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PubMed2002

The rate of loss of eyelid reflex following thiopental administration in hypo- and hypergonadism in rabbits.

BACKGROUND: The aim of this research was to explain whether different hormonal conditions caused by disturbed concentrations of estrogens and progesterone might lead to alteration of CNS reaction following administration of the hypnotic agent thiopental. The investigated factor was the rate of loss of the eyelid reflex after intravenous thiopental administration, since this corresponds with loss of consciousness. MATERIAL/METHODS: The investigation was performed in 24 sexually mature female Chinchilla rabbits divided into 4 groups of 6 rabbits each. The animals were oophorectomized (hypoprogesterone/hypoestrogen), hyperestrogen (sham surgery plus estradiol injections), hyperprogesterone (sham surgery plus 17 alpha-hydroxyprogesterone injections), or normal (sham surgery). Twelve weeks later, thiopental (40 mg/ml) was infused through the intravenous cannula at a constant rate (90 ml/hour) until loss of the eyelid reflex, at which time blood was sampled for determination of thiopental, b-estradiol, progesterone and 17 alpha-hydroxyprogesterone concentrations. The ANOVA and Tukey tests were applied in statistical analysis (p=0.05). RESULTS: Hyperprogesterone rabbits lost consciousness faster (138 +/- 34.6 sec), at a lower plasma thiopental concentration (46.3 +/- 6.6 microg/ml), and required less thiopental (24.63 +/- 6.44 mg/kg) than controls; hypoprogesterone rabbits lost consciousness slower (207.5 +/- 30.9 sec), at a higher plasma thiopental concentration (129.2 +/- 24.9 microg/ml), and required more thiopental (38.51 +/- 2.33 mg/kg) than controls. The time of sleep induction in the control group was 190 +/- 25.7 sec.; the serum thiopental concentration was 77.8 +/- 13.9 microg/ml, and the total thiopental consumption was 35.8 +/- 3.51 mg/kg. Estrogen status has no effect. CONCLUSIONS: Various hormonal states are accompanied by different CNS reactions to thiopental. Among the studied groups of sex steroids, only progestins significantly modify the CNS response to barbiturate infusion.

17-alpha-Hydroxyprogesterone↗
PubMed1996

The systemic and cerebral kinetics of thiopental in sheep: enantiomeric analysis.

Thiopental is used as a racemate (rac-thiopental). Enantiomeric pharmacokinetic differences could therefore influence the onset and duration of anesthesia of rac-thiopental. We studied the systemic and cerebral kinetics of R(+)- and S(-)-thiopental in five adult ewes after a 2-min intravenous infusion of 500 mg rac-thiopental sodium. Systemic kinetic values were determined from the time course of concentrations in arterial plasma; cerebral kinetic values were deduced from the time course of the concentration differences between arterial and superior sagittal sinus blood plasma. Enantiomeric differences were found in both sites, with the (R:S) ratio of thiopental enantiomer blood concentrations initially being > or = 1 then decreasing to < 1 after approximately 60 min. This is consistent with the finding of the mean total body clearance of R(+)-thiopental being 17% (SD 12%) greater than that of S(-)-thiopental (P = .04). Sagittal sinus plasma concentrations of both enantiomers followed closely behind those in arterial plasma and this is consistent with facile bidirectional exchange of thiopental between plasma and brain. No significant differences were found between enantiomers in the rates of brain influx or efflux. Onset and regression of anesthesia occurred while the enantiomer blood concentrations were similar. Hence published pharmacokinetic-pharmacodynamic models of the onset of thiopental effects probably are not significantly compromised by neglecting the enantiomeric duality of thiopental, but models based on its elimination kinetics could be compromised if enantiomeric differences are neglected.

Anesthetics, Intravenous↗
PubMed1991

Pharmacodynamic characterization of the electroencephalographic effects of thiopental in rats.

