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PubMed1991

Increase of thiopental concentration in tissues of the rat due to an anesthesia with halothane.

In rats anesthetized with halothane (CAS 151-67-7) (1.5 vol%) and rats without any further treatment (control) the early distribution phase of thiopental (CAS 76-75-5) (i.v. 30 mg/kg) was studied. In serum and 8 tissues thiopental concentration (T) was determined using ultraviolet detection at 305 nm after extraction and TLC. In rats anesthetized with halothane, T in serum was significantly higher during the 30 min following the thiopental injection (at least +27% and maximally +51%) as compared to the control (same dose), and several pharmacokinetic parameters (e.g. central volume of distribution) were found to be changed thereby; furthermore, at 3, 10 and 30 min T was significantly increased in liver, brain, heart, lung and spleen; in kidney and skeletal muscle a rise of T was also seen, however, it occurred later (after 10 and 30 min). T in fat tissue increased time-dependently; a T-difference in adipose tissue between both groups was not observed. Thiopental was "trapped" during the early distribution phase to a considerable extent in the vessel-rich tissues of rats simultaneously anesthetized with halothane; this pharmacokinetic interaction might be explained hemodynamically: in many tissues regional blood flow is reduced by halothane; thereby a delayed "washout" of thiopental from the vessel-rich tissues could take place and redistribution would be delayed; additional factors as e.g. an increased binding of thiopental at tissue proteins could also play a role. An unusually high T was found at least temporarily in myocardial tissue due to this interaction between the two anesthetics.

Anesthesia↗
PubMed1991

Increase of thiopental concentration in rat tissues due to anesthesia with isoflurane.

Thiopental distribution was studied in rats (30 mg/kg i.v.) anesthetized simultaneously with 1.25 "rat"-MAC isoflurane. The thiopental concentration in serum and several tissues was determined UV-photometrically at 305 nm after extraction and TLC. In the serum of rats anesthetized with isoflurane the thiopental concentration was significantly increased to +39----+74% in comparison to controls during 30 min following the barbiturate injection. Also in liver, brain, heart, kidney, lung and spleen of rats anesthetized with isoflurane the thiopental concentration was significantly increased at 3 and 10 min; at 30 min the difference vs. control had vanished in brain, heart, lung and spleen. Obviously, thiopental was transiently "trapped" during the early distribution phase to a considerable amount in these vessel-rich tissues when anesthesia with isoflurane was simultaneously performed; this pharmacokinetic interaction might be explained at least to some extent hemodynamically; in many tissues regional blood flow is reduced during anesthesia with isoflurane; thereby the "washout" of thiopental from the tissues and the redistribution are delayed.

Anesthesia, Inhalation↗
PubMed1990

pH-dependent interaction of halothane upon thiopental binding to human serum albumin.

At pH 7.4 the binding of thiopental to human serum albumin (HSA) was increased in the presence of halothane. In order to obtain information about the mechanism of this interaction, in vitro binding experiments by means of equilibrium dialysis were carried out at different pH values. At pH 4.97 the binding of thiopental to HSA 1% was low (23% bound) and not influenced by halothane. An increase of thiopental binding caused by halothane could be seen at pH 7.4 (55% bound vs. 41% in the control = without halothane) and at pH 8.23 (62% vs. 54%). At pH 10.15 an opposite interaction was found: in the presence of halothane thiopental binding was considerably decreased (36.2% vs. 47.0% in the control). Evaluation of the binding parameters of experiments using increasing substrate concentrations (Scatchard plot) revealed quite different changes of the two classes of binding sites of HSA for thiopental. It is assumed that halothane causes reversible conformational changes of the albumin molecule resulting in altered binding characteristics for thiopental.

Binding Sites↗
PubMed1989

A randomized comparison between midazolam and thiopental for elective cesarean section anesthesia. I. Mothers.

