15 micrograms X kg-1 X min-1, where a 48% reduction was found. Larger doses produced severe truncal, chest wall, and abdominal rigidity, precluding adequate ventilation and the determination of MAC.

Adjuvants, Anesthesia↗
PubMed1986

Failure of the platelet-halothane nucleotide depletion test as a diagnostic or screening test for malignant hyperthermia.

A platelet-halothane nucleotide or bioassay test has been suggested as an accurate means for diagnosis of malignant hyperthermia (MH). For the last three years we performed this test in all patients at risk for MH and in all normal control patients undergoing skeletal muscle biopsy in our diagnostic unit. The reliability of the platelet-halothane nucleotide test has been assessed on the basis of the presence or absence of a previous MH reaction and degree of relationship of relatives to those who have had reactions, and on the basis of caffeine-halothane contracture test values (positive or negative for MH). We have found no significant difference in platelet-halothane nucleotide test values in malignant hyperthermia susceptible (MHS) patients or relatives of MHS patients and normal controls, and no relationship between the nucleotide test and caffeine-halothane contracture test results. We conclude that the platelet-halothane nucleotide test is not of assistance in the diagnosis of or in the screening for MH.

Blood Platelets↗
PubMed1985

[Uptake and elimination of isoflurane and halothane by children and adults].

The rate of increase of alveolar concentrations (FA/FI) of isoflurane and halothane was studied in children and adults during general anaesthesia and controlled ventilation. After 30 min of body equilibrium, elimination curves of the volatile anaesthetics were determined by measurement of alveolar (FA/FA0; infrared technique) and venous concentrations (gas chromatography). The distribution and elimination half-times (t1/2 alpha, t1/2 beta), clearance (Cl), volume of central and peripheral compartment (V1, Vz) and the volume of distribution at steady state (Vss) were calculated from the intercepts and slopes of a two-compartment model. During the uptake of anaesthetic concentrations of isoflurane and halothane, the FA/FI ratio of each gas was found to rise significantly faster in children than in adults. The reason for the more rapid approach to equilibrium in children seems to be related to physiological differences. Irrespective of age, uptake of isoflurane was more rapid than that of halothane, as it is less soluble. Similarly, isoflurane was eliminated from the lung or blood faster than halothane. Moreover, anaesthetic wash-out in children differed from that in adults. In the paediatric age group t1/2 beta under isoflurane was shorter than in adults, whereas halothane excretion took longer in children. This could be accounted for by the larger volumes of distribution Vz and Vss in the young, due to higher organ affinity of halothane. From our data we conclude that age significantly affects uptake and elimination of volatile anaesthetics and the control of anaesthesia is easiest with isoflurane in paediatric patients.

Adult↗
PubMed1979

[The influence of ethanol, dithiocarb, diethylmaleate and phenobarbital on the metabolic elimination of halothane in rats (author's transl)].

Rats exposed to halothane (100 ppm) in a closed allglass-system eliminate halothane from the atmosphere of this system with a half-life (t0.5) of 0.99 h. In 24 h-fasted rats t0.5 was prolonged to 1.24 h. A single oral load of 4.8 g/kg ethanol as well as a 15% ethanol solution instead of drinking water for 28 days did not alter the metabolic elimination of halothane. On the other hand, ethanol (4.8 g/kg p.o.) applied 5 min before exposure to halothane markedly prolonged t0.5 to 3.79 h. Pretreatment with phenobarbital (80 mg/kg i.p. for 4 days) shortened t0.5 significantly to 0.79 h. Inhibition of the mixed-function oxidase system by dithiocarb (100 mg/kg i.p.) or diethyl maleate (1 ml/kg i.p.) markedly prolonged t0.5 to 7.53 and 1.57 h. respectively. The observed modifications of the halothane metabolism may be of interest in relation to the problem of halothane-induced hepatotoxicity.

Animals↗
PubMed1982

Effect of halothane on cardiac sarcoplasmic reticulum Ca2+-ATPase at low calcium concentrations.

The effect of halothane on cardiac sarcoplasmic reticulum Ca2+-ATPase activity was studied at low calcium concentrations (0.4-20 microM). Clinical concentrations of halothane (1%-3%, v/v) were found to depress Ca2+-ATPase activity more severely at lower calcium levels than at the higher calcium levels previously reported (greater than 0.1 mM). An increase in calcium concentration in the external medium of a preparation of isolated cardiac sarcoplasmic reticulum vesicles antagonized the halothane-induced depression of the Ca2+-ATPase activity. The depression of calcium-activated ATPase activity by halothane appears to take place by a competitive-type inhibition. The Ca2+-ATPase Vmax remained constant at 0.175 mumole/min/mg of protein with an increasing Km (0.47 microM-4.09 microM). Halothane depression of sarcoplasmic reticulum function may in part explain the ability of halothane to depress myocardial function.

