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PubMed1990

Halothane anaesthesia does not modify the cardiovascular response to phenylephrine in man.

Conflicting results exist regarding the ability of halothane to alter the vascular response to alpha 1 adrenergic agonists in animals. Because data from humans are lacking, we studied the haemodynamic response to phenylephrine (PHE) in eight patients about to undergo coronary artery bypass surgery before and during halothane anaesthesia. After obtaining baseline measurements in patients while awake, the responses to PHE infusion at 30, 40, and 50 micrograms.min-1 were determined. New baseline measurements were made following stabilisation during anaesthesia with halothane, one per cent inspired in oxygen, prior to surgical incision. Then the responses to identical PHE doses were measured again. Halothane did not influence the cardiovascular response to PHE: there was no dose-response shift for any cardiovascular variable. No arrhythmias or signs of ischaemia were observed. We conclude that one per cent halothane anaesthesia does not attenuate PHE-induced vasoconstriction in man.

Anesthesia, Inhalation↗
PubMed1980

Porcine malignant hyperthermia--failure of dantrolene dose response to diagnose susceptibility (halothane effect).

Dantrolene, a skeletal muscle relaxant, has been proven prophylactic and therapeutic for malignant hyperthermia (MH) in swine. This study examined the feasibility of using a dantrolene dose response as measured by indirectly evoked foretoe twitch depression as a means to safely discriminate MH susceptibility in swine. The effect of halothane on the dantrolene response was quantified. Subjects were five Poland China malignant hyperthermia susceptible (MHS) and five Hampshire malignant hyperthermia resistant (MHR) swine. Dantrolene dose response was determined twice in each anaesthetized subject, once with thiopentone and subsequently with thiopentone and halothane. Dantrolene in incremental doses, 0.15 mg.kg-1, was given to a cumulative dose of 2--3 mg.kg-1. Under thiopentone anaesthesia, the dantrolene dose responses were similar in MHS and MHR animals. The presence of halothane augmented dantrolene twitch depression in MHS but not MHR animals when compared to their response under thiopentone. Under halothane, the MHS animals had significantly augmented dantrolene response compared to MHR pigs, but three MHS animals had developed the MH syndrome prior to receiving dantrolene. We conclude that dantrolene muscle relaxant dose response cannot be used as a diagnostic test for MHS in swine. Halothane augments dantrolene twitch depression in MHS swine.

Animals↗
PubMed1994

Absence of anti-trifluoroacetate antibody after halothane anaesthesia in patients exhibiting no or mild liver damage.

It has been shown that the circulating antibodies, which bind to rat hepatic microsomal proteins obtained after in vivo exposure to halothane, are detectable by immunoblotting in patients with "halothane hepatitis (HH)," and that rabbit immunized anti-sera against trifluoroacetylated rabbit serum albumin (TFA-RSA) recognizes rat microsomal distorted polypeptides in almost the same way as do sera from patients with HH. In this paper, we report first the development of a novel method of synthesizing TFA-RSA using p-nitrophenyl TFA, and second the results of tests for circulating anti-TFA antibodies in the serum of 86 patients who had received halothane anaesthesia and developed no (67 patients) or mild (19 patients, the maximum activity of serum alanine aminotransaminase 519 IU.L-1) liver damage. Serum was selected from stored sera of post-transfusion patients. The new method of synthesizing TFA-RSA was convenient and was able to be done at neutral pH. Rabbit sera obtained after immunization with the newly synthesized TFA-RSA recognized the same polypeptides (109 kDa, 92 kDa, 80 kDa, 76 kDa, 64 kDa and 59 kDa) as the established anti-sera against TFA-RSA, and these reactions were inhibited in the presence of TFA-lysine. Circulating antibodies were not detected in our patients who had developed no or mild liver damage. The present finding supports the hypothesis that the appearance of circulating antibodies against microsomal distorted proteins are specific to patients with HH. Furthermore, we have shown here that the halothane-induced mild increase in ALT activity is not associated with the appearance of those circulating antibodies, supporting the pathophysiological difference between HH and halothane-induced mild hepatic damage.

Adolescent↗
PubMed1987

Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone.