In a randomized blind trial midazolam (0.3 mg kg-1) was compared with thiopental (4 mg kg-1), both combined with meperidine-nitrous oxide, for elective cesarean section anesthesia in 40 women. We found no statistically significant differences between thiopental and midazolam at induction, during operation or recovery with regard to maintenance doses, change in maternal neurologic status based on a modified Glasgow Coma Scale, systolic blood pressure, and heart rate. Induction time was 120 seconds with midazolam and 111 seconds with thiopental. There were significant differences with regard to diastolic blood pressure. Side effects occurred with approximately equal frequencies, but vomiting was significantly more frequent after thiopental. Perivenous tenderness and erythema occurred in four patients, all after thiopental. Midazolam appears to be a suitable alternative to thiopental for the induction and maintenance of anesthesia for elective cesarean section.

Adolescent↗
PubMed1987

[Intracranial pressure in patients with craniocerebral trauma after administration of propofol and thiopental].

Propofol (Disoprivan) is a rapid and effective hypnotic comparable with etomidate. Up to now, the effects on intracranial pressure (ICP) have only rarely been investigated, especially in cases with pre-existing increased ICP [4, 18]. The aim of this study was the evaluation of ICP after i.v. propofol administration in comparison with thiopental. Method. Five patients were studied, all of whom had had isolated head trauma. All were on controlled ventilation and were unconscious. Depending on the result of computer tomography, an epidural pressure transducer was implanted. ICP, blood pressure (BP), and heart rate (HR) were measured before and 1, 3, 5, 10, and 15 min after 1 mg/kg propofol; subsequently 2 mg/kg thiopental were administered and the same parameters documented. Cerebral perfusion pressure (CPP) and mean arterial pressure (MAP) were calculated. Results. ICP decreased in all five cases 5 min after the initial values were measured. Two patients showed an ICP decrease after thiopental. BP was reduced markedly by propofol and very slightly by thiopental. The CPP showed a small decrease in four patients after propofol and in two after thiopental. Conclusions. The data now available permit the conclusion that both propofol and thiopental can be used in patients with possibly elevated ICP. The marked cardiovascular side effects of propofol must be taken into consideration.

Adolescent↗
PubMed1985

Thiopental requirements may be increased in children reanesthetized at least one year after recovery from extensive thermal injury.

Clinical observations suggested that children long recovered from burn injury required larger doses of thiopental for a smooth anesthetic induction. A prospective randomized study examined children 6-16 yr old, with greater than 15% burn, and more than 1 year after injury, for loss of lid reflex (LR), corneal reflex (CR), and acceptance of the anesthesia mask (AM) 60 sec after administration of thiopental. Children were unpremedicated, received the thiopental (2.5%) through a rapidly running peripheral intravenous line, and received either 2, 3, 4, 5, 6, 7, or 8 mg/kg. LR, CR, and AM were examined at 30, 60, and 90 sec. Blood pressure and heart rate were recorded for those patients receiving 7 or 8 mg/kg thiopental. The mean age was 12.0 +/- 0.5 yr, weight 43.9 +/- 2.9 kg, % burn 44.7 +/- 2.9, time since burn 68.4 +/- 7.7 months, and time since previous thiopental 25.1 +/- 6.6 months. The estimated ED50 (95% confidence limits) for loss of LR was 4.78 (3.95-5.78) mg/kg; for loss of CR was 7.04 (4.87-10.10) mg/kg; and for AM was 6.74 (4.68-9.71) mg/kg. These doses of thiopental were significantly greater for LR and AM (P less than 0.001) but not CR (P = 0.15) compared to non-thermally injured children. There were no clinically important or statistically significant decreases in blood pressure while heart rate did increase 11 beats/min (P less than 0.05) in children who received 7 or 8 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Effects of thiopental on endothelium-dependent responses in rat aorta.

