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PubMed1993

Halothane and the reperfusion injury in the intact animal model.

We studied the effect of halothane on regional myocardial function during acute ischemia and reperfusion in an open-chest pig model. Anesthesia was induced with thiopental and fentanyl and maintained with an intravenous (IV) infusion of pentobarbital and fentanyl. Regional myocardial function was studied with microsonometers placed in the subendocardium supplied by the left anterior descending coronary (LAD) and circumflex coronary artery (LX). Systolic function was evaluated with reference to the end-systolic pressure-length relationship (ESPLR) and regional systolic shortening. Diastolic dysfunction was studied with postsystolic shortening (PSS). Ischemia was induced with 15 min of total occlusion of the LAD artery, and thereafter reperfusion was allowed for 120 min. Five groups were studied: one group received only pentobarbital and fentanyl (n = 10); the other groups received halothane 0.2% (n = 5), 0.4% (n = 7), 0.6% (n = 5), and 0.8% (n = 5). The pentobarbital and fentanyl infusion was adjusted in the halothane groups in an effort to maintain arterial blood pressure and heart rate within specified limits (when possible). Results indicate that regional dysfunction during acute ischemia was equal among all the groups. However, on reperfusion, halothane significantly reduced the incidence of ventricular arrhythmias. Halothane (0.6% and 0.8%) was associated with less regional postischemic systolic dysfunction during reperfusion when compared to the other groups. Hearts subjected to 0.6% and 0.8% halothane also were less stiff at the end of systole (i.e., the extrapolated ventricular volume at zero ventricular pressure was less) after 120 min reperfusion compared to animals receiving less halothane. However, diastolic dysfunction was equal among the groups during reperfusion. We conclude that, in this model, administration of halothane is associated with improved recovery of regional systolic function and potentially beneficial pressure-length relations at the end of systole after acute severe myocardial ischemia and reperfusion. Furthermore, administration of halothane was associated with fewer reperfusion arrhythmias compared to animals not receiving halothane.

Animals↗
PubMed1994

Halothane and pertussis toxin-sensitive G proteins in airway smooth muscle.

We hypothesized that halothane-induced depression of airway smooth muscle (AWSM) contractility is caused, in part, by an effect on pertussis toxin-sensitive guanosine triphosphate (GTP)-binding regulatory proteins (G proteins). To determine the effect of G protein inactivation on the ability of halothane to relax AWSM, isolated strips of canine tracheal smooth muscle were contracted with the muscarinic agonist acetylcholine and relaxed by halothane (0.2 to 1.6 minimum alveolar anesthetic concentration [MAC]). Half of the strips were treated with pertussis toxin 10 micrograms/mL. Because a pertussis toxin-sensitive G protein mediates muscarinic inhibition of adenylyl cyclase, depression of G protein function by halothane might also enhance the relaxing effects of beta-adrenoreceptor agonists. To test this possibility, in another series of experiments, the effect of pretreatment with 1.6 MAC halothane on the ability of isoproterenol to relax strips contracted with acetylcholine was studied; the converse order of drug presentation was also performed. Treatment with pertussis toxin did not affect the ability of halothane to relax AWSM; 1.6 MAC halothane produced a 42% +/- 8% (mean +/- SD) and 38% +/- 8% decrease in force in treated and untreated strips, respectively. Exposure to 1.6 MAC halothane did not significantly affect the dose-response relationship between isoproterenol and force. Conversely, exposure to isoproterenol (0.036 +/- 0.033 micron) did not significantly affect the dose-response relationship between halothane and force. These results do not support the presence of a significant effect of halothane on the function of pertussis toxin-sensitive G proteins.

Acetylcholine↗
PubMed2003

5-HT3 receptors partially mediate halothane depression of spinal dorsal horn sensory neurons.