The effects of using nitrous oxide (N2O) with halothane or pentobarbitone anaesthesia on the filtration of venous air emboli (VAE) by the pulmonary circulation were studied in dogs. Dogs anaesthetized with either pentobarbitone, pentobarbitone/N2O, halothane, or halothane/N2O were embolized with venous air into the right atrium at 0.25 to 0.35 ml.kg-1.min-1 for 30 min. The animals were in a supine, head down position. A Doppler ultrasonic probe located over the suprarenal aorta detected arterial bubbles that escaped filtration by the lungs. No bubbles were detected at 0.25 ml.kg-1.min-1, but at 0.30 ml.kg-1.min-1 the incidence was 11 per cent (pentobarbitone), 0 per cent (pentobarbitone/N2O), 33 per cent (halothane), and 63 per cent (halothane/N2O) and at 0.35 ml.kg-1.min-1, 44 per cent (pentobarbitone), 14 per cent (pentobarbitone/N2O), and 56 per cent (halothane). Half of the dogs receiving VAE with halothane/N2O at 0.30 ml.kg-1.min-1 died within the first 10 min of the air infusion. Thus, no animals were studied at the next higher dose (0.35 ml.kg-1.min-1). The results suggest that the occurrence of VAE with nitrous oxide anaesthesia may result in greater haemodynamic consequence and increased likelihood for spillover of the venous bubbles into the arteries if used with halothane as compared to pentobarbitone.

Anesthesia, Inhalation↗
PubMed1995

Mivacurium-induced neuromuscular blockade during sevoflurane and halothane anaesthesia in children.

The neuromuscular blocking effects of mivacurium during sevoflurane or halothane anaesthesia was studied in 38 paediatric patients aged 1-12 yr. All received premedication with midazolam, 0.5 mg.kg-1 po and an inhalational induction with up to 3 MAC of either agent in 70% N2O and O2. The ulnar nerve was stimulated at the wrist by a train-of-four stimulus every ten seconds and the force of adduction of the thumb recorded with a Myotrace force transducer. Anaesthesia was maintained with a one MAC end-tidal equivalent of either volatile agent for five minutes before patients received mivacurium (0.2 mg.kg-1) iv. The onset of maximal blockade occurred in 2.4 +/- 1.26 (mean +/- SD) min with halothane and 1.8 +/- 0.54 min with sevoflurane (NS). Four patients failed to achieve 100% block (3 halothane, 1 sevoflurane). The times from injection to 5, 75, and 95% recovery during sevoflurane (9.8 +/- 2.6, 19.5 +/- 4.4, and 24.2 +/- 4.8 min) were greater than during halothane anaesthesia (7.2 +/- 2.2, 15.0 +/- 4.0, 19.2 +/- 4.9 min, respectively (P < 0.005). All patients demonstrated complete spontaneous recovery of neuromuscular function (T1 > 95%, T4/T1 > 75%) during the surgery which lasted 24-63 min. All patients showed clinical signs of full recovery of neuromuscular blockade (i.e., headlift, gag, or cough). Pharmacological reversal was not required. It is concluded that following a single intubating dose of mivacurium, the time to maximum relaxation was not different during halothane and sevoflurane anaesthesia; recovery times to 5, 75 and 95% twitch height were longer during sevoflurane anaesthesia and neuromuscular reversal was not necessary.

Anesthesia Recovery Period↗
PubMed1994

Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta.

In a previous study, we demonstrated that halothane and isoflurane inhibit binding of thromboxane A2 to its receptors on human platelets and thus inhibit prostanoid-induced aggregation strongly. The aim of this study was to determine whether volatile anaesthetics inhibit prostanoid-induced vasoconstriction preferentially. Rat isolated aortic rings were mounted in organ baths and their isometric tension was measured. They were contracted with STA2 (a stable thromboxane A2 analogue), prostaglandin F2 alpha (PGF2 alpha), phenylephrine, and 20 mM KCl, and then exposed to halothane (0.5-3%), isoflurane (0.5-3%), and sodium nitroprusside (SNP, 10(-9)-3 x 10(-7) M). Halothane (2-3%) and isoflurane (2-3%) induced greater relaxation of aortic rings precontracted with STA2 and PGF2 alpha than of those precontracted with phenylephrine (P < 0.01). Halothane induced greater relaxation of rings precontracted with KCl than phenylephrine only at 3%, whereas isoflurance relaxed rings precontracted with KCl more than those with phenylephrine at 0.5, 2 and 3% (P < 0.05). In contrast, SNP relaxed rings precontracted with PGF2 alpha. KCl and phenylephrine equally, but induced smaller relaxations of those precontracted with STA2 (P < 0.05). We conclude that halothane and isoflurane inhibit prostanoid-induced vasoconstriction preferentially, possibly by interacting with prostanoid receptors.

