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PubMed1994

Calcium-dependent halothane activation of sarcoplasmic reticulum calcium channels from frog skeletal muscle.

The effect of halothane on calcium channels present in sarcoplasmic reticulum membranes isolated from frog skeletal muscle was studied at the single channel level after fusing the isolated vesicles into planar lipid bilayers. Addition of 91 microM halothane to the cytosolic compartment containing 1 microM free calcium activated the channel by increasing fractional open time from 0.11 to 0.59, without changing the channel conductance. The activation of the channels by halothane was calcium dependent. At resting calcium concentrations in the cytosolic compartment, halothane failed to activate the channel, whereas maximal activation was found at 10 microM calcium. The free energy of halothane binding to the channel decreased from -5.8 kcal/mol at 1 microM calcium to -6.6 kcal/mol at 10 microM calcium. Halothane increased the open time constants and decreased the closed time constants, indicating that it binds to both the open and the closed configurations of the channel.

Animals↗
PubMed1986

Halothane is less suppressive than pentobarbital on reflex and neural activation of pancreatic F-cell.

To determine the suitability of halothane anesthesia for studies of parasympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane on reflex, direct neural, and direct chemical activation of the parasympathetic input to the islet. Levels or output of pancreatic polypeptide (PP), an islet hormone under predominant cholinergic influence, were used as an indicator of the degree of parasympathetic activation and its potential suppression by anesthesia. Reflex stimulation of the parasympathetic nervous system by 2-deoxy-D-glucose (2-DG) in dogs anesthetized with halothane (0.8%) caused a fourfold increase in plasma PP levels, equivalent to the response in conscious dogs. In contrast, 2-DG at this dose and at a threefold higher dose did not alter PP levels in dogs anesthetized with pentobarbital (30 mg/kg iv), suggesting that halothane at this dose is not suppressive and that pentobarbital is very suppressive on reflex activation of the parasympathetic nerves to the pancreas. Bilateral electrical stimulation of the cervical vagi in halothane-anesthetized dogs elicited a sixfold increase in the pancreatic output of PP. The same stimulation caused only a twofold increase of PP output in pentobarbital-anesthetized dogs. These data suggests that halothane is also less inhibitory than pentobarbital on either peripheral neurotransmission or pancreatic F-cell responsiveness. The effect of direct activation of the F-cell by bethanechol did not differ between the two anesthesias. Therefore, the attenuated PP response to vagal stimulation in pentobarbital-anesthetized dogs is probably due to an action of pentobarbital on peripheral neurotransmission, perhaps at the intrapancreatic parasympathetic ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1987

Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia.

To determine the suitability of halothane anesthesia for studies of sympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane anesthesia (0.8% inspired concentration) on the sympathetic response to central neuroglucopenia. In dogs anesthetized with halothane, intravenous administration of the neuroglucopenic agent, 2-deoxy-D-glucose (2-DG; 100 mg/kg), produced increases of both systemic plasma epinephrine (EPI; delta = 269 +/- 86 pg/ml, P less than 0.025) and norepinephrine (NE; delta = 157 +/- 55 pg/ml, P less than 0.025) equivalent to those previously observed in conscious dogs. Measurement of plasma NE kinetics revealed that the plasma NE response to 2-DG during halothane was due to an increase in the rate of NE appearance that was identical to that of conscious dogs, rather than to an impairment of NE clearance. In contrast, 2-DG at this dose did not increase plasma EPI or NE levels in dogs anesthetized with pentobarbital sodium (30 mg/kg). Plasma glucose increased modestly after 2-DG (100 mg/kg) in both conscious and halothane-anesthetized dogs but not in the pentobarbital-anesthetized dogs. Although 2-DG at a threefold higher dose (300 mg/kg) caused plasma EPI, NE, and glucose (delta = 12 +/- 3 mg/dl, P less than 0.001) to increase in pentobarbital-anesthetized dogs, the responses to this higher dose of 2-DG were all significantly larger in halothane-anesthetized dogs (delta of plasma glucose = 30 +/- 8 mg/dl, P less than 0.005; P less than 0.0025 vs. pentobarbital).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Halothane and octanol block Ca2+ oscillations in pancreatic acini by multiple mechanisms.