UNLABELLED: We recently reported that gamma-aminobutyric acid type A- and strychnine-sensitive glycine receptor systems partially mediate halothane depression of spinal dorsal horn low-threshold neurons. Serotonin subtype 3 (5-HT(3)) receptors belong to the same ligand-activated ion-channel family as gamma-aminobutyric acid type A- and strychnine-sensitive glycine receptors, so we examined the possible involvement of 5-HT receptor systems in halothane depression of spinal sensory neurons. Extracellular recordings of spinal low-threshold neurons were obtained in decerebrate, spinally transected rats. Receptive field size and brush-induced activity were recorded in the presence or absence of 5-HT antagonists and in the presence or absence of 1.1% (1 minimum alveolar anesthetic concentration) halothane. In the absence of halothane, antagonists had no effect on receptive field size or brush-induced activity. In the presence of halothane, methysergide, a nonselective 5-HT antagonist, and tropisetron, a selective 5-HT(3) antagonist, significantly reversed the halothane-induced reduction in receptive field size but did not alter halothane depression of brush-induced activity. Methiothepin, a 5-HT(1) antagonist, and ketanserin, a 5-HT(2) antagonist, did not reverse halothane depression. These results support the hypothesis that 5-HT(3) receptors partially mediate some inhibitory effects of halothane on spinal dorsal horn neurons. IMPLICATIONS: The results of this study support the hypothesis that halothane depression of spinal sensory neuronal responses to low-intensity stimuli is mediated, to a minor extent, by serotonin subtype 3 neurotransmitter systems.

Anesthetics, Inhalation↗
PubMed1977

Absorption, biotransformation, and storage of halothane.

Current knowledge of the quantitative aspects of biotransformation of halothane and the fate of its metabolites are reviewed. Absorbed quantities of the inhalation anesthetic average 12.7 and 18 g during 1 and 2 hr, respectively, of anesthesia. Reported fractions of halothane recovered as urinary metabolites range from 10 to 25%. An analysis of reports of bromide ion accumulation in plasma during and following anesthesia suggests that metabolism of halothane continues for 20-40 hr after exposure and that 22-24% of absorbed halothane is metabolized following 8 hr of anesthesia. Half-times for excretion of trifluoroacetic acid (TFA), a principal urinary metabolite of halothane, tend to confirm that biotransformation proceeds for 2 to 3 days following exposure. Other urinary metabolites which occur in small amounts include a dehydrofluorinated metabolite of halothane conjugated with L-cysteine and N-trifluoroacetyl-n-ethanolamine, both of which are evidence of the occurrence of reactive intermediates during the metabolism of halothane. Support for free radical formation has come from in vivo and in vitro demonstrations of stimulation of lipoperoxidation of polyenoic fatty acids by halothane. Irreversible binding of halothane metabolites to microsomal proteins and phospholipids has been shown to depend on the microsomal P-450 cytochrome system. Irreversible binding is increased by microsomal enzyme induction and by anaerobic conditions. Hypoxia increases irreversible binding to phospholipids, augments the release of inorganic fluoride and is followed by centrilobular hepatic necrosis. It is concluded that one-fourth to one-half of halothane undergoes biotransformation in man. One fraction is excreted as trifluoroacetic acid, chloride and bromide. A second fraction is irreversibly bound to hepatic proteins and lipids. Under anaerobic conditions fluoride is released, binding to phospholipids is increased, and hepatic necrosis may occur.

Anesthesia, Inhalation↗
PubMed2000

Effects of the combination of halothane and serotonin uptake blockers on synaptic transmission in the rat dentate gyrus in vitro.