Animals↗
PubMed1980

Effects of halothane on the cyclic 3',5'-adenosine monophosphate enzyme system in human platelets.

A study of the effects of halothane on the cyclic 3',5'-adenosine monophosphate (cAMP) system in human platelets was undertaken since cAMP has been implicated in the regulation of the process of platelet aggregation and this anesthetic has been reported to decrease platelet aggregation and, in other tissues, to increase adenylate cyclase activity. When exposed to halothane 0.5 to 10 vol%, adenylate cyclase activity was increased in the platelet preparation in a dose-dependent manner, reaching a maximum at 5 vol% (93% increase above basal activity). Platelet aggregation was also inhibited by halothane in a dose-dependent manner, with a maximum effect at about 5 vol% halothane (a decrease of 70%). Kinetic analysis of platelet cAMP-phosphodiesterase suggested two forms of activity, neither of which was altered by halothone. The results that the impairment of platelet aggregation observed with halothane may be brought about by the halothane-induced activation of platelet adenylate cyclase, which may result in a higher cAMP level, inhibiting platelet aggregation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Halothane effect on beta-adrenergic receptors in canine myocardium.

Halothane depresses the inotropic state of the heart, possibly by decreasing the rate of formation of cyclic 3',5'-adenosine monophosphate (cAMP) through depression of the activity of adenylate cyclase, the cAMP-generating enzyme. As catecholamines regulate the inotropic state and adenylate cyclase activity by binding to myocardial beta-adrenergic receptors, the effect of halothane on binding to these receptors was studied to determine whether this was a site of halothane effect. Beta-adrenergic binding was measured at binding equilibrium in vitro in a canine myocardial membrane preparation in the absence and presence of halothane, 3 to 5 vol%, using as the radioligand 3H-dihydroalprenolol (3H-DHA), a beta-adrenergic antagonist with high affinity and radioactivity. In addition, the effect of halothane on the binding of l-isoproterenol, a beta-adrenergic agonist, was measured by displacement of 3H-DHA. The results indicate that halothane has no effect on either the affinity of canine myocardial beta-adrenergic receptors for 3H-DHA or l-isoproterenol, nor does it alter the number of available receptors at binding equilibrium.

Adenylyl Cyclases↗
PubMed1984

Hemodynamic consequences of halothane anesthesia during chronic anemia.

The hemodynamic effects of halothane anesthesia in chronically anemic mongrel dogs were evaluated. Control and anemic animals (13.7 +/- 0.4 g/dl hemoglobin mean +/- SE vs. 3.4 +/- 0.3 g/dl) were exposed to 0.75, 1.5, and 2.25% inspired halothane and changes in cardiac output (CO), heart rate (HR), dp/dt, heart work, heart efficiency, myocardial oxygen consumption (MVO2), mean arterial blood pressure (MABP), central venous pressure (CVP), left ventricular end-diastolic pressure (LVDP), left coronary blood flow (CBF), systemic vascular resistance (SVR), and myocardial lactate metabolism were measured and compared. Anemic dogs showed a significantly lower SVR at each halothane dose when compared with controls. In addition, SVR progressively decreased with increasing halothane in anemic dogs, while SVR remained unchanged in controls. CO, CBF, MVO2, and heart work all were significantly greater in anemic canines compared with controls with each halothane concentration. Heart efficiency, dp/dt, HR, and MABP were not significantly different in anemic and control dogs. Neither control nor anemic dogs demonstrated myocardial hypoxia as evidenced by a lack of myocardial lactate production. The results from this study suggest that anemic animals appear to tolerate large concentrations of halothane.

Anemia↗
PubMed1984

Hemodynamic effects of halothane in the newborn piglet.