This study has investigated halothane and octanol, reported inhibitors of gap junction permeability, for their effects on acinar cell intracellular Ca2+ concentration ([Ca2+]i) signaling. Halothane and octanol alone at maximal concentrations induced a sustained rise in [Ca2+]i of 23 +/- 4 and 29 +/- 5 nM, respectively. Cholecystokinin (CCK, 20 pM) induced [Ca2+]i oscillations in single acinar cells within the acinus to a peak of 275 +/- 17 nM, rising from a basal level of 55 +/- 3 nM. These oscillations were completely abolished by superfusion with both halothane (4 mM) and octanol (1 mM), concentrations that blocked the spread of Lucifer yellow from cell to cell within an acinus. Lower concentrations of octanol markedly reduced the oscillation frequency (0.2 and 0.5 mM octanol: reduction in oscillation frequency of 69 +/- 6 and 43 +/- 6%, respectively). These agents however, over the same concentration range, also exhibited similar inhibitory effects on [Ca2+]i oscillations in single cells dispersed from the acinus (reduction in oscillation frequency of 75 +/- 10 and 32 +/- 12% for 0.2 and 0.5 mM octanol, respectively), suggesting additional effects other than on gap junctions. Halothane inhibited inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] production in response to both 1 and 10 nM CCK (31 and 40% inhibition, respectively), possibly explaining its effects on [Ca2+]i oscillations, whereas octanol showed no significant inhibition. Octanol, unlike halothane, blocked Ins(1,4,5)P3-induced Ca2+ release from permeabilized acini, an effect that was most pronounced at a more physiological Ins(1,4,5)P3 concentration. Octanol did not affect Ins(1,4,5)P3 binding to Ins(1,4,5)P3 receptor preparation. In conclusion, although halothane and octanol block gap junction permeability in pancreatic acinar cells, these agents also affect Ins(1,4,5)P3 production and Ca2+ mobilization in response to agonist stimulation.

1-Octanol↗
PubMed1986

Effects of halothane on transmembrane potentials, Ca2+ transients, and papillary muscle tension in the cat.

The effects of halothane on cat papillary muscle were studied in vitro at different pacing rates (60, 75, 100, and 150 beats/min). Simultaneous measurements of transmembrane potentials, intracellular Ca2+ transients, and isometric tension were made before and after introduction of 1 and 2 minimal alveolar concentration halothane. Anesthetic concentrations in the superfusion bath were measured using a gas chromatography procedure. The Ca2+-sensitive photoprotein, aequorin, was microinjected into papillary muscle cells. Aequorin light emission is a function of free intracellular [Ca2+] [( Ca2+]i). The most prominent effects of halothane were a dose-dependent decrease in the contractile force and a decrease in [Ca2+]i, at all pacing rates. The negative inotropic effect of halothane was associated with only small changes in the papillary muscle action potential duration. Increasing the extracellular [Ca2+] produced an increase in [Ca2+]i and counteracted the negative inotropic effects of halothane. Addition of the Ca2+ channel blocker, verapamil, and halothane, produced an additive decrease in [Ca2+]i compared with the control.

Action Potentials↗
PubMed1992

Halothane anesthesia abolishes pulmonary vascular responses to neural antagonists.