Although the exact basis of their action remains unknown, volatile agents affect noradrenergic and serotoninergic systems. Imipramine and fluoxetine have documented effects on these neurotransmitter transmission systems. Given the common sites of action of these antidepressants and halothane, we examined their individual and combined effects on tonic excitatory post-synaptic potentials (EPSPs) and frequency dependent blockade in the rat dentate gyrus in vitro. Extracellular recordings of field EPSPs were maintained from the dentate gyrus, in the presence of picrotoxin (100 microM). Stimulation at 30 Hz (200 ms) allowed investigation of frequency dependent blockade. Once a stable equilibrium was established, halothane, imipramine and fluoxetine were administered via the perfusate and recordings were made. Halothane produced a dose dependent reduction in EPSP amplitude (EC50 0.28 mM; n = 12). Imipramine (1-10 microM) potentiated the EPSP amplitude (148.2 +/- 8.2%; imipramine 1 microM; n = 6). Fluoxetine (0.5-10 microM) reduced EPSP amplitude to 83.7 +/- 22.1% of control (n = 6). In the presence of halothane 0.2 mM, imipramine reduced the EPSP amplitude to 56.5 +/- 9.9% of control (imipramine 10 microM; n = 6; p < 0.05 compared with imipramine alone). Halothane (0.2 mM) demonstrated frequency dependent blockade. However, neither imipramine nor fluoxetine showed use dependent inhibition at the doses investigated. When combined with halothane 0.2 mM, fluoxetine 10 microM demonstrated frequency dependent blockade at the sixth pulse in the train compared with controls (13.8 +/- 4.7% vs 38.1 +/- 8.3%; n = 6; p < 0.05). The halothane-imipramine combination did not exhibit use dependent blockade greater than controls. The reversal of imipramine-induced EPSP potentiation by the preapplication of halothane has not been previously reported. It may be due to modulation of noradrenergic transmission by halothane. The frequency dependent blockade produced by the combination of fluoxetine 10 microM and halothane may be mediated by a nonspecific membrane effect on 5-HT uptake. These differing effects underline the broad action of volatile agents on synaptic mechanisms.

Anesthetics, Inhalation↗
PubMed1983

Further evidence on the inheritance of halothane reaction in pigs.

One thousand six hundred forty-one Pietrain, 163 Minnesota No. 1 and 158 Pietrain X Minnesota No. 1 crosses and their reciprocals were tested for porcine stress syndrome susceptibility using halothane gas between September 1975 and July 1981. The frequency of reactors in the Pietrain breed was 93.9%. Matings of reactor males to reactor females within the Pietrain breed resulted in 632 reactor and 14 nonreactor offspring. A boar, judged to be nonpenetrant on the basis of the halothane reaction of his parents and littermates, was shown by progeny test to be homozygous for the halothane allele. These data indicate that halothane sensitivity is due to a single autosomal recessive gene with a penetrance of about 98% and a frequency of .98 in this Pietrain herd. No halothane reactors were found in the 163 Minnesota No. 1 pigs tested. Only one Pietrain X Minnesota No. 1 gilt reacted positively to halothane and later, the same gilt produced both positive and negative offspring, indicating that she was most likely heterozygous. Blood group typing of 107 crossbred pigs provided insufficient information to predict accurately the halothane reaction, although some associations were observed between the A and H loci and halothane sensitivity. The time taken by Pietrain pigs to react to halothane was measured and recorded. Analysis of these data showed that progeny of some sires had significantly faster reaction times than others and that reaction time had decreased over the years. These results as well as other data presented here indicate the existence of certain modifier genes that influence halothane reaction.

Animals↗
PubMedDate not supplied

Suppressive effect of vitamin E on lipid peroxidation in halothane-administered guinea pig liver.

The effect of vitamin E on halothane-induced liver damage was studied in guinea pig halothane hepatitis. Twenty animals were divided into 3 groups, consisting of a control group, a halothane group and a vitamin E + halothane (H) group. The animals in the control group (n = 6) were allowed to inhale air only. The animals in the halothane group (n = 6) and the vitamin E + H group (n = 8) were allowed to inhale 1% halothane with air. Animals in the vitamin E + H group were additionally injected with 30 mg kg-1 of vitamin E 30 minutes prior to inhalation of halothane. Blood was aspirated from the heart immediately after sacrificing to measure the serum activity of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT). A microsomal suspension was prepared from the excised liver. Then the amount of thiobarbituric acid (TBA) reactive products in the microsomes were measured. The amount of tissue TBA-reactive products was increased by inhalation of halothane. The increase in the amount of TBA-reactive product was inhibited by the administration of vitamin E. The serum GPT activity was increased by halothane inhalation. Increased serum GOT and GPT activity were inhibited by the administration of vitamin E. These results demonstrated that vitamin E suppressed halothane-induced liver damage in the guinea pig by inhibiting lipid peroxidation.

