The Effect of Different Concentrations of Halothane Anaesthesia on the Electroencephalograph of Rock Doves (Columba livia)

Anaesthetic agents and doses used can significantly impact cerebrocortical responsiveness as assessed by electroencephalography (EEG). The objective of this study was to evaluate the effect of three different halothane concentrations on the EEG of Rock Doves using measures of frequency distribution and burst suppression. Eight healthy Rock Doves (Columba livia) were anaesthetized with halothane in oxygen, their tracheas intubated and their lungs mechanically ventilated. Five minutes of EEG were recorded at three multiples of minimum anaesthetic concentration (MAC), 1× MAC (1.6%), 1.5× MAC (2.4%) and 2× MAC (3.2%), presented in ascending then descending order. Fast Fourier transformation of the raw EEG record gave the median frequency (F50), spectral edge frequency (F95) and the total power (Ptot). Burst suppression, expressed as inactive compared to active EEG (%), was calculated on a representative two-minute section of the raw EEG. Data were analysed using repeated-measures one-way ANOVA with Tukey post hoc correction for comparison of 1×, 1.5× and 2× MAC. Three of eight birds demonstrated negligible (<1%) burst suppression. No effect of halothane concentration on burst suppression incidence was seen. A significant decrease in all measured frequency variables (F50, p = 0.04; F95p = 0.02; Ptotp < 0.0001) occurred between 1× and 2× MAC. Halothane anaesthesia at MAC multiples of 1×, 1.5× and 2× in the Rock Dove can be considered suitable where cortical responsiveness is desired.

Comparative evaluation of halothane anaesthesia in medetomidine–butorphanol and midazolam–butorphanol premedicated water buffaloes (Bubalus bubalis)

Six clinically healthy male water buffaloes (Bubalus bubalis) 2–3 years of age and weighing 290–325 kg were used for 2 different treatments (H1 andH2). The animals of groupH1 were premedicated with medetomidine (2.5 g/kg, i.v.) and butorphanol (0.05 mg/kg, i.v.), while in groupH2 midazolam (0.25 mg/kg) and butorphanol (0.05 mg/kg) were used intravenously. Induction of anaesthesia was achieved by 5%thiopental sodium inH1 (3.85±0.63 mg/kg) and H2 (6.96 ± 0.45 mg/kg) groups. The anaesthesia was maintained with halothane in 100 % oxygen through a large animal anaesthetic machine. Better analgesia and sedation with a significantly lower dose of thiopental for induction and significantly higher values of sternal recumbency time and standing time were recorded in group H1 than in group H2 , whereas no significant (P > 0.05) difference for the halothane concentration was observed between groups H1 and H2. Significant decrease in heart rate was observed in group H1 whereas it significantly increased in group H2. In both groups, RR decreased during the preanaesthetic period, which increased significantly (P<0.01) after halothane administration. In both groups a significant (P<0.01) fall in RT was recorded from 20 min to the end of observation period. A significant (P < 0.05) fall in MAP was observed in group H1 from 15 min until the end, while in group H2 MAP increased nonsignificantly (P > 0.05) after premedication and a significant (P<0.05) occurredafter thiopental administration. In both groups a significant (P<0.01) increase in CVP and a significant (P<0.01) decrease in SpO2 were observed after premedication which persisted up to 120 min. ECG changes included significant (P<0.01) decrease and increase in QRS amplitudes in groupsH1 andH2 respectively, a significant (P < 0.05) increase in PR interval was recorded at 15 min in group H1, a significant (P<0.05) decrease in PR interval in groupH2 , a significant (P<0.05) decrease in T wave amplitude in groupH1, and a significant (P<0.01) increase in duration of T wave in groupH1 . It is concluded that both combinations can be used safely in buffaloes for surgery of 2 h duration but better sedation, analgesia and muscular relaxation and more dose sparing effect on anaesthetics and shorter recovery times were observed in group H1.

Partial intravenous anaesthesia in 5 horses using ketamine, lidocaine, medetomidine and halothane

A partial intravenous protocol was used successfully to maintain anaesthesia in 5 healthy horses. Horses were premedicated with acepromazine, romifidine and butorphanol, induced with guaifenesin and ketamine and maintained on a constant rate infusion of lidocaine, ketamine and medetomidine together with halothane inhalation anaesthesia. Mean end-tidal halothane concentration to maintain a surgical plane of anaesthesia was 0.8 ± 0.2 %. Mean dobutamine requirement to maintain mean arterial pressure above 9.31 kPa was 0.42 ± 0.3 µg/kg/min. The administration of relatively low doses of lidocaine, ketamine and medetomidine together with halothane resulted in haemodynamically stable anaesthesia, followed by smooth recovery.