We investigated the effects of the inhalational anesthetic halothane on autonomic nervous system (ANS) regulation of the baseline pulmonary vascular pressure-flow (P/Q) relationship compared with that measured in the conscious state. Multipoint pulmonary vascular P/Q plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q. P/Q plots were generated in the same dogs in the conscious state and during halothane anesthesia (approximately 1.2% end tidal) in the intact (no drug) condition and after administration of selective ANS antagonists. In conscious dogs, sympathetic alpha 1-adrenoreceptor block with prazosin decreased (P less than 0.01) the pulmonary vascular pressure gradient [pulmonary arterial pressure-pulmonary arterial wedge pressure (PAP-PAWP)] over the entire range of Q studied; i.e., inhibition of endogenous alpha 1-adrenoreceptor activity caused pulmonary vasodilation. In contrast, alpha 1-adrenoreceptor block had no effect on PAP-PAWP at any value of Q during halothane anesthesia. In conscious dogs, sympathetic beta-adrenoreceptor block with propranolol increased (P less than 0.01) PAP-PAWP over the entire range of Q studied; i.e., inhibition of endogenous beta-adrenoreceptor activity resulted in pulmonary vasoconstriction. However, beta-adrenoreceptor block had no effect on PAP-PAWP at any value of Q during halothane anesthesia. Finally, cholinergic receptor block with atropine decreased (P less than 0.05) PAP-PAWP at values of Q greater than 100 ml.min-1.kg-1 in conscious dogs but had no effect on PAP-PAWP at any value of Q during halothane anesthesia. These results indicate that endogenous ANS regulation of the baseline pulmonary vascular P/Q relationship observed in conscious dogs is abolished during halothane anesthesia.

Adrenergic alpha-Antagonists↗
PubMed1995

Halothane reduces force and intracellular Ca2+ in airway smooth muscle independently of cyclic nucleotides.

Halothane relaxes airway smooth muscle in part by a direct effect on the smooth muscle cell. The purpose of this study was to investigate the possible role of cyclic nucleotides in this direct effect. Strips of canine tracheal smooth muscle in vitro were contracted with acetylcholine (ACh) and then exposed to 0.7-2.6% halothane. Isometric force and the intracellular concentrations of adenosine cyclic 3',5'-monophosphate ([cAMP]i) guanosine cyclic 3',5'-monophosphate ([cGMP]i), and free calcium ([Ca2+]i, using the fluorescent Ca(2+)-sensitive dye fura 2) were measured. ACh caused significant increases in force, [cAMP]i, [cGMP]i, and [Ca2+]i. Subsequent exposure of the strips to halothane caused an additional increase in [cAMP]i, decreases in force and [Ca2+]i, and no effect on [cGMP]i. The additional increase in [cAMP]i was similar to that produced by a concentration of isoproterenol (0.03 microM) that caused equipotent relaxation. Indomethacin abolished the increase in [cAMP]i produced by ACh and abolished the additional increase in [cAMP]i produced by halothane. In contrast, indomethacin had no effect on the decreases in force and [Ca2+]i. These findings suggest that in canine tracheal smooth muscle contracted with ACh 1) halothane increases [cAMP]i by a cyclooxygenase-dependent mechanism and 2) the increase in [cAMP]i produced by halothane is not responsible for the relaxation or the decrease in [Ca2+]i.

1-Methyl-3-isobutylxanthine↗
PubMed1997

Halothane inhibits agonist-induced potentiation of rMLC phosphorylation in permeabilized airway smooth muscle.

Agonist-induced increases in CA2+ sensitivity are mediated in part by mechanisms that increase phosphorylation of the regulatory myosin light chain (rMLC) at constant cytosolic Ca2+ concentration ([Ca2+]i). The current study tested the hypothesis that halothane inhibits acetylcholine (ACh)-induced potentiation of rMLC phosphorylation in beta-escin-permeabilized canine tracheal smooth muscle. ACh plus GTP significantly potentiated the increase in isometric force and rMLC phosphorylation induced by 0.8 microM free Ca2+. However, whereas the potentiation of isometric force was sustained, the potentiation of rMLC phosphorylation was biphasic, peaking at 0.5 min and then declining by approximately 10 min to a steady-state level significantly above that induced by 0.8 microM free Ca2+ alone. This finding suggests that mechanisms in addition to changes in rMLC phosphorylation may mediate ACh-induced Ca2+ sensitization, as has been reported for vascular smooth muscle. Halothane (0.91 +/- 0.10 mM) significantly inhibited ACh plus GTP-induced potentiation of rMLC phosphorylation and isometric force after 2 (peak rMLC phosphorylation) and 15 (steady-state rMLC phosphorylation) min of stimulation. However, the effect of halothane on the potentiation of isometric force was significantly less than that expected from its effect on rMLC phosphorylation (i.e., halothane changed the relationship between rMLC phosphorylation and isometric force). These results demonstrate that halothane inhibits the ACh-induced increase in Ca2+ sensitivity by inhibiting the membrane receptor-coupled mechanisms that increase rMLC phosphorylation at constant submaximal [Ca2+]i. Possible additional effects of halothane on rMLC phosphorylation-independent mechanisms cannot be ruled out.