We have developed a chronically instrumented rat model that uses changes in electroencephalographic wave forms to estimate continuously the degree of central nervous system (CNS) depression induced by thiopental. Such changes were subject to aperiodic signal analysis, a technique that breaks down the complex EEG into a series of discreet neurologic "events" which are then quantitated as waves/sec. We thus obtained a continuous measure of CNS drug effect. In addition we continuously recorded central arterial blood pressure and heart rate and monitored ventilatory status using arterial blood gas determinations. We also determined, with frequent arterial blood sampling, the distribution and elimination of thiopental in individual animals. The time lag occurring in the curve representing arterial concentration of thiopental vs. EEG effect suggests that arterial plasma is not kinetically equivalent to the EEG effect site. Application of semiparametric pharmacodynamic modeling techniques enabled us to estimate equilibration rate constant (Keo) for concentrations of thiopental between arterial plasma and the effect site. The half-life for equilibration of thiopental with the EEG (CNS) effect was less than 80 sec. Knowledge of the rate of equilibration permitted characterization of the relationship between the steady state plasma concentrations and CNS effect of thiopental, as measured by activation and slowing of the EEG. At concentrations of thiopental below 5 micrograms/ml, EEG activity was 180% higher than during the baseline awake state. Thiopental produced an activated EEG over more than 20% of the concentration-effect relationship. Further increases in the concentration of thiopental at the site of effect depressed EEG activity progressively until complete suppression of the EEG signal occurred (at which time, the concentration was approximately 80 micrograms/ml). This report describes our model and its application to the assessment of the pharmacodynamics of thiopental as manifested by changes on the EEG.

Animals↗
PubMed1976

Gas chromatographic assay for free and total plasma levels of thiopental.

A rapid gas chromatographic assay for the determination of free and total plasma thiopental is described. Free thiopental was obtained by ultrafiltration through Amicon Centroflo membrane cones. Gas chromatographic assay utilized secobarbital as an internal standard and employed on-column methylation of the barbiturates to improve peak resolution. In 73 blood samples from 22 patients total thiopental concentrations ranged from 4.2 to 134 mug/ml plasma, with a mean of 28 mug/ml. Free thiopental values ranged from 8.6 to 22.7 per cent of total, with a mean of 13.7 per cent free thiopental and a standard deviation of 3.2 per cent. At a total thiopental level of 10 mug/ml, unbound thiopental averaged 10.7 per cent with ultrafiltration, compared with 11.5 per cent with equilibrium dialysis. Assays of thiopental by gas chromatography and 14C scintillation counting gave similar results. There were progressive increases in the percentages of thiopental that were unbound when thiopental was added to plasma, purified crystalline albumin (4.5 g/l), and normal serum albumin (5 g/l), and a solution of purified protein fractions (5 g/l). Differences in protein binding determined by this method and previously reported methods are discussed.

Chromatography, Gas↗
PubMed1981

Hypothermia plus thiopental: prolonged electroencephalographic suppression.

Duration of EEG suppression was compared to three groups of patients undergoing hypothermic cardiopulmonary bypass (CPB) at 25-30 degrees C under halothane-nitrous oxide anesthesia. Group I (n = 8) received three doses of thiopental (8 mg/kg i.v.): 1) for induction of anesthesia, 2) immediately after the institution of CPB, and 3) just after emergence from CPB. Group II (n = 5) received no thiopental. Group III (n = 4) received thiopental, 8 mg/kg administered intravenously, during CPB only. An unexpectedly prolonged duration of EEG suppression (26.1 min) was noticed in Group I patients with thiopental and hypothermia in combination, as compared with 4.8 min of suppression in Group II patients during hypothermic CPB without thiopental. To rule out a possible cumulative effect of thiopental administration, Group III patients were studied. With only a single dose of thiopental, administered during CPB, 29.3 min of EEG suppression was noticed. Mild cardiovascular depression occurred with thiopental administration during induction of anesthesia, whereas mild-to-moderate depression was associated with thiopental administration following emergence from CPB. It appears that thiopental and hypothermia, when administered in combination in modest doses during CPB, result in profound depression of cerebral electrical activity and presumably cerebral metabolism.