Alanine Transaminase↗
PubMed1989

[Halothane anesthesia of several hours' duration in swine of the German Landrace breed, selected for resistance to malignant hyperthermia].

The malignant hyperthermia syndrome is widely spread in pigs of the German Landrace. This has precluded the use of halothane anesthesia. The advent of homozygous halothane-negative strains stimulated us to test whether such animals were suitable for longduration halothane anesthesia. Nine sows of the German Landrace (n = 4, homozygous halothane-positive (H+); n = 5, homozygous halothane-negative (-)) were used. Anesthesia was induced by Azaperon/Metomidat-HCL followed by intubation and exposure to halothane. All 4 halothane-positive animals died within 45-90 min following the onset of halothane administration, while all 5 halothane-negative animals survived a 4-5 h deep anesthesia without problems. Thus, homozygous hylothane-positive strains of German Landrace pigs may be surgically anesthetized for long durations with halothane anesthesia.

Anesthesia↗
PubMed1985

Prolonged hyporesponsiveness of vascular smooth muscle contraction after halothane anesthesia in rabbits.

Halothane diminishes smooth muscle contractility in vascular tissue. In order to further characterize this phenomenon we undertook a series of in vivo and ex vivo experiments. Pressor dose-response curves to the selective alpha 1-adrenergic agonist, phenylephrine, were constructed in groups of rabbits before, during and 2 hr after halothane anesthesia and the dose of phenylephrine that induced a 25 torr increase in mean arterial pressure (ED25) was derived by polynomial regression analysis. ED25 torr increased significantly during halothane anesthesia, and rabbits remained in this insensitive state when the ED25 was assessed 2 hr after anesthesia. The halothane-induced loss of responsiveness was corroborated by ex vivo experiments utilizing aortic rings from halothane-anesthetized rabbits. The maximal contraction to norepinephrine (NE) was significantly lower in halothane-treated aortic rings and only slowly returned to normal by 4 hr. The EC50 (the dose causing a 50% maximal contraction) for NE was significantly greater in aortic rings from halothane-anesthetized rabbits. This loss of sensitivity, reflected by the higher EC50 was not restored by 4 hr of ex vivo incubation in a halothane-free medium. We conclude that halothane induces loss of sensitivity to adrenergic agonists that persists for several hours after termination of the halothane anesthetic.

Anesthesia↗
PubMed1987

A randomized prospective controlled study of the metabolism and hepatotoxicity of halothane in humans.

In a randomized prospective controlled study in humans, the metabolism and hepatic effects of a single administration of halothane were compared with enflurane and meperidine. Pre- and postoperative antipyrine pharmacokinetics, intraoperative indocyanine green clearance, liver histology, and postoperative liver function tests were determined in 24 patients undergoing abdominal surgery who were randomly allocated to receive either halothane (0.5%, group I), enflurane (0.8%, group II), or meperidine (group III) as a supplement to a common basal anesthetic regimen consisting of thiopental, nitrous oxide/oxygen/muscle relaxant. In addition, end-tidal concentrations of the volatile reductive metabolites of halothane, chlorodifluoroethylene (CDF), and chlorotrifluoroethane (CTF) were determined in group I patients and serum and urinary inorganic fluoride were determined in both group I and II patients. Indocyanine green clearance was measured before anesthesia (stage I), during basal anesthesia (stage II), in the presence of surgical stimuli (stage III), and after introduction of the selected anesthetic agent (stage IV). CDF and CTF were detectable within 20 min of the start of halothane anesthesia in every patient receiving halothane. Peak serum fluoride concentrations occurred at 2 and 24 hr in the enflurane and halothane groups, respectively, whereas urinary fluoride excretion was elevated postanesthesia in the enflurane group only. There was no difference between the pre- and postoperative disposition of antipyrine in group II or III, but after anesthesia, antipyrine clearance was significantly decreased (P less than 0.02) and plasma half-life increased (P less than 0.05) in group I patients (halothane). Concentrations of serum alanine aminotransferase (ALT) and bilirubin were significantly elevated (P less than 0.5) postoperatively in groups I and II but unchanged from preoperative values in group III patients. Three of the 24 liver biopsies taken at the end of stage IV showed several foci of acute liver cell necrosis; of these, two patients were from group I and one from group II. There were no significant differences in liver cell morphology (P greater than 0.5) in biopsies taken at the end of stage IV compared with biopsies at the end of stage III, from groups I and II. The results of this study show that reductive metabolism of halothane occurs routinely in patients undergoing halothane anesthesia under conditions of normoxia. This may be the cause of the changes in antipyrine clearance after halothane anesthesia.