Effects of pretreatment with thiopental on endothelium-dependent vasodilator responses elicited by drugs in rat aortic rings were investigated. The vasodilators employed were acetylcholine and histamine (endothelium- and receptor-dependent), A23187 (endothelium-dependent but receptor-independent) and sodium nitroprusside (endothelium-independent); they were tested 15 or 60 min after aortic preparations were exposed during 15 min to thiopental. Pretreatment with the barbiturate reversibly inhibited relaxation elicited by either acetylcholine and histamine, but a high concentration of the anesthetic was needed (3.1 mg/ml). On the contrary, thiopental did not modify the relaxation elicited by sodium nitroprusside or A23187. In addition, the barbiturate inhibited basal and acetylcholine-stimulated production of nitrites (an indicator of nitric oxide output) in aortic rings. In conclusion, thiopental inhibited the endothelium-dependent relaxation elicited by either acetylcholine or histamine. Although the barbiturate also inhibited nitric oxide production, the reduction in the relaxant response provoked by it does not seem to be the result of direct guanylate cyclase or nitric oxide synthase alterations, since thiopental did not modify the effect of sodium nitroprusside or A23187. Disturbances elicited by thiopental on endothelial receptors or on signal transduction elements may indirectly provoke nitric oxide synthase inhibition.

Animals↗
PubMed1998

[Comparison of the vascular effects of propofol and those of thiopental in patients under cardiopulmonary bypass].

The effects of propofol (1 mg.kg-1) and thiopental (2.5 mg.kg-1) on the vascular smooth muscle were investigated in 10 cardiac patients on cardiopulmonary total bypass using a constant perfusion flow. Radial mean arterial blood pressure (mAP) decreased to 85 +/- 5% (P < 0.01, vs preinjection) in the post-injection late phase (2-3 min) after propofol, and to 90 +/- 6% (P < 0.01) after thiopental. MAP after thiopental showed a transient initial increase to 115 +/- 8% (P < 0.01) in the post-injection early phase (-1 min). Skin blood flow (SBF) in the middle finger-tip increased to a peak of 450 +/- 120% (P < 0.01) in the post-injection late phase after propofol, and to 240 +/- 60% (P < 0.05) after thiopental. The increase in SBF after propofol was greater than that after thiopental (P < 0.05). The decrease in mAP and the increase in SBF under the constant perfusion flow are considered mainly due to a direct drug action of dilating peripheral vessels. In conclusion, this in vivo human study suggests that propofol (1 mg.kg-1) causes more potent vasodilatation in the peripheral vessels than thiopental (2.5 mg.kg-1).

Aged↗
PubMed2001

Effects of propofol and thiopental on the central nervous system during nociceptive stimulation in cats.

PURPOSE: Nociceptive stimulation may increase central nervous system (CNS) activity during anesthesia. However, it is not known whether propofol and thiopental have a similar inhibitory effect on the CNS during nociceptive stimulation. Therefore, we compared the antinociceptive effects of propofol and thiopental in cats. METHODS: In 12 cats, anesthesia was induced with 4% halothane in oxygen and maintained with 0.5% halothane in oxygen. The cortical electroencephalogram (EEG) and the electrical activity from the midbrain reticular neurons (R-MUA) were measured before and after sciatic nerve stimulation. The cats were then allocated to receive cumulative doses of either propofol (n = 6) or thiopental (n = 6) i.v. at 5-min intervals. Two minutes after each dose, the cortical EEG and the R-MUA were compared before and after sciatic nerve stimulation. RESULTS: Propofol and thiopental depressed the basal R-MUA to a similar degree at each dose. Sciatic nerve stimulation increased the R-MUA, and there were no differences in the maximum R-MUA values between propofol and thiopental. The cortical EEGs after each dose of anesthetic without stimulation showed similar patterns, and the patterns of change with stimulation were also similar for these two anesthetics. CONCLUSION: Propofol and thiopental have similar antinociceptive effects in cats.

Journal Article↗
PubMed1984

Extraction of clinical information from electroencephalographic background activity: the combined use of brain electrical activity mapping and intravenous sodium thiopental.