Adult↗
PubMed1984

Thiopental potentiation of isolated rabbit pulmonary artery contractions with alpha receptor agonists.

The effects of thiopental sodium on the adrenergic neuroeffector junction were studied in isolated rabbit pulmonary arteries. Basal tension was not altered by thiopental (2 X 10(-5) and 10(-4) M) but was increased by high concentrations of thiopental (5 X 10(-4) M). Thiopental (10(-4) and 5 X 10(-4) M) potentiated contractions induced by transmural electrical stimulation. Contractile responses to exogenously applied low concentrations of norepinephrine (NE) were potentiated by thiopental (2 X 10(-5), 10(-4) and 5 X 10(-4) M), whereas those to high concentrations were not altered. In strips previously incubated in 1-[7,8-3H]-NE (10(-7) M), the release of [3H] induced by transmural stimulation (5 Hz) was not altered by thiopental (10(-4) and 5 X 10(-4) M). Potentiation by thiopental (10(-4) M) of the responses to transmural stimulation was not affected by prior application of cocaine or hydrocortisone. Contractions induced by alpha receptor agonists (phenylephrine and methoxamine) were potentiated by thiopental (10(-4) M), while those induced by acetylcholine were not altered. Contractile responses to potassium chloride were attenuated by thiopental (10(-4) M). Amobarbital sodium and pentobarbital sodium (10(-4) M, respectively) attenuated contractions induced by NE. It may be concluded that thiopental specifically increases the responsiveness of postsynaptic alpha receptors to NE.

Acetylcholine↗
PubMed1994

Plasma, brain, and spinal cord concentrations of thiopental associated with hyperalgesia in the rat.

BACKGROUND: Although low doses of barbiturates are widely believed to increase sensitivity to pain, studies of the electrophysiologic effects of these drugs on the neurons involved in nociception in the spinal cord have detected only depressant effects. The goal of the studies reported here was to quantify the hyperalgesia resulting from low-dose thiopental infusions and to measure the associated concentrations of thiopental in the plasma, brain, and spinal cord. METHODS: Nociception was measured using the threshold for motor response to pressure stimulation of the tail (nociceptive threshold) and tail flick latency in the rat. Thiopental was administered by intravenous infusions designed to produce plasma concentrations that either slowly increased or remained at a steady state. Plasma and tissue thiopental concentrations were measured by high-performance liquid chromatography. RESULTS: We observed a reduction in nociceptive threshold that was correlated with the plasma thiopental concentration over the range 2-20 micrograms.ml-1 (7.6-76 microM). The relationship was nonlinear. Nociceptive threshold reached a nadir (36% less than control values) at a mean plasma thiopental concentration of 13.7 micrograms.ml-1 (51.9 microM). The steady-state study showed a similar reduction in nociceptive threshold, with an equilibrium plasma thiopental concentration of 7.6 +/- 1.3 micrograms.ml-1 (28.8 +/- 4.9 microM). Concentrations of thiopental in brain and spinal cord samples were 1.7 +/- 0.03 and 3.5 +/- 1.7 micrograms.g-1, respectively. CONCLUSIONS: These studies confirm previous reports of hyperalgesia in association with small doses of thiopental. Reductions in nociceptive threshold and tail flick latency were observed in association with spinal cord concentrations of thiopental in a range reported by others to depress the electrophysiologic activity of neurons involved in nociception.

Animals↗
PubMed1994

Dexmedetomidine decreases thiopental dose requirement and alters distribution pharmacokinetics.