Antipyrine↗
PubMed1987

Porcine malignant hyperthermia: false negatives in the halothane test.

Purebred Pietrain pigs presumed (on the basis of pedigree) to be homozygous for malignant hyperthermia (MH) susceptibility were subjected to a 3% halothane challenge test. A few (6%) pigs that should have been MH susceptible on the basis of parental genotype did not develop muscle rigidity in response to repeated halothane tests. Three of these animals were brought into the laboratory, and muscle biopsy specimens were obtained for in vitro analysis. Bundles of intact muscle cells dissected from biopsy specimens were electrically stimulated, and mechanical responses were monitored during exposure to halothane. In all instances, the muscle bundles from the halothane-negative (ie, not sensitive to halothane), but genetically susceptible, pigs gave in vitro responses that were similar of those of halothane-positive MH-susceptible pigs in that tetanic tension was depressed, tetanus relaxation was slowed, and small contractures were produced upon halothane exposure. Thus, the presence of a halothane-sensitive abnormality in the skeletal muscles, in and of itself, is not always sufficient for development of in vivo muscle rigidity during a brief halothane test. Furthermore, when the halothane testing of pigs is conducted by recommended techniques, false negatives still occur in a small percentage of the genetically MH-susceptible animals.

Animals↗
PubMed1985

Immunological studies on the mechanism of halothane-induced hepatotoxicity: immunohistochemical evidence of trifluoroacetylated hepatocytes.

The fulminant hepatotoxicity caused by halothane has been thought to have an immunological basis because this toxicity occurs most often after repeated administration of halothane and because sera from patients recovering from severe halothane hepatotoxicity contain antibodies that bind to the surface membranes of hepatocytes of rabbits treated with halothane. In order to determine whether the major reactive metabolite of halothane, trifluoroacetyl halide, covalently binds to hepatocytes, we have developed specific and sensitive peroxidase enzyme-linked immunosorbent assays and an indirect immunofluorescence staining method for identifying trifluoroacetylated (TFA)-hepatocytes. Liver sections prepared from rats at 4 hr after halothane administration were stained preferentially in the centrilobular region with anti-TFA serum whereas livers of control rats showed no staining. The specificity of the assay for the TFA group was confirmed by the complete inhibition of the staining with 200 microM N-epsilon-TFA-L-lysine in the diluted antiserum. On the other hand, 2 mM halothane or L-lysine did not inhibit this staining. Moreover, treatment of rats with deuterated halothane resulted in significantly less staining than did halothane. At 24 hr after halothane administration, hepatocytes isolated and stained by indirect immunofluorescence showed a linear and granular pattern on their surface membranes. These results indicate that trifluoroacetyl halide either reacts directly with constituents of the plasma membranes or with other cellular components which become incorporated into the plasma membranes.

Animals↗
PubMed1985

Transient inhibitory effect of isoflurane upon oxidative halothane metabolism.