Traditional visual inspection of electroencephalographic (EEG) tracings and computer-assisted topographic mapping were compared in their abilities to detect and locate supratentorial lesions following intravenous sodium thiopental administration. Of the 13 subjects, 8 had atrophic and 5 had mass lesions, all defined by computed tomographic scan and 11 confirmed at operation. EEGs made before and after thiopental administration were evaluated separately from topographic maps of statistical difference between EEGs at multiple frequency ranges made before and after thiopental injection. Topographic mapping of statistical difference accurately detected all thirteen lesions, whereas EEG detected eight. In addition to demonstrating reduced beta production overlying structural abnormalities, topographic mapping revealed regionally augmented beta, especially over irritative lesions. Moreover, localization was possible with the topographic method after the first thiopental injection, whereas a second injection was required for EEG localization by visual inspection. Changes in slow (delta) activity were also useful in delineation of atrophic lesions, in which delta was usually augmented but occasionally regionally reduced. Multielectrode studies with topographic mapping appear essential in delineating cerebral abnormalities, because both slow and fast activities may be increased or reduced over such areas. The relative response of EEG background activity to thiopental at different frequencies may assist lesion characterization as well as localization.

Adolescent↗
PubMed2001

Intravenous midazolam significantly enhances the lethal effect of thiopental but not that of ketamine in mice.

Intravenous (i.v.) drug combinations are used in clinical anaesthesia in order to combine the desired effects and minimize toxicity from large doses of single agents. This fundamental assumption has not been systematically evaluated. We examined its validity by testing the influence of midazolam on the lethal effect of i.v. thiopental and ketamine in mice. Dose-response curves were constructed for the lethal effect of i.v. thiopental and ketamine, and for the loss of righting reflex effect by midazolam, in sexually mature male ICR mice weighing 20-40 g. For each curve, six or seven groups of eight to 10 mice each were used. A quarter of the median effective dose (ED50) for loss of righting reflex by midazolam was combined with the two other drugs to deduce dose-response curves for the lethal effect of the combinations. The ED50 for loss of righting reflex by i.v. midazolam was 43.5 mg x kg(-1) (95% confidence interval [CI], 40.4-46.5). The median lethal dose (LD 50) of i.v. thiopental was 50.6 mg x kg(-1) (95% CI, 50.0-54.9) and that of ketamine 42.9 mg x kg(-1) (95% CI, 32.3-52). In the presence of 10 mg x kg(-1) midazolam, the LD50 of thiopental was reduced to 20 mg x kg(-1) (17.7-22.2), but that of ketamine remained 44.4 mg x kg(-1) (37.7-54.9). Midazolam increased the lethal effect of thiopental 2.5-fold, but did not affect that of ketamine. Interactions at the toxic level between commonly used anaesthetic agents may differ from those at the hypnotic or analgesic levels, which should prompt evaluation of such combinations before their introduction to routine clinical use.

Anesthetics, Dissociative↗
PubMed1976

Inhibition of glucose phosphorylation in rat brain by thiopental.

The purpose of the present investigation was to shed some light on the suppression of the glycolytic pathway by anesthetics. The antimetabolite 6-aminonicotinamide (6-AN) was used to discriminate between the key enzymes hexokinase and phosphofructokinase which are suggested to be involved in the effect of anesthetics on glycolysis. The cerebral energy metabolism was studied in the isolated perfused rat brain after the addition of thiopental (0.15 mM) to the perfusion medium, after the administration of 6-AN (35mg/kg i.p.) to the intact animals 15 h before perfusion was started, as well as in brain preparations treated in the same manner with both 6-AN and thiopental. After a perfusion period of 30 min brain levels of the following substrates and metabolites were determined: phosphocreatine, ATP, ADP, AMP, glycogen, glucose, glucose 6-phosphate, fructose 6-phosphate, pyruvate, lactate, alpha-ketoglutarate, blutamate, ammonia, and 6-phosphogluconate. The metabolic alterations in the isolated rat brain caused by 6-AN or thiopental were such as reported in the literature. When the isolated brains of the 6-AN pretreated rats were perfused with thiopental we found as the most interesting result that the concentration of glucose 6-phosphate was reduced in comparison to that in brains only treated with 6-AN but still significantly higher than that in controls. The glucose concentration was significantly elevated and the lactate concentration decreased considerably. The effect of thiopental on cerebral glycolysis was interpreted as an inhibition of hexokinase activity.

