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PubMedDate not supplied

Echocardiographic analysis of human left ventricular diastolic volume and cardiac performance during halothane anesthesia.

Using M-mode echocardiography we found that 0.5, 1.0, and 1.5% end-tidal halothane induced dose-related increases in left ventricular volume and decreases in left ventricular performance in seven normal unpremedicated subjects. During controlled respiration with normocarbia, the diastolic minor axis of the heart, which is related to the cube root of left ventricular volume, increased to a maximum of 107. 7 +/- 1.9 (% +/- SE of control) at 1.5% end-tidal halothane from a control value of 43.5 +/- 1.3 (mm +/- SE). Two ejection-phase performance variables, percentage shortening and mean velocity of circumferential shortening decreased to 60.1 +/- 6.1 (% +/- SE of control) and 62.4 +/- 6.5, (% +/- SE of control) at 1.5% halothane from respective control values of 29.7 +/- 2.61 (% +/- SE) and 0.94 +/- 0.08 (circumferences/second +/- SE). Surgical stimulation did not significantly affect these changes. Under these experimental conditions, we conclude that halothane dilates the heart, and that echocardiography can be used to monitor the depressant effect of halothane on the heart.

Adult↗
PubMedDate not supplied

Naloxone fails to antagonize halothane-induced depression of the longitudinal muscle of the guinea pig ileum.

The influence of halothane, or naloxone, or halothane followed by naloxone was investigated in the in vitro myenteric plexus longitudinal muscle preparation of the guinea pig ileum. Halothane alone in 1.5 to 2.0% (v/v) concentration caused about 50% depression of the twitch and decreased both spontaneous acetylcholine (ACh) release (p less than 0.02) and volley output of ACh (p less than 0.02). Very high concentrations (greater than 1 micron) of naloxone caused a nonspecific, postsynaptic depression of the twitch. Higher than 100 nM concentrations of naloxone increased spontaneous ACh release, but had no effect on the volley output of ACh. Over a wide concentration range, from 15 nM to 3 micron, naloxone did not antagonize in the longitudinal muscle preparation the effects of halothane on any of the parameters investigated. These findings indicate that the sites of action of halothane and naloxone in this preparation are not identical.

Acetylcholine↗
PubMedDate not supplied

Depression of lung mucociliary dlearance by thiopental and halothane.

It has previously been demonstrated that an induction dose of thiopental, 25 mg/kg, without continuing anesthesia did not depress peripheral lung mucociliary clearance in the dog, whereas 2 hours of anesthesia with halothane, 1.2 MAC, did depress clearance. To determine whether this was because thiopental depresses the mucociliary apparatus less than halothane, this study compared mucociliary clearance after 2 hours of anesthesia with halothane with clearance after 2 hours of anesthesia with thiopental, 40 mg/kg. With thiopental, 40 mg/kg, 50% mucociliary clearance of tantalum from peripheral airways required 280 +/- 65 (SEM) minutes, which was comparable to clearance obtained with halothane, 1.2 MAC, 382 +/- 27 (SEM) minutes. Hence thiopental depresses mucociliary clearance as much as halothane does when both are administered in equivalent anesthetic doses for equal periods of time.

Anesthesia, Inhalation↗
PubMed1990

Antibody assays for the detection of patients sensitized to halothane.

Sera from patients with a clinical diagnosis of halothane hepatitis have been shown to contain antibodies that react with liver microsomal proteins (100, 76, 59, 57, and 54 kDa) covalently altered by the trifluoroacetyl (TFA) halide metabolite of halothane. In the present study, rapid and sensitive enzyme-linked immunosorbent assays for the detection of these antibodies have been evaluated. A recently described method that utilizes TFA-rabbit serum albumin as test antigen was studied employing a large population of halothane hepatitis and control patients. Several problems were discovered with the assay that were not previously recognized. The assay was then compared directly with methods that utilize as test antigens either liver microsomes or purified TFA proteins from halothane-treated rats. Sixty-seven percent of patients with a clinical diagnosis of halothane hepatitis tested positive for antibodies when the test antigens were either TFA-rabbit serum albumin or liver microsomes. This value was increased to 79% when the purified TFA-57 kDa, TFA-76 kDa, and TFA-100 kDa proteins were used as test antigens. These results indicate that the specificity and sensitivity of enzyme-linked immunosorbent assay methods for the detection of patients' antibodies may be increased significantly by utilizing the purified TFA microsomal proteins as test antigens.