Acetylcholine↗
PubMed1999

Immune response in infants undergoing application of cast: comparison of halothane and balanced anesthesia.

PURPOSE: To study the immunological effects of two types of anesthesia on the immune response in infants during a minimally stressful surgical procedure. METHODS: The effects of inhalational halothane (halothane + N2O + O2, spontaneous breathing, n = 12) and conventional balanced anesthesia (thiopental + N2O + O2 + fentanyl + vecuronium, mechanical ventilation, n = 12) on immune function were measured in a crossover study in 12 infants undergoing application of casts to the lower extremity or hip joint. Leukocyte and differential counts, lymphocyte subpopulations, spontaneous lymphocyte proliferative responses as well as responses to phytohemagglutinin (PHA), concavalin A (ConA) and pokeweed mitogen (PWM), and serum cortisol concentration were measured before, immediately after and four hours after the end of anesthesia. RESULTS: Halothane anesthesia was associated with a higher percentage of T helper cells than conventional balanced anesthesia [47.1+/-1.8 (SEM)%, 48.1+/-2.3% and 50.7+/-1.9% before, immediately and four hours after anesthesia vs. 45.7+/-1.7%, 44.0+/-2.3% and 45.1+/-1.9%, respectively, by groups, P<0.05]. Leukocyte count and the percentages of activated T cells, natural killer cells and B cells showed similar alterations in both groups, and no alterations were observed in the percentages of T lymphocytes or T cytotoxic cells. Lymphocyte transformation response to PWM was decreased four hours after anesthesia in the halothane but not in the balanced anesthesia group. CONCLUSION: Anesthesia of short duration during minimal surgical stress alters lymphocyte subpopulations and lymphoproliferative responses in infants and, furthermore, halothane anesthesia and balanced anesthesia have different effects.

Anesthesia↗
PubMed1997

Halothane inhibition of acetylcholine-induced relaxation in rat mesenteric artery and aorta.

PURPOSE: The effect of halothane was compared on acetylcholine (ACh)-induced relaxation of the mesenteric artery and the aorta in rats. METHODS: The responses of isolated rat aortic and mesenteric arterial ring segments precontracted with phenylephrine to ACh (10(-8)-10(-5) M), in the presence of halothane 0-3%, were compared using isometric force tension recordings. Effects of NG-nitro-l-arginine (L-NOARG, 3 x 10(-5), methylene blue (MB, 5 x 10(-6) M), oxyhaemoglobin in (OxyHB, 10(-7) M), and various potassium channel inhibitors; tetraethylammonium (TEA, 10(-5) M, 10(-3) M), apamin (AP, 10(-7) M), charybdotoxin (ChTx, 10(-7) M) and glibenclamide (GC, 10(-5) M) on ACh-induced relaxation in mesenteric artery were tested. Using radioimmunoassay, ACh (10(-6) M)-induced guanosine 3':5'-cyclic monophosphate (cGMP) accumulation of mesenteric arterial rings pretreated with L-NAORG were also measured. RESULTS: L-NOARG partially inhibited ACh-induced relaxation in mesenteric arterial rings (P < 0.05, maximum relaxation reduced by approximately 50%), whereas it abolished them in aortic rings. The remaining relaxation resistant to L-NOARG in mesenteric arterial rings was insensitive to additional MB or OxyHB, and was not accompanied by increases in cGMP contents of rings. Halothane inhibited endothelium-dependent relaxation in aorta and mesenteric arterial rings. This inhibitory effect was larger in aorta. Halothane also inhibited NO independent EDHF-dependent relaxation in the mesenteric arterial rings, CONCLUSION: Despite a similar inhibitory effect on the EDHF relaxing pathway, halothane has a larger effect on endothelium-dependent relaxation in the aorta (NO dependent mainly) than in the mesenteric rings (NO and EDHF dependent).