The duration of inhibition of halothane oxidative metabolism by isoflurane was studied in rats exposed for 2 hr to an anesthetic concentration of isoflurane (0.6% inspired), followed by a 2-hr exposure to a subanesthetic concentration of halothane (0.06% inspired), starting either 0.5, 4, or 24 hr after the end of the isoflurane exposure. Other rats were exposed to halothane, isoflurane, or a mixture of both. Tissue levels of total nonvolatile fluorine were used as a measure of oxidative metabolism of halothane and hepatic levels of 1,1,1-trifluoro-2-chloroethane and 1,1-difluoro-2-chloroethylene as a measure of reductive metabolism of halothane. Isoflurane administered simultaneously with or 30 min prior to halothane significantly inhibited oxidative metabolism of halothane, but this inhibition was transient and was no longer apparent when halothane was administered 4 or 24 hr after the end of isoflurane anesthesia. The reductive metabolism of halothane was unaffected. This study suggests that isoflurane may transiently modify the action of some drugs administered during the perianesthesia period by inhibiting their oxidative metabolism. Differences in elimination kinetics of nonvolatile fluorine-containing metabolites after isoflurane and halothane exposure suggest the presence of an unidentified isoflurane metabolite.

Animals↗
PubMed1981

["Hepatitis" following halothane-anesthesia (author's transl)].

"Hepatitis" following halothane-anesthesia is a rare complication, occurring once after about 2500 halothane-anaesthesias. The mortality is estimated to be 20-25%. The disease can be diagnosed by exclusion of other causes only. The differential diagnosis of postoperative jaundice is therefore briefly reviewed. Three hypotheses of possible pathogenic mechanisms are discussed, namely the theory of toxic products of the metabolism of halothane, the theory of delayed hypersensitivity to a metabolite and the theory of coincidence with preexisting unknown liver disease. None of these theories has been proved definitely. The use of halothane is contraindicated if a patient suffered from unexplained pyrexia and jaundice after a previous exposure to halothane. Gamma radiation decomposes halothane to hexachlorofluorobutene, a know hepatotoxin. The repeated use of halothane during irradiation therapy is therefore contraindicated. The risk of "hepatitis" after halothane anaesthesia increases if the patient is exposed to halothane twice within four weeks, especially if he is obese and older than 40 years. The risks and advantages of repeated halothane exposures have to be weighed against the risks of alternative techniques. The increased mortality after repeated anaesthesias within short periods of time, irrespective of the technique used, has to be considered.

Adult↗
PubMed1995

[Effect of halothane on the energy metabolism of isolated perfused rat kidney as analysed by 31P-NMR].

The effects of halothane on energy metabolism of isolated perfused rat kidney were studied by 31P-NMR spectroscopy. Rat kidney was perfused by physiological medium containing halothane. Perfusion was carried out continuously in addition to ischemic period of 30 or 10 minutes. In continuous perfusion study, halothane concentration below 4% did not affect renal ATP level but halothane above 6% decreased ATP level significantly. In ischemic study, changes of renal energy metabolism were not influenced by halothane below 4% throughout the experiment, but halothane above 6% decreased ATP levels significantly after reperfusion. From the viewpoint of energy metabolism, it can be said that a low concentration of halothane does not damage renal cells but a high concentration of halothane has possibility to damage them. During and after ischemic insult, halothane does not diminish renal damage, but on the contrary a high concentration of halothane reversely worsens it.

Adenosine Triphosphate↗
PubMed1993

Potassium channel blockade and halothane vasodilation in conducting and resistance coronary arteries.

On the basis of reports that volatile anesthetics, such as halothane, open membrane potassium channels in several tissues, it was investigated whether coronary vasodilation by halothane is mediated by a similar mechanism. The ability of glyburide, a blocker of ATP-sensitive K+ (KATP) channels, and tetraethylammonium (TEA+), a blocker of Ca(2+)-activated K+ channels, to modify halothane-induced vasodilation was assessed in two vascular preparations. First, coronary resistance vessel tone was measured in isolated rat hearts arrested with tetrodotoxin and, second, conducting vessel responsiveness was evaluated in ring segments of the porcine epicardial coronary artery contracted with prostaglandin F2 alpha. Halothane alone markedly vasodilated the perfused hearts and attenuated the agonist contraction of the coronary rings. Blockade of KATP channels with glyburide alone did not affect the base-line vascular tone or responsiveness but it inhibited cromakalim vasodilation. TEA+ alone caused vasoconstriction. In hearts perfused at constant pressure, glyburide significantly attenuated the halothane-induced increase in coronary flow by 56% and perfusion with a high K+ buffer reduced the halothane-induced vasodilation response by 94%. In endothelium-denuded coronary rings, glyburide did not affect halothane-induced relaxation but KATP channel blockade potentiated halothane-caused relaxation in endothelium-intact rings. The attenuation of halothane-induced vasodilation by TEA+ seen in the perfused hearts did not achieve statistical significance and no halothane/TEA+ interaction was evident in the coronary rings. Thus, the data from the perfused heart experiments suggest that halothane relaxes rat coronary resistance vessels, in part, by opening K+ channels.