BACKGROUND: alpha 2-Adrenergic agonists such as dexmedetomidine can be used to reduce the dose requirement of intravenous and volatile anesthetics. Whereas dexmedetomidine and volatile anesthetics interact pharmacodynamically (reduction of MAC), the mechanism of interaction between dexmedetomidine and intravenous anesthetics is not known. METHODS: Fourteen male ASA physical status 1 patients were randomly assigned to serve as control subjects (n = 7) or to be treated with dexmedetomidine (n = 7; 100, 30, and 6 ng.kg-1.min-1 for 10 min, 15 min, and thereafter, respectively). After 35 min, in all patients, thiopental (100 mg/min) was infused until burst suppression appeared in the raw tracing of the electroencephalogram. By using concentrations of thiopental in plasma and the electroencephalogram as a continuous pharmacologic effect measure, the apparent effect site concentrations for thiopental were estimated in both groups. Three-compartment pharmacokinetics were calculated for thiopental. RESULTS: Dexmedetomidine reduced the thiopental dose requirement for electroencephalographic burst suppression by 30%. There was no difference in estimated thiopental effect site concentrations between dexmedetomidine and control patients, suggesting the absence of a major pharmacodynamic interaction. Dexmedetomidine significantly decreased distribution volumes (V2, V3, and Vdss) and distribution clearances (Cl12 and Cl13) of thiopental. CONCLUSIONS: The thiopental dose-sparing effect of dexmedetomidine on the electroencephalogram is not the result of a pharmacodynamic interaction but rather can be explained by a dexmedetomidine-induced decrease in thiopental distribution volume and distribution clearances. Dexmedetomidine reduces thiopental distribution, most probably by decreasing cardiac output and regional blood flow.

Adrenergic alpha-Antagonists↗
PubMed1996

Effects of pre- and postischemic administration of thiopental on transmitter amino acid release and histologic outcome in gerbils.

BACKGROUND: The mechanism by which barbiturates protect neurons against ischemia is unclear, particularly when they are given after ischemia or reperfusion begins. Because an excess release of excitatory neurotransmitters causes postsynaptic membrane depolarization, which triggers neuronal damage in ischemia, the effects of thiopental on histologic outcome, ischemia-induced amino acid release, and anoxic depolarization in gerbils were studied. METHODS: The effects of different doses of thiopental administered before or after ischemia were examined morphologically by assessing delayed neuronal death in hippocampal CA1 pyramidal cells produced by forebrain ischemia for 3 min in gerbils. The ischemia-induced changes in output of aspartate, glutamate, glycine, taurine, and gamma-aminobutyric acid were measured using a microdialysis-high-performance liquid chromatography procedure, and the differences among a halothane-anesthetized group, a thiopental-administered group, and a group given thiopental after a period of ischemia were evaluated. The changes induced in the direct-current potential in the hippocampal CA1 area by forebrain ischemia were compared in animals anesthetized with halothane and those given thiopental. RESULTS: Preischemic administration of thiopental at all doses decreased the risks for delayed neuronal death (P < 0.01). Post-ischemic administration at a dosage of 2 mg.kg-1.min-1 for 60 min protected neurons, but the same dose for 10 min did not ameliorate the cell injury. Forebrain ischemia produced marked increases in all amino acids 3 to 6 min after the start of recirculation in the halothane-anesthetized gerbils, whereas thiopental anesthesia (2 mg.kg-1.min-1) reduced these increases throughout the experimental period, except for glycine (P < 0.01). The initiation of thiopental after reflow did not markedly diminish these increases. Thiopental anesthesia prolonged the onset of anoxic depolarization and reduced its maximal amplitude. CONCLUSIONS: Thiopental helps protect the brain from ischemia, although treatment with this agent after ischemia requires a larger dose than that before ischemia. The effect of preischemic treatment may be related to the suppression of the excitatory amino acid release and the direct-current potential shift.

Animals↗
PubMed2005

Thiopental-induced apoptosis in lymphocytes is independent of CD95 activation.