Animals↗
PubMed1990

Effect of dexmedetomidine, a selective and potent alpha 2-agonist, on cerebral blood flow and oxygen consumption during halothane anesthesia in dogs.

The effect of the alpha 2-agonist dexmedetomidine on the cerebral blood flow (CBF) and the metabolic rate for oxygen was studied by a sagittal sinus outflow technique in dogs during halothane anesthesia. Dexmedetomidine was given in a dose (10 micrograms/kg) reported to reduce the anesthetic requirement of halothane by 90%. During 0.9% halothane anesthesia dexmedetomidine caused a significant reduction in CBF without influencing the metabolic rate for oxygen. Reducing the halothane concentration to 0.1% caused no further change in CBF, but increased the metabolic rate for oxygen 19%. The cerebral vasoconstrictive effect, combined with the 90% reduction in MAC for halothane, indicates that dexmedetomidine might be a useful adjunct to inhalation anesthetics during neurosurgery in situations where an increase in CBF should be avoided.

Adrenergic alpha-Agonists↗
PubMed1991

Adverse interaction between bupivacaine and halothane on ventricular contractile force and intraventricular conduction in the dog.

Regional anesthesia with bupivacaine in pediatric patients is often accompanied by light levels of halothane general anesthesia. To determine the potential cardiotoxicity of these two drugs when used together, we defined the interaction between moderate plasma bupivacaine concentrations (1270-1760 ng/mL) and halothane (end-tidal concentrations, 0.5%-1.0%) on ventricular contractility and conduction in 22 closed-chest dogs anesthetized with chloralose. Bupivacaine alone (1-mg/kg intravenous bolus plus a 0.1-mg.kg-1.min-1 constant rate infusion) resulted in significant increases in ventricular conduction time (VCT) and effective refractory period (VERP) and nonsignificant decreases in dP/dtmax and blood pressure. The addition of halothane resulted in hypotension and in progressively increasing plasma bupivacaine levels secondary to reduced hepatic clearance, which led to further dose-related significant increases in VCT and VERP and to significant decreases in dP/dtmax and blood pressure. In other dogs given halothane but in which bupivacaine levels were held constant (1400 ng/mL), VCT remained constant and VERP lengthened slightly, whereas dP/dtmax decreased. We conclude that the combination of bupivacaine and halothane can cause adverse effects on ventricular contractility and intraventricular conduction.

Anesthesia↗
PubMed1991

Effects of cardiopulmonary bypass and cardioplegia on regional and global cardiac actions of halothane in dogs.

Cardiopulmonary bypass (CPB) with aortic cross-clamping represents a controlled period of global cardiac ischemia. We hypothesized that CPB (asanguineous prime), with aortic cross-clamping and repeated cardioplegia, alters myocardial function, which would be manifested as an exaggerated myocardial depression caused by halothane after CPB. In nine dogs anesthetized with fentanyl and midazolam, halothane dose-response curves (0.0%-2.0%) were compared before and after CPB. A reduced mean arterial blood pressure (46.4 +/- 3.7 vs 85.8 +/- 5.9 mm Hg), associated with a marked hemodilution (hematocrit, 19% +/- 1% vs 41% +/- 2%), was observed after CPB. Cardiac output and systolic shortening were not significantly different after versus before CPB during fentanyl-midazolam anesthesia. Normalized to fentanyl-midazolam hemodynamics, halothane dose-response curves before and after CPB were identical for all variables except cardiac output, where halothane caused a slight but statistically significantly more pronounced decrease after CPB compared with before CPB. The effect of halothane on left ventricular function, therefore, is relatively unaffected by CPB with cardioplegia.

Animals↗
PubMed1991

Halothane attenuates small arteriole vasodilation to serotonin (5-HT) in skeletal muscle.