Animals↗
PubMed1993

Halothane anesthesia is neuroprotective in experimental spinal cord injury: early hemodynamic mechanisms of action.

The neuroprotective potential of halothane anesthesia was explored in a weight-drop model of spinal trauma in the rat (N = 252). In initial experiments, animals were subjected to 25, 50 or 100 g cm impact injuries at T10 during pentobarbital or halothane anesthesia and their outcomes determined using somatosensory-evoked potentials, blinded neurologic evaluations for two weeks, and post-mortem analysis of spinal serotonin levels. Subsequently, halothane anesthesia was combined with either pentobarbital or nitrous oxide or given as a late treatment to pentobarbital anesthetized rats subjected to 50 g cm injuries. A series of acute studies were then performed in order to assess the hemodynamic and respiratory concomitants of halothane vs. pentobarbital, as well as the effect of mechanical ventilation and bicarbonate treatment upon halothane neuroprotection. Finally, the effect of a 50 g cm impact upon local white matter spinal cord blood flow was measured during halothane or pentobarbital anesthesia using laser-Doppler flowmetry. Results demonstrate an active neuroprotective action for halothane anesthesia that is not altered by the presence of other anesthetics and is most prominent at severe injury levels. The data suggest the importance of immediate injury responses in this action. Late halothane treatment was ineffective when given as early as 10 minutes postinjury while both the electrophysiological and hemodynamic effects of halothane vs. pentobarbital were apparent during this 10 minute period. Thus, halothane was associated with the prevention of spinal ischemia during the first 10 minutes after trauma in comparison to pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1996

Halothane constricts bovine pulmonary arteries by release of intracellular calcium.

In the canine lung, when compared with the conscious state, halothane causes vasoconstriction that is independent of blood flow. However, traditionally inhalational anesthetics have been shown to attenuate hypoxic pulmonary vasoconstriction and have therefore been considered pulmonary vasodilators. We have shown, in isolated bovine pulmonary artery, that halothane produces a transient contractile response. A variety of smooth muscle cellular mechanisms could be responsible for the vasoconstriction produced by halothane. The purpose of this study was to test the hypothesis that the halothane-induced contraction was caused by the release of sarcoplasmic reticular Ca++. Isometric tension was measured in isolated rings of bovine pulmonary artery with intact endothelium. Three protocols were followed. Rings were exposed to cyclopiazonic acid or ryanodine (modulators of sarcoplasmic reticular Ca++) (protocol 1), caffeine (protocol 2) verapamil or nicardipine (protocol 3). Halothane-induced contraction was measured before, during and after exposure to drug. In nominally Ca(++)-free buffer cyclopiazonic acid and ryanodine attenuated the halothane-induced contraction. Similar responses were seen with cyclopiazonic acid and ryanodine treatment when caffeine was substituted for halothane. The calcium channel blockers nicardipine and verapamil did not significantly alter the halothane-induced contraction. Our data in bovine pulmonary artery segments are consistent with halothane effects seen in vascular smooth muscle from several other tissues and species. The results of our experiments support the conclusion that the release of intracellular Ca++ from sarcoplasmic reticular stores is responsible for the halothane-induced vasoconstriction that has been observed in this tissue.

Anesthetics, Inhalation↗