BACKGROUND: Barbiturate coma is used in patients with traumatic brain injury whenever increases in intracranial pressure remain unresponsive to less aggressive therapeutic regimens. However, barbiturate-mediated neuroprotection correlates with lymphopenia, which increases the risk of infection. The mechanisms by which barbiturates lead to lymphopenia remain to be determined. METHODS: Freshly isolated human lymphocytes and Jurkat cells were incubated with the barbiturate thiopental for 24 and 48 h. Apoptosis was measured by fluorescein isothiocyanate-Annexin and propidium iodide staining, rhodamine 123 staining, and the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method. Caspase-3 activity was detected by Western blot and substrate cleavage assay. RESULTS: Thiopental dose-dependently (5-500 microg/ml) increased apoptosis in Jurkat cells from basal levels (4.4 +/- 1.9%) to 29.7 +/- 2.8% after 24 h and 39.7 +/- 3.2% after 48 h, whereas in lymphocytes, thiopental-induced necrosis was observed. Parallel to apoptosis, thiopental dose-dependently increased caspase-3-like activity in Jurkat cells. However, the pan-caspase inhibitor z-VAD-fmk (20 microm) only marginally reduced thiopental-induced (250 microg/ml) apoptosis in Jurkat cells (20.2 +/- 2.5 to 17.2 +/- 2.5%) and necrosis in lymphocytes (39.2 +/- 7.5 to 30.7 +/- 14%). In contrast, anti-CD95-induced apoptosis in Jurkat cells (27.0 +/- 2.0%) was completely blocked by z-VAD-fmk (8.1 +/- 1.8%). Neither expression of CD95 on Jurkat cells nor pretreatment with a neutralizing anti-CD95 antibody influenced thiopental-induced apoptosis, indicating that thiopental induces apoptosis independently of the CD95 system. The nuclear factor kappaB inhibitor gliotoxin accelerated both thiopental- and CD95-mediated apoptosis, indicating a mutual control mechanism of thiopental- and CD95-induced apoptosis. CONCLUSIONS: Thiopental directly induces cell death in lymphocytes and Jurkat cells by a CD95-independent mechanism.

Apoptosis↗
PubMed1992

Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts.

The authors examined direct myocardial and coronary vascular responses to the anesthetic induction agents etomidate, ketamine, midazolam, propofol, and thiopental and compared their effects on attenuating autoregulation of coronary flow as assessed by changes in oxygen supply/demand relationships. Spontaneous heart rate, atrioventricular conduction time during atrial pacing, left ventricular pressure (LVP), coronary flow (CF), percent oxygen extraction, oxygen delivery, and myocardial oxygen consumption (MVo2) were examined in 55 isolated guinea pig hearts divided into five groups of 11 each. Hearts were perfused at constant pressure with one of the drugs administered at steady-state concentrations increasing from 0.5 microM to 1 mM. Adenosine was given to test maximal CF. At concentrations below 10 microM no significant changes were observed; beyond 50 microM for midazolam, etomidate, and propofol, and 100 microM for thiopental and ketamine, each agent caused progressive but differential decreases in heart rate, atrioventricular conduction time (leading to atrioventricular dissociation), LVP, +dLVP/dtmax, percent oxygen extraction, and MVo2. The concentrations (microM) at which +dLVP/dtmax was reduced by 50% were as follows: etomidate, 82 +/- 2 (mean +/- SEM); propofol, 91 +/- 4; midazolam, 105 +/- 8; thiopental, 156 +/- 11; and ketamine, 323 +/- 7; the rank order of potency was etomidate = propofol = midazolam greater than thiopental greater than ketamine; results were similar for LVP. At the 100 microM concentration, CF was decreased 11% +/- 2% by ketamine and 5% +/- 3% by thiopental but was increased 17% +/- 6% by etomidate, 21% +/- 5% by midazolam, and near maximally to 57% +/- 10% by propofol; MVo2 was decreased 8% +/- 4% by thiopental, 10% +/- 5% by ketamine, 19% +/- 5% by midazolam, 29% +/- 7% by etomidate, and 37% +/- 5% by propofol; oxygen delivery/MVo2 was unchanged by thiopental and ketamine but was increased 62% +/- 7% by midazolam, 71% +/- 9% by etomidate, and 150% +/- 15% by propofol. Between 100 microM and 1 mM, thiopental and ketamine did not increase CF but decreased MVo2 and percent oxygen extraction, whereas propofol maximally increased CF and decreased MVo2 and midazolam and etomidate had intermediate effects. These results indicate that on a molar basis, propofol, and less so midazolam and etomidate, depress cardiac function moderately more than thiopental and ketamine, and that propofol markedly attenuates autoregulation by causing coronary vasodilation. With doses used to induce anesthesia, propofol and thiopental appear to depress cardiac function more than ketamine or etomidate.