Acetylcholine↗
PubMed1997

Halothane and isoflurane enhance melanoma tumour metastasis in mice.

PURPOSE: To investigate the incidence of tumour metastasis from B16 melanoma tumour cells in experimental animals following exposure to equipotent concentrations of halothane or isoflurane, and to differentiate if exposure to one anaesthetic resulted in greater metastases than the other. METHODS: Experimental animals (C57B1 mice), were randomized to receive 1.3 MAC hours of halothane or isoflurane anaesthesia. The control group of animals received oxygen alone under identical conditions. Fifteen minutes after completion of anaesthesia, control and experimental groups were given 1 x 10(5) B16 melanoma cells intravenously. After 21 days, all animals were autopsied, and the metastatic nodules in their lungs were counted. The difference in the numbers of metastatic nodules between control and experimental groups of animals was analyzed for significance by the Mann Whitney "U test". RESULTS: More metastases were observed in the animals exposed to halothane (37.28 +/- 5.08, P < 0.0001), or isoflurane anaesthesia (28.24 +/- 4.07, P < 0.0014) than in the control animals (12.22 +/- 1.52). CONCLUSION: Exposure to halothane or isoflurane anaesthesia increased the number of pulmonary metastases in C57B1 mice compared with the control groups but there was no difference in metastases among animals treated with halothane or isoflurane.

Anesthetics, Inhalation↗
PubMed1994

A comparison of sevoflurane with halothane, enflurane, and isoflurane on bronchoconstriction caused by histamine.

This study was conducted to assess the effect of sevoflurane on lung resistance and compliance, and its responsiveness to histamine. We studied eight dogs to compare the effect of sevoflurane, isoflurane, enflurane, and halothane on bronchoconstriction caused by histamine. Baseline values of pulmonary resistance (RL) and dynamic pulmonary compliance (Cdyn) were measured prior to administration of histamine. Histamine (2, 4, and 8 micrograms.kg-1) were administered iv, and the values of RL and Cdyn at the time of peak effect were recorded. Under 1 or 2 MAC anaesthesia, sevoflurane as well as the other three anaesthetics had no bronchoactive effects. The four anaesthetics, including sevoflurane, demonstrated inhibitory effect on increases in RL and decreases in Cdyn caused by histamine. At 1 MAC anaesthesia, % changes in RL caused by 2, 4, or 8 micrograms.kg-1 of histamine were 38 +/- 11, 85 +/- 21, or 132 +/- 24% (mean +/- SE) for halothane, and 65 +/- 11, 132 +/- 15, or 172 +/- 19% for sevoflurane, respectively. Sevoflurane was less effective than halothane in preventing increases in RL. In preventing decreases in Cdyn, sevoflurane was less effective than halothane only at 8 micrograms.kg-1 of histamine under 1 and 2 MAC anaesthesia. There was no difference in attenuating effect on changes in RL and Cdyn between sevoflurane and isoflurane or enflurane. We concluded that sevoflurane was less potent than halothane in attenuating changes in RL and Cdyn in response to iv histamine.

Airway Resistance↗
PubMed1998

[Protective effects of halothane on ischemic reperfusion injury on rat perfused hearts].

UNLABELLED: We evaluated the possible cardioprotective effects of halothane in isolated rat hearts. Langendorff perfusion was initiated by using Krebs-Henseleit Buffer (KHB) heated at 37 degrees C. CONTROL GROUP: After 15 mins Langendorff perfusion, global ischemia was induced for 40 mins at 37 degrees C by clamping aorta, followed by 60 mins of reperfusion. Experimental group: Global ischemia was induced at the same time course as the control group and during reperfusion, halothane administered at the concentration of 1%, 2%, 3%. Cardiac function (heart rate, coronary flow, Vmax of the left ventricule) and intracelluar calcium level was measured during pre-ischemia, ischemia and reperfusion period. Recovery of cardiac function after ischemia was better in the 1% halothane group than in the control group but suppression on cardiac function inclined to increase concentration dependently. Compared to the control group, increase of intracellular calcium level after ischemia was suppressed in the halothane administered group at all concentration level. These data suggests that a low dose halothane administration shows a cardioprotective effects during reperfusion.