6-Aminonicotinamide↗
PubMed2002

Functional magnetic resonance imaging of swine brain during change in thiopental anesthesia into EEG burst-suppression level--a preliminary study.

Deepening anesthesia produces well known changes in electroencephalogram (EEG) and evoked potentials, differing in pathological and normal brain. Yet, it is not known how the T2*-weighted signal changes in the healthy brain during deepening anesthesia. We studied the effect of thiopental bolus on functional magnetic resonance imaging (fMRI) in the healthy brain using porcine model. In five pigs (2-3 months, 20-25 kg), the control bolus prior to fMRI resulted in a change into burst-suppression. After the recovery of continuous EEG, fMRI (4 min) was performed with a single bolus of thiopental (11.4-17.1 mg/kg) administered 1 min after the onset of imaging. This was repeated in four of five pigs. Positive (6-8%) or negative (-3 to -8%) signal intensity changes correlated to the thiopental bolus injection were seen in the group average fMRI response. Positive response was 1.6% and negative response 2.3% of the total brain region of interest (ROI) voxels. Responding voxels were distributed more prominently in the thalamic ROI (4.5%) than in the cortical ROI (2.2%). The group average of unthresholded voxel time courses showed that the net effect of thiopental bolus was a small (0.5%) but a clear positive change in the thalamic region, while variance changed in the global level. In conclusion, this study is the first to show that significant signal intensity changes occur in fMRI response during the sudden deepening of thiopental anesthesia. However, these responses are neither anatomically constant nor global in the healthy swine brain.

Anesthesia Recovery Period↗
PubMed2004

Effect of thiopental sodium on the release of glutamate and gamma-aminobutyric acid from rats prefrontal cortical synaptosomes.

To investigate the effect of thiopental sodium on the release of glutamate and gamma-aminobutyric acid (GABA) from synaptosomes in the prefrontal cortex, synaptosomes were made, the spontaneous release and the evoked release by 30 mmol/L KCl or 20 micromol/L veratridine of glutamate and GABA were performed under various concentrations of thiopental sodium (10-300 micromol/L), glutamate and GABA concentrations were determined by reversed-phase high-performance liquid chromatography. Our results showed that spontaneous release and evoked release of glutamate were significantly inhibited by 30 micromol/L, 100 micromol/L and 300 micromol/L thiopental sodium, IC50 of thiopental sodium was 25.8 +/- 2.3 micromol/L for the spontaneous release, 23.4 +/- 2.4 micromol/L for KCl-evoked release, and 24.3 +/- 1.8 micromol/L for veratridine-evoked release. But GABA spontaneous release and evoked release were unaffected. The study showed that thiopental sodium with clinically related concentrations could inhibit the release of glutamate, but had no effect on the release of GABA from rats prefrontal cortical synaptosomes.

Animals↗
PubMed1983

Anaesthetic induction with alfentanil: comparison with thiopental, midazolam, and etomidate.

The speed, side effects and cardiovascular changes associated with anaesthetic induction and endotracheal intubation following alfentanil (20 micrograms/kg/min, IV), thiopental (84 micrograms/kg/min, IV), etomidate (5 micrograms/kg/min, IV) and midazolam (20 micrograms/kg/min, IV) prior to halothane-nitrous oxide general anaesthesia were evaluated and compared in 80 patients undergoing elective general surgical operations. Anaesthetic induction was fastest with etomidate and thiopental (approximately one minute) and slowest with midazolam (about two minutes). Systolic arterial blood pressure (SBP) was decreased at the moment of unconsciousness with thiopental but unchanged with the other compounds. Heart rate (HR) was increased at unconsciousness with midazolam and thiopental but unchanged with etomidate and alfentanil. After intubation HR was increased in all groups except those induced with alfentanil. Arrhythmias were infrequent (5 per cent or less in all groups). Rigidity during induction only occurred with alfentanil (55 per cent) and pain on injection only with etomidate (35 per cent) and alfentanil (5 per cent). Postoperative vomiting was infrequent in all groups (15 per cent) except etomidate (55 per cent). No patient remembered any aspect of laryngoscopy or the operation and all rapidly regained consciousness at the end of operation. The results of this study demonstrate that with the exception of rigidity (which is easily overcome with succinylcholine) and a slightly slower onset of action, alfentanil compares favourably as an induction agent with thiopental and is better than midazolam and etomidate. Alfentanil is superior to all three other induction agents with respect to cardiovascular stability during induction and intubation.