Adenosine↗
PubMedDate not supplied

The influence of selected antiarrhythmic drugs on the hemodynamic parameters in rabbits during anesthesia. Part II. Thiopental anesthesia.

The aim of the study was to investigate the combined influence of thiopental and antiarrhythmic drugs: procainamide, N-acetylprocainamide, verapamil or propranolol on hemodynamic parameters in rabbits: arterial blood pressure, heart rate, cardiac output, stroke volume, peripheral vascular resistance, renal and hepatic blood flows. Propranolol used during thiopental anesthesia deepened the decrease of hepatic and renal blood flow resulting from the action of the anesthetic drug. Verapamil in a dose that did not change hepatic blood flow caused significant decrease of that parameter during thiopental anesthesia. Other hemodynamic changes observed after administration of antiarrhythmic drugs during thiopental anesthesia are essentially similar to those resulting from the action of antiarrhythmic drugs alone. The administration of procainamide or N-acetylprocainamide during thiopental anaesthesia in rabbits had no significant influence on hemodynamic changes evoked by thiopental alone. Verapamil injected to rabbits together with thiopental caused a significant decrease of blood flow in the liver, which was not observed after thiopental alone or verapamil alone. Propranolol injection together with thiopental caused a decrease of blood pressure, heart rate, cardiac output but an increase of vascular peripheral resistance, which was similar to the action of propranolol alone. Propranolol administered during thiopental anesthesia caused a significant decrease of the renal and hepatic blood flow, more marked than after the injection of that beta-blocker alone.

Anesthetics, Intravenous↗
PubMed1981

Effect of sulfadimethoxine on thiopental distribution and elimination in rats.

The effect of sulfadimethoxine on the distribution and elimination of thiopental was examined by comparing the change in the steady-state volume of distribution (Vss) determined from both in vivo plasma elimination and in vitro serum and tissue binding studies in rats. The plasma disappearance of thiopental after a 12-mg/kg iv dose followed a biexponential decline in both the control and sulfadimethoxine-treated rats. The plasma thiopental concentrations under the steady-state plasma sulfadimethoxine concentration (500 micrograms/ml) were significantly lower than those of the control rats. In the sulfadimethoxine-treated rats, the pharmacokinetic parameter beta significantly decreased while Vss significantly increased to 3.6-fold that of the control rats. With sulfadimethoxine, a significant increase was observed in the apparent dissociation constant (Kd) of thiopental to serum protein by equilibrium dialysis, but the total number of binding sites was not altered. The in vitro serum free fraction of thiopental was increased to about 2.6-fold in the presence of sulfadimethoxine. The free fraction of thiopental in the main distribution tissues (liver, muscle, and adipose) was determined by equilibrium dialysis with and without sulfadimethoxine. No significant changes were observed in the presence of sulfadimethoxine. The calculated Vss, determined by the free fractions from in vitro binding experiments, also showed a significant increase. The ratio of Vss with sulfadimethoxine to that of the control rats was 2.8. The total clearance did not change, but the intrinsic clearance decreased to one-half of that of the control rats due to the increase of the serum free fraction by sulfadimethoxine. It was concluded that sulfadimethoxine caused a displacement of thiopental in plasma protein binding, which significantly increased the free fraction of thiopental, and this result may explain the significant increase of Vss and the decrease of both beta and intrinsic clearance. Tissue binding of thiopental, however, was unaffected by sulfadimethoxine.

Animals↗
PubMed1983

Pharmacokinetics and anesthetic potency of a thiopental isomer.