In order to better understand the mechanism of hypotension and bradycardia in newborn infants under halothane anesthesia, we studied the changes in the four determinants of cardiac output in newborn piglets given 0.5 and 1% end tidal halothane. Cardiac index (CI) was measured by thermodilution. Preload was estimated from the left ventricular diastolic dimension determined by echocardiography and from the left ventricular end-diastolic pressure. Total peripheral resistance index was calculated to assess afterload. Contractility was estimated from left ventricular peak dP/dT, and from left ventricular shortening fraction and mean rate of circumferential fiber shortening determined by echocardiography. All indices of contractility decreased to approximately 50% of baseline values during administration of 1% halothane, whereas heart rate (HR) was reduced to 74% of baseline. Preload and afterload did not change significantly. Mean arterial pressure (MAP) and CI decreased to 67% and 74% of control values, respectively. Smaller, proportional reductions in all variables occurred when 0.5% halothane was administered. Control values of MAP were the only measurements significantly related to piglet age. When five additional animals underwent atrial pacing at the control HR during 1% halothane anesthesia, MAP and CI decreased to 66 and 71% of control values, respectively. dP/dT/DP40, a dP/dT point measurement independent of preload and afterload changes, decreased to 49% of control during pacing. Therefore, the major effect of halothane in newborn piglets is its potent negative inotropic action, not peripheral vasodilation or bradycardia.

Aging↗
PubMed1977

Effects of halothane on ganglionic discharges.

The effects of halothane on ganglionic transmission were studied by recording extracellular potentials from the postganglionic nerve of the isolated hamster stellate ganglion. Halothane, at concentrations greater than 0.1 mM, decreased the potentials evoked by preganglionic stimuli at 0.2 Hz. Halothane also blocked discharges elicited by 1,1-dimethyl-4-phenylpiperazinium, a selective nicotinic agonist, and discharges elicited by the nicotinic actions of exogenous acetylcholine. Repetitive preganglionic stimulation (30 Hz, 5 seconds) in the presence of nicotine (10(-3) M), or hexamethonium (10(-3) M), evoked asynchronous discharges in the postganglionic nerve. These discharges were suppressed by low concentrations of atropine, and were probably due to the muscarinic actions of neurotransmitter. Halothane depressed these discharges at approximately the same concentration that it depressed the compound action potential elicited by low frequency preganglionic stimulation in the untreated ganglion. Halothane had no effect on the discharges elicited by 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343), a selective muscarinic agonist, or the discharges elicited by the muscarinic actions of acetylcholine. These results are most readily explained by hypothesizing that halothane acts at two sites in the ganglion. It appears to depress the postsynaptic response to the nicotinic actions of the neurotransmitter, acetylcholine. Also, it probably depresses transmitter release from the presynaptic nerve endings during repetitive stimulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1983

Halothane and halothane/succinylcholine induced malignant hyperthermia (porcine stress syndrome) in a population of Ontario boars.

This paper recounts a study of the prevalence of malignant hyperthermia in a population of boars entering the Record of Performance Test Station at New Hamburg, Ontario over a period of ten months. The literature is briefly reviewed and an account of the present status of malignant hyperthermia (porcine stress syndrome) in Ontario boars using the halothane or halothane/succinylcholine screening tests is presented. It was determined in this population of boars that there was a 1.5% prevalence rate of malignant hyperthermia susceptible boars. This was based on a five minute halothane challenge carried out on 786 boars from 107 herds. The halothane reactors came from a total of eight herds or 7.5% of the total number of herds. A majority of 58.3% of the animals reacted after the three minute mark of the halothane challenge. In contrast, an 18.0% prevalence rate was determined using halothane/succinylcholine challenge on 123 boars. This further identified an additional eight herds with the problem, bringing the total to 16 or 15% of the total number of herds. It is suggested that the prevalence of malignant hyperthermia in Ontario breeding herds is much higher than was originally thought and that the halothane challenge is an inadequate screening test for this trait if the intention is to remove the genetic trait from the breeding herd. At the same time halothane challenge testing will identify those animals which have a strong susceptibility to the trait and if used on key breeding stock will help to maintain some control on the condition until a more definitive test is readily available.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Halothane inhibition of canine myocardial adenylate cyclase--modulation by endogenous factors.

We have hypothesized that the halothane-induced depression of myocardial contractility can be explained, at least in part, by halothane's depression of adenylate cyclase, previously demonstrated in whole homogenates of myocardial tissue. Canine myocardial sarcolemmal membranes, which contain the adenylate cyclase of myocardial cells, were separated from other cellular constituents. Halothane did not depress catecholamine-stimulated adenylate cyclase activity in this preparation. Reconstitution of the sarcolemmal membrane preparation with a 100,000 X g adenylate cyclase-free supernatant restored the depressant effect of halothane on adenylate cyclase stimulated by guanosine triphosphate (GTP) 100 microM alone (-55%, P less than 0.01) or in combination with l-isoproterenol 1 microM (-38%, P less than 0.05) or 2.5 microM (-40%, P less than 0.01). Dilution of the supernatant to half-strength decreased the magnitude of the halothane-induced depression of adenylate cyclase activity to 19% (P less than 0.01); at one-quarter dilution, the effect was no longer significant. This study demonstrates the presence of endogenous modulators of the action of halothane on canine myocardial adenylate cyclase that can be reversibly separated from the adenylate cyclase complex.