Mg2+Dependence of Halothane-induced Ca2+Release from the Sarcoplasmic Reticulum in Skeletal Muscle from Humans Susceptible to Malignant Hyperthermia

Background Recent work suggests that impaired Mg(2+) regulation of the ryanodine receptor is a common feature of both pig and human malignant hyperthermia. Therefore, the influence of [Mg(2+)] on halothane-induced Ca(2+) release from the sarcoplasmic reticulum was studied in malignant hyperthermia-susceptible (MHS) or -nonsusceptible (MHN) muscle. Methods Vastus medialis fibers were mechanically skinned and perfused with solutions containing physiologic (1 mm) or reduced concentrations of free [Mg(2+)]. Sarcoplasmic reticulum Ca(2+) release was detected using fura-2 or fluo-3. Results In MHN fibers, 1 mm halothane consistently did not induce sarcoplasmic reticulum Ca(2+) release in the presence of 1 mm Mg(2+). It was necessary to increase the halothane concentration to 20 mm or greater before Ca release occurred. However, when [Mg(2+)] was reduced below 1 mm, halothane became an increasingly effective stimulus for Ca(2+) release; e.g., at 0.4 mm Mg(2+), 58% of MHN fibers responded to halothane. In MHS fibers, 1 mm halothane induced Ca(2+) release in 57% of MHS fibers at 1 mm Mg(2+). Reducing [Mg(2+)] increased the proportion of MHS fibers that responded to 1 mm halothane. Further experiments revealed differences in the characteristics of halothane-induced Ca(2+) release in MHS and MHN fibers: In MHN fibers, at 1 mm Mg(2+), halothane induced a diffuse increase in [Ca(2+)], which began at the periphery of the fiber and spread slowly inward. In MHS fibers, halothane induced a localized C(2+)a release, which then propagated along the fiber. However, propagated Ca(2+) release was observed in MHN fibers when halothane was applied at an Mg(2+) concentration of 0.4 mm or less. Conclusions When Mg(2+) inhibition of the ryanodine receptor is reduced, the halothane sensitivity of MHN fibers and the characteristics of the Ca release process approach that of the MHS phenotype. In MHS fibers, reduced Mg(2+) inhibition of the ryanodine receptor would be expected to have a major influence on halothane sensitivity. The Mg dependence of the halothane response in MHN and MHS may have important clinical implications in circumstances where intracellular [Mg(2+)] deviates from normal physiologic concentrations.

Antagonism of the Antinocifensive Action of Halothane by Intrathecal Administration of GABA-A Receptor Antagonists

Background The hind brain and the spinal cord, regions that contain high concentrations of gamma-aminobutyric acid (GABA) and GABA receptors, have been implicated as sites of action of inhalational anesthetics. Previous studies have established that general anesthetics potentiate the effects of gamma-aminobutyric acid at the GABAA receptor. It was therefore hypothesized that the suppression of nocifensive movements during anesthesia is due to an enhancement of GABAA receptor-mediated transmission within the spinal cord. Methods Rats in which an intrathecal catheter had been implanted 1 week earlier were anesthetized with halothane. Core temperature was maintained at a steady level. After MAC determination, the concentration of halothane was adjusted to that at which the rats last moved in response to tail clamping. Saline, a GABAA, a GABAB, or glycine receptor antagonist was then injected intrathecally. The latency to move in response to application of the tail clamp was redetermined 5 min later, after which the halothane concentration was increased by 0.2%. Response latencies to application of the noxious stimulus were measured at 7-min intervals during the subsequent 35 min. To determine whether these antagonists altered baseline response latencies by themselves, another experiment was conducted in which the concentration of halothane was not increased after intrathecal administration of GABAA receptor antagonists. Results Intrathecal administration of the GABAA receptor antagonists bicuculline (0.3 micrograms) or picrotoxin (0.3, 1.0 micrograms) antagonized the suppression of nocifensive movement produced by the small increase in halothane concentration. In contrast, the antinocifensive effect of the increase in halothane concentration was not attenuated by the GABAB receptor antagonist CGP 35348 or the glycine receptor antagonist strychnine. By themselves, the GABAA receptor antagonists did not alter response latency in rats anesthetized with sub-MAC concentrations of halothane. Conclusions Intrathecal administration of bicuculline or picrotoxin, at doses that do not change the latency to pinch-evoked movement when administered alone, antagonized the suppression of noxious-evoked movement produced by halothane concentrations equal to or greater than MAC. These results suggest that enhancement of GABAA receptor-mediated transmission within the spinal cord contributes to halothane's ability to suppress nocifensive movements.