In developing a high-performance liquid chromatographic assay for thiopental [5-ethyl-5-(1-methylbutyl)-2-thiobarbituric acid], a thiopental isomer [5-ethyl-5-(1-ethylpropyl)-2-thiobarbituric acid] was found. This isomer occurs (6-7%) in supposedly pure thiopental and in the commercially available thiopental sodium administered to patients for induction of anesthesia. A similar type of isomer also occurs in pentobarbital, the oxybarbiturate analogue of thiopental. Because the disposition and anesthetic potency of the isomer is unknown, its pharmacokinetic properties were determined in humans and its anesthetic potency in mice. In five surgical patients, the terminal elimination half-life, clearance, and volume of distribution at steady state of the isomer were not statistically different from those of thiopental. In mice, the isomer proved to be as effective as thiopental for induction of anesthesia. The LD50 and sleep time at one-half the LD50 did not statistically differ between the two compounds in mice. The close structural similarity of thiopental and the isomer results in similar pharmacokinetic and anesthetic properties. It does not appear critical that the isomer be separated from thiopental in subsequent pharmacological research.

Anesthetics↗
PubMed1991

A comparison of etomidate and thiopental anesthesia for cardioversion.

Sixteen ASA class II or III male patients (aged, 52 to 66 years) undergoing elective cardioversion were randomly assigned to receive either thiopental or etomidate according to an observer-blinded, parallel study design. The appropriate drug was administered in 2-mL aliquots every 15 seconds until the patient no longer responded to verbal commands, at which time cardioversion was attempted. The total dose for induction was 0.22 +/- 0.2 mg/kg and 3.2 +/- 0.4 mg/kg for etomidate and thiopental, respectively. The cardiorespiratory data after induction were evaluated for maximal percent change from baseline. The baseline heart rate was 106 +/- 6 beats/min and 98 +/- 8 beats/min for the etomidate and thiopental groups, respectively (mean +/- SEM). The heart rate decreased 5% after induction with etomidate and increased 7% with thiopental (P less than 0.05). The baseline mean arterial pressure (MAP) was 96 +/- 3 mm Hg and 105 +/- 11 mm Hg for the etomidate and thiopental groups, respectively (mean +/- SEM). The MAP decreased 4% with etomidate and 3% with thiopental. Respiratory rate was significantly increased by 22% after etomidate compared with a 22% decrease in respiratory rate with thiopental (P less than 0.05). Seven of eight patients in the thiopental group required only one countershock, whereas four of eight patients in the etomidate group required only one shock. One patient in each group could not be successfully cardioverted. Recovery time and clinical side effects were similar between groups except for mild myoclonus in the etomidate group. Titration to effect of either etomidate or thiopental provided satisfactory anesthesia for elective cardioversion in hemodynamically stable patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2005

Determination of thiopental in urine sample with high-performance liquid chromatography using iodine-azide reaction as a postcolumn detection system.

The reaction between iodine and azide ions induced by thiopental was utilized as a postcolumn reaction for chromatographic determination of thiopental. The method is based on the separation of thiopental on an Nova-Pak CN HP column with an acetonitrile-aqueous solution of sodium azide as a mobile phase, followed by spectrophotometric measurement of the residual iodine (lambda=350 nm) from the postcolumn iodine-azide reaction induced by thiopental after mixing an iodine solution containing iodide ions with the column effluent containing azide ions and thiopental. Chromatograms obtained for thiopental showed negative peaks as a result of the decrease in background absorbance. The detection limit (defined as S/N=3) was 20 nM (0.4 pmol injected amount) for thiopental. Calibration graphs, plotted as peak area versus concentrations, were linear from 40 nM. The elaborated method was applied to determine thiopental in urine samples. The detection limit (defined as S/N=3) was 0.025 nmol/ml urine. Calibration graphs, plotted as peak area versus concentrations, were linear from 0.05 nmol/ml urine. Authentic urine samples were analyzed, thiopental was determined at nmol/ml urine level.

Acetonitriles↗
PubMed2001

Thiopental inhibits NF-kappaB activation in human glioma cells and experimental brain inflammation.