Acetylcholine↗
PubMed1991

BAY K 8644 and nifedipine alter halothane but not caffeine contractures of malignant hyperthermic muscle fibers.

The purpose of these experiments was to determine if the Ca2+ agonist BAY K 8644 and the Ca2+ antagonist nifedipine alter the mechanical responses of malignant hyperthermia-susceptible (MHS) skeletal muscle to halothane and caffeine. Muscle fiber bundles were dissected from MHS porcine skeletal muscle and exposed to BAY K 8644 (10 microM), nifedipine (1 microM), low-Ca2+ media [Ca2+ replaced by 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid], or diltiazem (30 microM) administered alone and with halothane (3%) or caffeine (0.5-0.8 mM). When administered alone, both halothane and BAY K 8644 evoked a significant change in resting tension (i.e., contracture) of 193.7 +/- 61.0 and 51.9 +/- 21.5 mN/cm2, respectively. When administered in combination, BAY K 8644 had no effect on the magnitude of the halothane contracture (195.2 +/- 58.6 mN/cm2) but reduced its onset time from 306.7 +/- 36.3 to 105.9 +/- 8.9 s. Nifedipine, low Ca2+, and diltiazem significantly reduced the halothane contracture (103.1 +/- 30.3, 123.1 +/- 20.6, and 112.6 +/- 16.2 mN/cm2, respectively) but had no effect on its onset time. In addition, low Ca2+ reduced the magnitude of the BAY K 8644 contracture (8.2 +/- 2.1 mN/cm2). BAY K 8644 also increased contractures induced by low caffeine concentrations (0.5-2.0 mM) but did not alter contractures induced by 4.0 and 8.0 mM caffeine, whereas nifedipine, low Ca2+, and diltiazem had no effect on these contractures. These results suggest that extracellular Ca2+ influx may have some influence on halothane but not on caffeine contractures of MHS skeletal muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Effects of BAY K 8644, nifedipine, and low Ca2+ on halothane and caffeine potentiation.

The purpose of this investigation was to examine the effects of the Ca2+ agonist BAY K 8644 and the Ca2+ antagonist nifedipine on halothane- and caffeine-induced twitch potentiation of mammalian skeletal muscle. Muscle fiber bundles were taken from normal Landrace pigs and exposed to BAY K 8644 (10 microM), nifedipine (1 microM), and low Ca2+ media administered alone and in combination with halothane (3%) or with increasing concentrations of caffeine (0.5-8.0 mM). Both BAY K 8644 and halothane potentiated twitches by approximately 80%; when they were administered in combination, twitch potentiation was nearly double that caused by either drug alone. In the presence of nifedipine, halothane increased twitches by less than 30%. Low Ca2+ significantly depressed twitches by approximately 25% but also inhibited halothane's inotropic effect. BAY K 8644 augmented caffeine potentiation but only at low caffeine concentrations (0.5-2.0 mM). Nifedipine and low Ca2+ failed to inhibit caffeine's inotropic effects. These results suggest that halothane potentiates twitches via a mechanism that involves or is influenced by extracellular Ca2+.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Ventilation and thoracoabdominal asynchrony during halothane anesthesia in infants.