Anesthetics, Inhalation↗
PubMed2005

Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons.

PURPOSE: Although general anesthetics may decrease neuronal excitation, their detailed effects on spontaneous excitatory postsynaptic currents (EPSCs) remain controversial. We investigated and compared the effects of halothane on N-methyl-D-asparate (NMDA) and non-NMDA receptor-mediated postsynaptic currents. METHODS: Spontaneous synaptic currents were recorded by the patch clamp technique in cultured rat cortical neurons. They were isolated by specific pharmacological blocking agents and their electrophysiologic properties were examined. RESULTS: The frequency of NMDA EPSCs was preferentially decreased as compared with that of non-NMDA EPSCs at halothane 1.2 mM. The total net charge of EPSCs mediated by NMDA and non-NMDA receptors was depressed to 56% +/- 6% (mean +/- SD) and 71% +/- 7% of control by halothane 0.6 mM, and to 11% +/- 9% and 59% +/- 11% of control by halothane 1.2 mM, respectively. CONCLUSION: These results show that halothane causes decrease of excitatory synaptic activity, with NMDA EPSCs being more sensitive than non-NMDA EPSCs.

Algorithms↗
PubMed2006

Halothane affects focal adhesion proteins in the A 549 cells.

Halothane is a volatile anaesthetic, which is known to induce alterations in cellular plasma membranes, modulating the physical state of the membrane lipids and/or interacting directly with membrane-bound proteins, such as integrin receptors. Integrin-mediated cell adhesion is a general property of eukaryotic cells, which is closely related to cell viability. Our previous investigations showed that halothane is toxic for A 549 lung carcinoma cells when applied at physiologically relevant concentrations and causes inhibition of adhesion to collagen IV. The present study is focused on the mechanisms underlying halothane toxicity. Our results imply that physiologically relevant concentrations of halothane disrupt focal adhesion contacts in A 549 cells, which is accompanied with suppression of focal adhesion kinase activity and paxillin phosphorylation, and not with proteolytic changes or inhibition of vinculin and paxillin expression.We suggest that at least one of the toxic effects of halothane is due to a decreased phosphorylation of the focal contact proteins.

Cell Adhesion↗
PubMed1992

31P NMR and freeze fracture studies of sarcoplasmic reticulum membranes from normal and malignant hyperthermic pigs: effect of halothane and dantrolene.

The effects of halothane and dantrolene on sarcoplasmic reticulum membranes isolated from normal and malignant hyperthermia pig muscle have been investigated using 31P NMR and freeze fracture electron microscopy. The dynamical and structural changes are estimated from the second moment, as calculated from 31P NMR spectra. For both membranes, addition of halothane induces a similar decrease in the spectral second moment. At high concentration of halothane, freeze fracture replicas show small unilamellar vesicles or mixed micelles, uniformly sprayed in the case of malignant hyperthermia membranes but mainly aggregated for the normal ones. The effect of halothane on both membranes is partially inhibited by adding dantrolene. These results suggest that (i) the malignant hyperthermia syndrome is not directly related to the polar heads of phospholipids and (ii) dantrolene counteracts unspecifically the disturbing effect of halothane at the lipid level.

Animals↗
PubMed1975

Action of halothane on human erythrocytes. Mechanisms of cell lysis and production of sealed ghosts.

1. Suspension of human erythrocytes in halothane-saturated physiological media induces major cell deformation. 2. Release of halothane from erythrocyte suspensions after equilibrium with the anaesthetic produces complete hemolysis. 3. The membrane fragments isolated after halothane release are in the form of biconcave ghosts, impermeable to macromolecules (lactoperoxidase) and small molecules (ATP). 4. The protein composition of the membranes differs from that of ghosts produced by hypotonic lysis in the lack of components previously shown to be adsorbed at low ionic strength. 5. A hypothesis is presented explaining the action of halothane in terms of both its action on membranes and its capacity to modify water structure. 6. Halothane-induced hemolysis constitutes a simple method for the large-scale production of hemoglobin-depleted, sealed erythrocyte ghosts under physiological ionic conditions.