Inhaled anesthetics may have an effect on the microcirculation through selective alteration of receptor-mediated control. Halothane was chosen because its actions in the microcirculation have been determined previously. Serotonin has received recent attention as a potential mediator of vascular changes in a number of disease states. We obtained concentration-response curves for serotonin-induced constriction of large arterioles and dilation of small arterioles (less than 60 microns diameter) in the cremaster muscle of halothane-anesthetized and decerebrate rats. Cremaster muscles were prepared for microscopic viewing, leaving the neural and vascular supply intact. Serotonin concentration-response curves were obtained before and after receptor antagonist application. Large arteriole constriction was not affected by halothane. Dilation of small arterioles was decreased in halothane-anesthetized animals but enhanced in the presence of methysergide, a nonspecific antagonist. These data indicate that halothane interferes with occupancy of 5-hydroxytryptamine receptors.

Animals↗
PubMed1991

Halothane does have protective properties in the isolated ischemic rat heart.

To determine whether halothane has protective effects on the ischemic heart, the influence of various concentrations (0.5%-1.5%) of halothane on metabolic and functional recovery during reperfusion after 60-min hypothermic (20 degrees C) and 40-min normothermic cardioplegic arrest was determined in the isolated rat heart. Halothane was administered either before and after arrest or intermittently during arrest. Hearts not receiving halothane demonstrated a reduction in adenosine triphosphate (ATP) content from a control value of 20.35 +/- 1.66 mumol/g dry wt (mean +/- SEM) (before arrest) to 9.34 +/- 1.12 mumol/g dry wt at the end of arrest (P less than 0.001). The myocardial ATP content, when measured 20 min after arrest and during reperfusion, remained decreased (9.57 +/- 0.62 mumol/g dry wt). Under these experimental conditions, aortic flow was reduced from 43.62 +/- 2.40 mL/min before arrest to 1.80 +/- 1.80 mL/min 20 min after arrest and during reperfusion (P less than 0.001). The administration of adrenaline after 20 min of reperfusion resulted in partial recovery to 22.01 +/- 8.36 mL/min. Administration of halothane (0.5%) before the cardioplegic period was associated with a reduction of ATP at the end of the normothermic arrest (4.02 +/- 0.38 mumol/g dry wt; P less than 0.01), but the ATP increased significantly (13.45 +/- 0.32 mumol/g dry wt) when measured after the arrest and after 20 min of reperfusion and stimulation with adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Depression of calcium channel blocker binding to rat brain membranes by halothane.

The present study evaluates the action of volatile anesthetics on the voltage-dependent Ca2+ channels in isolated rat brain membranes, measured as changes in binding of the Ca2+ channel blocker [3H]isradipine to these membranes. Equilibrium binding studies with increasing concentrations of [3H]isradipine (0.01-1 nM) in the presence of halothane (1.9%), isoflurane (2.3%), and enflurane (4.8%) at 25 degrees C were performed. Only halothane produced a significant depression in the specific binding of isradipine to the brain membranes at 0.5 and 1.0 nM [3H]isradipine (P = 0.028 and 0.018, respectively). Isoflurane and enflurane had such inconsistent effects that the data were inconclusive. Halothane produced a significant dose-dependent inhibition of binding, the maximum inhibition being 44% (P less than 0.005). Nonlinear regression analysis fit of the binding data indicates halothane produced a 48% decrease (P less than 0.05) in the maximal number of binding sites (Bmax) with no effect on the dissociation constant (Kd). As voltage-dependent Ca2+ channels are important in mediating neurotransmission, the marked decrease in channel number (Bmax) associated with halothane exposure suggests that this phenomenon might be related to the mechanism of general anesthesia.

Animals↗
PubMed1992

Halothane and isoflurane inhibit endothelium-dependent relaxation elicited by acetylcholine.