To evaluate the ventilatory consequences of high chest wall compliance during anesthesia in infants, we assessed the effects of halothane at different fractions of minimal alveolar concentration (0.75, 1.0, and 1.5 MAC) on ventilation and movements of the rib cage and abdomen in infants < or = 12 mo of age (group I) and children (group II) > or = 12 mo of age. Minute ventilation decreased in group I, (20.6%, 0.75 to 1.5 MAC), but the change in group II did not reach the level of statistical significance. Tidal volume decreased with halothane level between 0.75 and 1.5 MAC, and its fall was greater in group I (32.7 +/- 11.2 vs. 22.6 +/- 9.3% in group II, P < 0.05). Duty cycle, or ratio of inspiratory to total time (TI/TT), increased in group II with halothane level but did not change in group I, resulting in a decreased TI in group I at higher halothane levels. Thoracic paradox increased with halothane level in group I but not group II. The increase in thoracic paradox in association with the fall in tidal volume between 0.75 and 1.5 MAC was greater in group I than group II (P < 0.05). We conclude that smaller infants depend more on inspiratory intercostal muscle activity to stabilize the thorax, leading to a greater degree of depression of ventilation during halothane depression of inspiratory intercostal activity.

Abdominal Muscles↗
PubMed1998

Prolonged exposure to halothane and associated changes in carbohydrate metabolism in rat muscles in vivo.

Halothane, an anesthetic presently used in animal experimentation, is reported to stimulate glycogen breakdown in isolated preparations of rat skeletal muscles, suggesting that it may not be a suitable anesthetic for the study of glycogen metabolism in rats in vivo. The purpose of this study was to establish whether prolonged exposure to halothane in rats in vivo is associated with accelerated glycogenolysis. Exposure of rats to halothane for up to 1 h was not accompanied by either any change in the levels of glycogen or increase in activity ratios of glycogen phosphorylase in muscles, irrespective of their fiber compositions. In marked contrast, the levels of lactate, inorganic phosphate, glucose 1-phosphate, glucose 6-phosphate, fructose 1,6-bisphosphate, and fructose 2, 6-bisphosphate changed progressively during anesthesia. Accordingly, the interpretation of muscle metabolite levels must be performed with caution in experiments involving prolonged exposure to halothane. Overall, our findings indicate that the reported halothane-mediated stimulation of glycogen breakdown in vitro is likely to be an artifact and that halothane is a suitable anesthetic for experiments concerned with glycogen metabolism in rats.

Anesthetics, Inhalation↗
PubMed1984

Halothane sensitizes cutaneous nociceptors in monkeys.

The effects of halothane on the responses of C-fiber (CMHs) and A-fiber (AMHs) nociceptive afferents sensitive to mechanical and heat stimuli were studied in monkeys. The response to heat stimuli was studied with use of a laser thermal stimulator that provided stepped increases in skin temperature over a 7.5-mm-diameter area with rise times to the desired temperature near 100 ms. Recordings were obtained from single fibers that innervated the glabrous skin of the hand using a teased-fiber dissection technique. In initial studies the response of 32 CMHs and 45 AMHs in monkeys anesthetized with pentobarbital sodium (3-6 mg X kg-1 X h-1) was compared with the response of 12 CMHs and 23 AMHs in monkeys anesthetized with a combination of halothane (0.8%) and N2O (67%). A standardized set of 10 3-s heat stimuli ranging from 41 to 49 degrees C delivered every 30 s were applied to the receptive field. Both AMHs and CMHs had a lower threshold and greater response to suprathreshold heat stimuli under conditions of halothane-N2O anesthesia. The threshold to mechanical stimuli, as tested by von Frey hairs, was not significantly different. Five CMHs and 5 AMHs were studied in a crossover study in which responses to the 41-49 degrees C stimuli were obtained first under halothane-N2O (0.8%-67%) anesthesia, then under an ultrashort acting barbiturate, methohexital (2-9 mg/kg over 15 min), and finally once again under halothane-N2O anesthesia. For the five CMHs, the mean cumulative response was 1.8 times greater, whereas for the five AMHs the response was 4.7 times greater under halothane as opposed to barbiturate anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Cutaneous responsiveness of lumbar spinal neurons in awake and halothane-anesthetized sheep.