Adenylyl Cyclase Inhibitors↗
PubMed1980

Halothane anesthesia and aqueous humor dynamics in laboratory animals.

Halothane anesthesia decreased intraocular pressure (IOP) by approximately 4 mm Hg in both normal rabbits and monkeys. The administration of nitrous oxide or 100% oxygen had no effect on IOP. Although PO2 and PCO2 increased following halothane administration in rabbits, similar blood changes occurred without IOP reduction in control rabbits receiving 100% oxygen. Outflow facility in both species as measured by tonography remained unchanged by halothane administration. Aqueous humor flow as estimated by tonography decreased by about 39% in rabbits and 31% in monkeys. Posterior chamber aqueous humor ascorbate was significantly elevated 90 min after halothane administration in rabbits. The ratio of the aqueous humor flow coefficient to diffusion coefficient for ascorbate (kfa/kdpa) was reduced approximately 47% following the administration of halothane. Halothane did not alter the in vitro accumulation of 131I-hippuran or 86Rb by rabbit ciliary body--iris preparations.

Anesthesia, Inhalation↗
PubMed1982

Hypoxia may be more important than reductive metabolism in halothane-induced hepatic injury.

To evaluate the relative importance of halothane metabolism and liver hypoxia in the occurrence of hepatic injury, the injury produced in hypoxic rats exposed to identical MAC hours of halothane but at various concentrations of halothane was compared. Groups of male Sprague-Dawley rats were pretreated with phenobarbital for 4 days, and 24 hours later they were exposed to 10 hours of 10% oxygen and concomitantly 0.2 MAC hours of halothane at the following anesthetic concentrations: 0.02% for 10 hours, 0.1% for 2 hours, 0.5% for 24 minutes, or 2.5% for 4.8 minutes. A control group received only 10% oxygen for 10 hours. Liver specimens taken 24 hours later demonstrated concentration-dependent damage; high concentrations given briefly produced more damage than lower concentrations given for long periods. As hepatic clearance of halothane by metabolism appears to be a saturable phenomenon, these results suggest that hypoxia per se may be more important than halothane metabolism in causing liver damage.

Animals↗
PubMed1980

Measurement of halothane by ultraviolet spectroscopy.

Halothane absorbs strongly in the ultraviolet region of the spectrum. This property has been employed to measure the concentration of halothane in samples in which the effect of halothane on enzyme kinetics was being studied. Halothane can be completely extracted into heptane, displays a concentration-dependent linear increase in absorbance over a broad concentration range, and has a molar extinction coefficient of 447 M cm-1 at 208 nm. The procedure described for the measurement of halothane will enable other investigators who do not have a gas chromatograph to measure the concentration of halothane.

Chromatography, Gas↗
PubMed1980

Halothane-induced suppression of cell-mediated immunity in normal and tumor-bearing C3Hf/He mice.

The present investigation was designed to demonstrate whether depression of cell-mediated immunity in tumor-bearing hosts is potentiated by halothane anesthesia. Both the in vivo and in vitro effects of halothane anesthesia on splenic lymphocytes from normal and tumor-bearing C3Hf/He mice were examined by lymphocyte transformation. The stimulation index (SI) of lymphocytes from normal C3Hf/He mice exposed to 1.5% halothane/98.5% oxygen anesthesia was significantly less than that of lymphocytes from normal C23Hf/He mice exposed to oxygen (SI of 25.3 and 33.6, respectively) (p < 0.001). Lymphocytes from tumor-bearing C3Hf/He mice demonstrated the greatest degree of immunosuppression by halothane when compared to those of normal (non-tumor-bearing) mice. That the tumor was the principal immunosuppressive factor was demonstraed by the SI of 34.6 for the non-tumor-bearing mouse lymphocytes and 4.1 for those of the mice with fibrosarcomas (p < 0.001). Lymphocytes from tumor-bearing hosts exposed to 1.5% halothane anesthesia demonstrated diminished lymphocyte transformation compared with those from control (tumor-bearing) mice exposed to oxygen (SI of 1.7 and 4.4, respectively) (p < 0.001). In both tumor-bearing and normal mice, there was a significant suppression of the cell-mediated immune response when the animals were exposed to halothane compared to exposure to oxygen. Results of this investigation demonstrate that halothane anesthesia potentiates the suppression of cell-mediated immunity observed in tumor-bearing hosts.

Animals↗