Adenosine Triphosphatases↗
PubMed1993

Association of anti-58 kDa endoplasmic reticulum antibodies with halothane hepatitis.

We recently showed that when rats were administered the inhalation anesthetic halothane, a 58 kDa liver endoplasmic reticulum protein became covalently trifluoroacetylated by the trifluoroacetyl chloride metabolite of halothane. Although the 58 kDa protein showed 99% identity to that of the deduced amino acid sequence of a cDNA reported to correspond to phosphatidylinositol-specific phospholipase C-alpha, it did not have phosphatidylinositol-specific phospholipase C activity. It was concluded that the reported cDNA of phosphatidylinositol-specific phospholipase C-alpha actually encoded for the 58 kDa endoplasmic reticulum protein of unknown function. Other researchers have come to the same conclusion and have shown that the 58 kDa protein has protein disulfide-isomerase and protease activities. We now report that patients with halothane hepatitis have serum antibodies that react with both purified trifluoroacetylated and native rat liver 58 kDa proteins. These results suggest that when patients are exposed to halothane a human liver orthologue of the rat liver trifluoroacetylated-58 kDa protein is formed. In certain patients, this protein may become immunogenic and lead to the formation of specific antibodies and or specific T-cells, which may react with both trifluoroacetylated and native 58 kDa proteins, and ultimately be responsible, at least in part, for the hepatitis caused by halothane.

Animals↗
PubMed1987

Mechanisms of halothane action on synaptic transmission in motoneurons of the newborn rat spinal cord in vitro.

Action of halothane on synaptic transmission was studied on the isolated newborn rat spinal cord. Clinical doses of halothane (less than or equal to 3%) suppressed mono- and polysynaptic reflexes, dorsal root reflexes, excitatory and inhibitory postsynaptic potentials as well as the spontaneous synaptic potentials caused by impulse bombardment. However, the spontaneous miniature inhibitory postsynaptic potentials observed after blocking impulse activities by tetrodotoxin were not all suppressed by halothane. During halothane administration, the membrane potential of motoneurons was hyperpolarized by several millivolts, associated with an increase in input conductance. However, the threshold potential level for spike generation was virtually unaffected. Depression of synaptic transmission in spinal motoneurons by halothane is suggested to be due to two factors: a reduction in the amount of transmitter release secondary to interference with Ca2+ entry into nerve terminals, either by partial blockade of impulse invasion or voltage-dependent Ca2+ channels; and an increase in the depolarizing current necessary for excitation of motoneurons owing to hyperpolarization and decreased input resistance.

Action Potentials↗
PubMed1991

Therapeutic window of halothane anesthesia for reversal of delayed neuronal injury in gerbils: relationship to postischemic motor hyperactivity.

The effect of postischemic halothane anesthesia on locomotor activity and delayed neuronal injury in the hippocampal CA1 sector was examined in gerbils subjected to 5-min forebrain ischemia. Locomotor activity was assessed for 48 h after ischemia using an animal activity monitor, and CA1 injury was evaluated by counting the number of surviving neurons following 7 days of recirculation. Sham-treated animals exhibited a slight decrease of motor activity for about 1 day after surgery. Gerbils subjected to ischemia without postischemic halothane anesthesia developed significant motor hyperactivity (18 times higher than control activity) between 1.7 h and 6.7 h of recirculation. Surviving CA1 neurons in this group amounted to only 17% of those in the control animals. Postischemic halothane anesthesia during the initial 1.7 h of recirculation abolished subsequent motor hyperactivity and protected 84% of all CA1 neurons. Postischemic halothane anesthesia during 1.7 h-3.3 h of recirculation and 3.3-5 h of recirculation did not abolish motor hyperactivity except during the period of anesthesia, and did not protect hippocampal CA1 neurons (only 24% and 10% neuronal survival, respectively). These results demonstrate that the therapeutic window of halothane anesthesia for protection of hippocampal injury precedes the phase of locomotor hyperactivity, and that the appearance of the latter predicts delayed neuronal death.

Anesthesia↗