1. To compare the responsiveness of lumbar spinal neurons to peripheral sensory stimuli under normal physiological conditions and under halothane anesthesia, we performed a study in sheep that were prepared chronically. This permitted recordings to be made in the same animals either when they were awake and free from recent surgery, drugs, and training and only partially restrained or when they were anesthetized with halothane. 2. We recorded 261 units in dorsal and ventral horns under conscious conditions. Of these, 19% had no detectable receptive field (RF) and 44% had responses dominated by proprioceptive inputs; these units were not investigated in detail. The remaining 96 neurons (37%) had clearly defined cutaneous RFs. Of these, most (72%) had wide-dynamic-range (WDR; convergent, multireceptive) properties, 19% were low-threshold mechanoreceptive (LTMR), and 9% were high-threshold mechanoreceptive (HTMR). These units with cutaneous RFs were investigated in greater detail. 3. The spontaneous activity under these awake conditions was low (< 4 spikes/s) for nearly all units in all three categories. The mechanical threshold of the most sensitive (central) part of the cutaneous RF was assessed with von Frey bristles. Thresholds were < 5 mN for all LTMR neurons, < 1-30 mN for WDR neurons, and > 80 mN for HTMR neurons. The size of the low-threshold cutaneous RFs was significantly larger for WDR neurons (mean 46 cm2) and HTMR neurons (45 cm2) than for LTMR neurons (24 cm2). The RFs were distributed all over the ipsilateral hindlimb. Large RFs were mostly proximal, whereas small RFs were distributed relatively evenly over the limb. 4. Recordings were made from a further 165 units while the animals were under halothane anesthesia. With 86 neurons having cutaneous peripheral RFs, the proportions having LTMR, HTMR, or WDR characteristics were very similar to those in awake animals. Under halothane the ongoing activity of WDR units was slightly (but significantly) less. The threshold to von Frey bristle stimulation was significantly higher only for WDR units, in both dorsal and ventral horns. The mean size of cutaneous RFs was significantly larger in all classes of units recorded under halothane anesthesia. For WDR units this was true for cells in both dorsal and ventral horns. This effect on mean values was due to a larger proportion of units with very large fields under anesthesia, particularly in the dorsal horn. 5. Comparison of the data from conscious animals with published results of acute experiments indicates that acute recording conditions do not distort the relative distribution and resting characteristics of these three functional categories of lumbar spinal neurons as much as might have been expected. 6. Halothane does not have major effects on the resting sensory responsiveness of spinal neurons with cutaneous RFs. The increase in RF area, which contrasts with most results from acute studies, is likely to be due to a dampening of descending inhibitory control mechanisms.

Anesthesia↗
PubMed1995

Halothane-induced synaptic depression at both in vivo and in vitro reconstructed synapses between identified Lymnaea neurons.

1. In the present study we tested the ability of the general anesthetic, halothane, to affect synaptic transmission at in vivo and in vitro reconstructed peptidergic synapses between identified neurons of Lymnaea stagnalis. 2. An identified respiratory interneuron, visceral dorsal 4 (VD4), innervates a number of postsynaptic cells in the central ring ganglia of Lymnaea. Because VD4 has previously been shown to exhibit immunoreactivity for FMRFamide-related peptides, it was hypothesized that these peptides may be utilized by VD4 during synaptic transmission. In the intact, isolated CNS of Lymnaea, we have identified novel connections between VD4 and the pedal A (PeA) cells. We demonstrate that VD4 makes inhibitory connections with the PeA neurons, in particular PeA4, and that these synaptic responses are mimicked by exogenous application of FMRFamide. 3. The synaptic transmission between VD4 and the PeA cells in an intact, isolated CNS preparation was completely blocked in 2%, but not 1% halothanc. Interestingly, the postsynaptic responses (PeA) to exogenous FMRFamide were maintained in the presence of both 1 and 2% halothane. 4. To determine the specificity of the observed responses and to determine the precise synaptic site of anesthetic action, we reconstructed the VD4/PeA synapses in vitro. After isolation from their respective ganglia, both cell types extended processes and established neuritic contact. We demonstrated that not only did the presynaptic neuron reestablish the appropriate inhibitory synapses with the PeA neurons, but that the PeA cells also maintained their responsiveness to exogenous FMRFamide. 5. Superfusion of the in vitro synaptically connected VD4 and PeA cells with 2% halothane completely abolished the synaptic transmission between these cells. However, even higher concentrations of 4% halothane failed to block the responsiveness of the PeA neurons to exogenous FMRFamide. Moreover, both 1 and 2% halothane enhanced the duration of the postsynaptic response to exogenously applied FMRFamide. These data suggest that the halothane-induced depression of synaptic transmission most likely occurred at the presynaptic level. 6. This study provides the first direct evidence that peptidergic transmission in the nervous system may also be susceptible to the actions of general anesthetics. In addition, we utilized a novel approach of in vitro reconstructed synapses for studying the effects of general anesthetics on monosynaptic transmission in the absence of other synaptic influences.