The purpose of this study was to determine whether volatile anesthetics modify the release of endothelium-derived relaxing factor. We examined the effects of halothane and isoflurane on endothelium-dependent relaxation and 3',5'-cyclic guanosine monophosphate formation elicited by acetylcholine and ionophore A23187 in isolated rat aorta. Halothane and isoflurane (1%-2%) significantly attenuated acetylcholine-induced relaxation of the phenylephrine-contracted aorta but had no significant effect on relaxation induced by A23187, nitroprusside, and nitroglycerin. Basal and A23187 (10(-7) M)-stimulated levels of 3',5'-cyclic guanosine monophosphate were slightly lowered by halothane and isoflurane (2%). In contrast, the increase of 3',5'-cyclic guanosine monophosphate elicited by acetylcholine (10(-5) M) was significantly attenuated by halothane (2%) and abolished by isoflurane (2%). These findings indicate that halothane and isoflurane strongly inhibit the release of endothelium-derived relaxing factor elicited by acetylcholine.

Acetylcholine↗
PubMed1992

Plasma lidocaine concentrations during epidural blockade with isoflurane or halothane anesthesia.

Because isoflurane maintains hepatic blood flow at higher flows than halothane, we proposed that the elimination of lidocaine would be different between these two volatile anesthetics. The plasma lidocaine concentrations were determined in 14 female patients undergoing epidural blockade plus isoflurane anesthesia and compared with those obtained during halothane anesthesia for lower abdominal surgery. General anesthesia was maintained with isoflurane (0.46% +/- 0.04% [mean +/- SE] inspired, n = 7) or halothane (0.48% +/- 0.05% inspired, n = 7) and 67% nitrous oxide in oxygen. All patients received 2% lidocaine solution, 10 mL as a bolus dose and continuous administration at a rate of 10 mL/h, through the epidural catheter. The plasma lidocaine concentrations over 180 min after the epidural injection in patients receiving isoflurane were similar to those in patients receiving halothane. The results suggest that low inspired concentrations of isoflurane do not reduce plasma lidocaine concentrations in patients during epidural blockade, compared with halothane.

Adult↗
PubMed1993

Anesthetic interaction between midazolam and halothane in humans.

The present study was undertaken in humans to determine the anesthetic efficacy of midazolam in terms of its ability to reduce halothane minimum alveolar anesthetic concentration (MAC). Fifty women scheduled for simple or radical hysterectomy were allocated randomly to one of four groups; group A was given no midazolam as a control; groups B, C, and D were given midazolam intravenously by a bolus of 0.1, 0.2, and 0.4 mg/kg followed by infusion of 1, 2, and 4 micrograms.kg-1 x min-1, respectively. Halothane MAC was 0.78%, 0.47%, 0.38%, and 0.23% at mean serum midazolam concentrations of 0, 134, 250, and 539 ng/mL in groups A, B, C, and D, respectively. The interaction between halothane and midazolam in the anesthetic efficacy conformed to an exponential fit. The results indicate that midazolam produces marked reduction of halothane MAC in humans at serum concentrations lower than that required to cause sleep. Lastly, midazolam's potentiation of halothane has a saturated nature.

Adult↗
PubMed1993

Effects of halothane anesthesia on vasoconstrictor response to NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, in sheep.

This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in chronically instrumented, halothane-anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P < 0.05) in both groups. However, L-NAME produced a sharp increase in mean arterial and pulmonary artery pressures only in the control group, whereas the pressor response in the halothane group was attenuated. Cardiac output, which was significantly lower after L-NAME administration in both groups, increased after L-arginine. The results suggest that halothane does not significantly alter the EDRF/NO-mediated effects on the vasculature but potentiates the cardiac depressant effect of L-NAME.

Anesthesia, Inhalation↗
PubMed2003

Halothane and isoflurane have additive minimum alveolar concentration (MAC) effects in rats.

UNLABELLED: Studies suggest that at concentrations surrounding MAC (the minimum alveolar concentration suppressing movement in 50% of subjects in response to noxious stimulation), halothane depresses dorsal horn neurons more than does isoflurane. Similarly, these anesthetics may differ in their effects on various receptors and ion channels that might be anesthetic targets. Both findings suggest that these anesthetics may have effects on movement in response to noxious stimulation that would differ from additivity, possibly producing synergism or even antagonism. We tested this possibility in 20 rats. MAC values for halothane and (separately) for isoflurane were determined in duplicate before and after testing the combination (also in duplicate; six determinations of MAC for each rat). The sum of the isoflurane and halothane MAC fractions for individual rats that produced immobility equaled 1.037 +/- 0.082 and did not differ significantly from a value of 1.00. That is, the combination of halothane and isoflurane produced immobility in response to tail clamp at concentrations consistent with simple additivity of the effects of the anesthetics. These results suggest that the immobility produced by inhaled anesthetics need not result from their capacity to suppress transmission through dorsal horn neurons. IMPLICATIONS: Despite differences in their capacities to inhibit spinal dorsal horn cells, isoflurane and halothane are additive in their ability to suppress movement in response to a noxious stimulus.