Association between halothane and oxygenated solvents by 1H NMR spectroscopy

Using 1H NMR spectroscopy the complex-formation equilibria between halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) and methyl tert-butyl ether or tetrahydrofuran in various inert solvents (hexane, heptane, decane, cyclohexane) were measured as a function of temperature. For two different association models (ideal solution and athermal solution), assuming only the formation of a 1:1 H-bonded complex, the equilibrium constants and the standard enthalpies of the complex-formation reaction were calculated. The ideal solution model provides values of the equilibrium constant that differ for different inert solvents. The athermal solution model makes this false solvent effect much smaller. For the low halothane concentration used, its dimerization was neglected. This assumption was verified experimentally. Keywords: 1H NMR, association, complex formation, halothane.

A System Model for Halothane Closed-Circuit Anesthesia

Background Previously, the authors described a physiologic model for closed-circuit inhalational anesthesia. The basic version of this system model was clinically validated for isoflurane. An extended version adopted nonpulmonary elimination causing a constant fraction of anesthetic to be irreversibly lost. This version improved the accuracy of the model for enflurane. The model's performance for other inhalational anesthetics that are not biochemically inert, such as halothane, remained to be evaluated. Methods The current study quantified the predictive performance of four versions of the model by comparison of the predicted and measured alveolar halothane concentration-time profiles in 53 patients. Version A did not incorporate nonpulmonary elimination, whereas version D adopted a nonlinear hepatic nonpulmonary elimination following Michaelis-Menten kinetics. A and D used fixed partition coefficients. Their counterparts, A' and D', were formulated to examine the impact of age-adjusted partition coefficients on the accuracy of our model. Each concentration measured by mass spectrometry was compared to four predicted concentrations calculated by four computer simulations (one per version). For each patient, the authors calculated the root mean squared error (rmse; typical error size), bias (systematic component), and scatter of the prediction errors. Results Fifty-three patients were anesthetized with 330 ml of liquid halothane via 426 bolus injections during more than 61 h; 21,890 alveolar concentrations (average 0.6 vol%) were measured. Version D' showed the best overall performance with an rmse of 19.6 +/- 7.2%, a bias of 0.5 +/- 15.9%, and a scatter of 13.2 +/- 3.5% (mean +/- SD). Conclusions The model incorporating nonpulmonary elimination and age-adjusted partition coefficients (D') is sufficiently reliable and accurate to represent halothane closed-circuit anesthesia. This system model, with its various versions, is a valuable tool to predict the dynamics of isoflurane, enflurane, and halothane for clinical, educational, and research purposes.

Breathing patterns in infants and children under halothane anesthesia: effect of dose and CO2

We studied the amplitude, timing, and shape of the airflow waveform at the mouth of spontaneously breathing children under two sets of conditions: 1) in 30 children aged 9 wk-4.5 yr at 2, 1, and 0% inspired halothane concentration and 2) in 22 children aged 5 mo-7 yr during hyperoxic CO2 rebreathing while recovering from anesthesia. Compared with control values, the relative changes in breath parameters at 1 and 2% halothane were, respectively, as follows: total cycle time -19 and -31%, tidal volume (VT) -30 and -44%, minute ventilation -11 and -17%, and VT/inspiratory time (TI) -16 and -20%. Parameters of timing and breath shape did not change except for the significant but small increase in TI/total cycle time (by 6 and 8%, respectively). With CO2 rebreathing, parameters reflecting inspiratory drive increased significantly in all patients as shown by the slopes of the regressions of these parameters against end-tidal PCO2. Mean slopes expressed in %control value per millimeter of mercury CO2 were 12.1 for minute ventilation, 8.3 for VT, and 10.67 for VT/TI. Parameters reflecting the timing and breath shape remained essentially unchanged. Our results suggest that, in children under halothane anesthesia, the amplitude, timing, and shape of the breathing pattern are controlled independently. In particular, the amplitude and timing of the breath may vary widely without any significant change in the shape.