Anesthetics, Inhalation↗
PubMedDate not supplied

Cellular actions of halothane on cat cerebral arterial muscle.

The effects of halothane on intracellular membrane potential (Em) and force development in cat MCA were studied. Halothane (0.07-0.14 mM/1) relaxed isolated MCA which had developed myogenic tone. Measurement of Em showed that halothane depolarized this preparation in a dose-dependent fashion in the face of vessel relaxation, demonstrating uncoupling of electrical and mechanical activity. Halothane markedly inhibited the contractile effects of histamine and serotonin suggesting that, apart from its direct action on cerebral arterial tone, it also blunts the action of vasoactive agents. When this preparation is partially depolarized from -62 to -50 mV with excess K+, halothane, while having only a small (1.2 mV) additional depolarizing effect, consistently elicits contraction rather than relaxation. Thus, the action of this particular volatile anesthetic on cerebral arteries can depend upon the resting level of Em. These studies indicate that halothane relaxes myogenic tone in cat MCA by an intracellular mechanism, but that the direction of its effect (i.e., relaxation vs. contraction) may depend upon the prior level of Em and muscle cell activation.

Animals↗
PubMed1981

An evaluation of the Hellige Transoxode (Servomed Oxymonitor SM 361 System): response to halothane and enflurane in vitro.

The effects of halothane (0.5-2%) and enflurane (1-4%) on two Transoxode transcutaneous oxygen (TcPO2) electrodes (Hellige Servomed Oxymonitor SM.361 system) were serially tested in atmospheres of nitrogen, air and 50% nitrous oxide in oxygen. Both TcPO2 electrodes reduced and "read" halothane but no enflurane. Calibration drift was significantly greater (p less than 0.05) after electrode exposure to halothane; 5.40 s.e.m. 1.37 kPa vs enflurane; -0.60 s.e.m. 0.93 kPa. Halothane has a direct effect in rendering the Transoxode inaccurate, which is probably clinically less important than the indirect cardiovascularly medicated influence of both halothane and enflurane on TcPO2 levels. A reduction in the electrode polarisation voltage is recommended to obviate the direct effect of halothane on Transoxode performance.

Air↗
PubMedDate not supplied

Comparative evaluation of a new inhalation anesthetic, BAX-3224, and halothane in Macaca speciosa.

Two groups of 8 monkeys were anesthetized with either BAX-3224, a new fluorinated methyl-propyl ether, or with halothane, 3 hours daily for a total of 30 hours. Vomiting incidence was 12.5 percent with BAX-3224 during both induction and recovery, compared with 3.7 percent for halothane during induction and 7 percent for halothane during recovery. Induction time did not change during the course of study with either agent. Respiration was spontaneous and cardiopulmonary function was stable. Electroretinographic (ERG) responses were consistent, flicker-light responses similar, but visual evoked responses (VER) were not present during BAX-3224 anesthesia. A 33 percent incidence of electroencephalographic (EEG) silence occurred with BAX-3224, which was consistent with absence of VER. Hematologic and serum chemistry values were similar for both agents. Serum fluoride ion concentrations, measured before exposure and 4 times during the 10-day study, did not change after administration of either agent. This finding was significant for BAX-3224, a fluorinated ether. No cardiac arrhythmias were observed during BAX-3224 anesthesia, compared with a 17 percent incidence during halothane induction. Recovery time was 32 minutes following BAX-3224 and 14 minutes after halothane. BAX-3224 produced anesthesia similar to that of halothane, did not induce changes incompatible with recovery from anesthesia, and showed great potential as a new volatile liquid anesthetic agent with excellent biologic stability.

Anesthesia, Inhalation↗