Thiopental is one of the intravenous anesthetics used widely. Several reports have demonstrated that thiopental inhibits the immune responses. We investigated whether or not thiopental inhibits the production of tumor necrosis factor-alpha (TNF-alpha) induced by lipopolysaccharide (LPS) in human glioma cells (A-172). Moreover, we determined whether or not thiopental modulates activation of the transcription factor NF-kappaB, a factor that regulates expression of the genes that code for proinflammatory cytokines in A-172 cells and in experimental murine brain inflammation. Thiopental inhibited TNF-alpha production induced by LPS in A-172 cells. Electrophoretic mobility shift assays demonstrated that thiopental inhibited NF-kappaB activation induced by LPS in A-172 cells. In experimental murine brain inflammation induced by intracerebroventricular injection of LPS, intraperitoneal injection of thiopental inhibited NF-kappaB activation. Western blot analysis indicated that this inhibition was linked to preservation of IkappaBalpha protein expression in A-172 cells. The chloramphenicol acetyltransferase assay revealed that NF-kappaB-dependent reporter gene expression was suppressed in A-172 cells exposed to thiopental. These findings are consistent with the idea that thiopental exerts antiinflammatory effects in cultured cells and experimental murine brain inflammation, through suppression of TNF-alpha production via inhibition of NF-kappaB activation.

Anesthetics, Intravenous↗
PubMed1991

Rectal thiopental compared with intramuscular meperidine, promethazine, and chlorpromazine for pediatric sedation.

STUDY OBJECTIVES: We studied the hypothesis that rectal thiopental is an effective agent for emergency department pediatric sedation and may have advantages over a more traditional regimen. DESIGN: Rectal thiopental 25 mg/kg was compared with the combination of meperidine 2 mg/kg, promethazine 1 mg/kg, and chlorpromazine 1 mg/kg in a prospective, randomized, double-blinded study. TYPE OF PARTICIPANTS: Children between 18 months and 6 years of age presenting to our teaching hospital ED for laceration repair were entered after the clinical decision was made to sedate. Patients with altered sensorium, medical contraindications to sedation, or medication allergy were excluded. INTERVENTIONS: After informed consent, each patient received IM injection (drug combination or placebo) and rectal suspension (rectal thiopental or placebo) simultaneously. MEASUREMENTS AND MAIN RESULTS: Vital signs, pulse oximetry, and pediatric Glasgow Coma Scores were recorded before and every 15 minutes after sedation until discharge. Intradermal lidocaine and suturing began when the patient appeared adequately sedated, and response was numerically scored. Patients were discharged when able to stand. Twenty-nine patients 34 +/- 13 months old were studied. Fifteen patients received rectal thiopental, and 14 received the drug combination. Analysis using the Wilcoxon two-sample test revealed no differences in age, sex, weight, or wound location between groups. The time course of sedation was different for the two treatment regimens. At 15 and 30 minutes after administration, patients who received rectal thiopental were more deeply sedated than those who received the drug combination, as evidenced by significantly lower Glasgow Coma Scores (P less than .05). Accordingly, time from medication administration to suturing was 29 +/- 12 minutes in the thiopental group and 54 +/- 33 minutes (P less than .01) in the drug combination group. Patients in the thiopental group also recovered more quickly and were discharged approximately one-half hour earlier than those in the drug combination group (89 +/- 25 vs 120 +/- 44 minutes, P less than .05). No difference in response to lidocaine injection or suturing was demonstrated between the groups. Laceration repair time was comparable between the groups. There were eight sedation failures (three of 15 in thiopental group and five of 14 in drug combination group, P = NS). Vital signs remained stable, no adverse reactions occurred, and no patient had decreased oxygen saturation to less than 95%. CONCLUSION: Rectal thiopental is superior to this drug combination for pediatric sedation because it can be administered painlessly, has a more rapid onset and offset of action, and is of equal safety and efficacy at the dosage studied.

Administration, Rectal↗