Anesthetics, Inhalation↗
PubMed2004

Halothane and propofol modulation of gamma-aminobutyric acidA receptor single-channel currents.

Halothane and propofol enhance the activity of the gamma-aminobutyric acid (GABA) system, which is one of the most important systems in the mechanism of anesthesia. To determine whether halothane and propofol enhance GABAergic responses by the same mechanism, we performed single-channel patch-clamp experiments with rat cortical neurons in primary culture. Each of the open-time and closed-time distributions of GABA(A) receptor single channels was expressed by a sum of fast and slow time constants. Neither halothane nor propofol changed the single-channel conductance. Halothane increased the probability of the channel being open via a prolongation of the slow phase of open time, whereas propofol increased the channel open probability via a shortening of the slow phase of closed time. Thus, although both halothane and propofol augmented the channel open probability, thereby causing an increase in charge transfer during inhibitory transmitter action, they acted by different mechanisms.

Algorithms↗
PubMed1992

Difference between halothane and barbiturate anesthesia in the influence of cerebral ischemia on the vagal baroreflex in dogs.

In halothane-anesthetized dogs, a decrease in baroreflex sensitivity (BRS) of approximately 20% was observed during the reperfusion period following 5-min global cerebral ischemia. When compared with our previous study on animals under pentobarbital anesthesia, the extent of the decrease in BRS was smaller and apparently more severe ischemia was necessary to damage the vagal component of the baroreflex. Substitution of halothane with pentobarbital during the reperfusion period failed to affect either BRS or the ratio of the vagal component. In another group, pre- and post-ischemic measurements of BRS was performed under halothane anesthesia, but the ischemic insult was given under thiopental anesthesia. In these animals, the extent of decrease in BRS (about 50%) was greater than that in animals subjected to ischemia under halothane anesthesia. The present results suggest that the anesthetics used during the ischemic insult may affect the extent of post-ischemic dysfunction of the baroreflex. The vagal component of the baroreflex may be more resistant to ischemia under halothane anesthesia than under barbiturate anesthesia.

Anesthesia↗
PubMed2005

Halothane sensitizes the guinea-pig heart to pharmacological IKr blockade: comparison with urethane anesthesia.

Potential utility of halothane-anesthetized guinea pigs for detecting drug-induced repolarization delay was analyzed in comparison with urethane-anesthesia (n = 4 for both groups). Basal QT interval was significantly greater under halothane-anesthesia than urethane-anesthesia (192 +/- 7 vs 132 +/- 5 ms, respectively), whereas the reverse was true for the heart rate (190 +/- 7 vs 248 +/- 11 beats/min, respectively). The typical I(Kr)-blocker dl-sotalol (0.1 to 3 mg/kg, i.v.) induced dose-related bradycardia and QT interval prolongation under each anesthesia. The extent of maximum prolongation in the QT interval was greater under halothane-anesthesia than urethane-anesthesia (+101 +/- 15 vs +49 +/- 3 ms, respectively), whereas that of peak change in the heart rate was smaller under the former than the latter (-49 +/- 8 vs -63 +/- 5 beats/min, respectively). Pretreatment of the animals under urethane-anesthesia with the selective I(Ks) blocker chromanol 293B (n = 6) increased the extent of the dl-sotalol-induced QT interval prolongation to +57 +/- 8 ms, which was only 0.56 times of that under the halothane-anesthesia, whereas the pretreatment increased the peak change in the heart rate to -76 +/- 12 ms. These results indicate that the halothane-anesthesia may effectively sensitize the guinea-pig heart to pharmacological I(Kr) blockade.

Action Potentials↗