Adjuvants, Anesthesia↗
PubMed2006

Elementary Ca2+ release events in mammalian skeletal muscle: effects of the anaesthetic drug thiopental.

We examined the effect of clinically relevant doses of thiopental (10-100 microM) on Ca2+ release from the sarcoplasmic reticulum of chemically skinned skeletal muscle fibres of the mouse. Elementary Ca2+ release events (ECRE) were recorded with confocal microscopy and were detected and analysed by an automated algorithm. Thiopental at 25 microM evoked a marked increase in ECRE frequency (events/100 microm/s) from 0.64 +/- 0.32 to 1.56 +/- 0.38 (P < 0.001). Incubation with 5 microM ryanodine significantly reduced spontaneous and evoked ECRE frequencies to 0.08 +/- 0.08 (P < 0.001) and 0.39 +/- 0.25 (25 microM thiopental, P < 0.001) respectively. Thiopental-evoked ECRE show different morphological characteristics compared to spontaneous events. Maximum relative amplitudes (DeltaF/F0)max and spatial width (full width at half maximum) of the events were substantially increased. Full duration at half maximum was increased and some very long events (200 ms compared to approximately 30 ms standard) were produced. The rise times as an indicator of the channel open time were slightly increased. Furthermore, the occurrence of repetitive ECRE was observed. These events, in contrast to previous observations in amphibian skeletal muscle fibres, displayed a multitude of different release patterns. In particular, a repetitive ECRE mode with successively decaying amplitudes was identified and the inter-event intervals were analysed. Estimation of the underlying Ca2+ release current suggests that during repetitive events with a decaying amplitude a decreasing amount of Ca2+ was released within the individual release event. Possible underlying mechanisms are discussed. In summary, thiopental seems to be a potent RyR1 agonist and substantially alters the gating mechanisms of RyR Ca2+ release channel clusters already in clinically relevant doses, i.e. doses administered during general anaesthesia.

Algorithms↗
PubMed1988

GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

Animals↗
PubMed1987

Effect of barbitone sodium and thiopental sodium on brain dopamine, noradrenaline, serotonin and 5-hydroxyindoleacetic acid content in Arvicanthis niloticus.

The quantitative estimation of total dopamine (DA), noradrenaline (NE), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) content in the whole brain tissue of normal Nile grass rat, Arvicanthis niloticus, gives and average of 631 +/- 12 ng DA/g, 366 +/- 12 ng NE/g, 617 +/- 15 ng 5-HT/g and 431 +/- 10 ng 5-HIAA/g fresh brain tissue. The effect of barbitone sodium and thiopental sodium on the total DA, NE, 5-HT and 5-HIAA content in the brain tissue of the Nile grass rat, Arvicanthis niloticus, was studied. The total DA, NE, 5-HT and 5-HIAA contents were determined 5 hr after i.p. injection of different doses of barbitone sodium (20, 40 and 80 mg/ml/100 g body wt) and thiopental sodium (5, 10 and 20 mg/ml/100 g body wt). The effect of different time intervals (1, 10, 30 min, 1, 2.5, 5, 8, 16, 24 and 48 hr) on the total brain DA, NE, 5-HT and 5-HIAA content was investigated after i.p. injection of 40 mg of barbitone sodium and 10 mg of thiopental sodium/ml/100 g body wt. Both barbitone sodium and thiopental sodium caused an increase in DA, NE and 5-HT content and a decrease in 5-HIAA content in the brain tissue of Arvicanthis niloticus. The increase in the whole brain contents of DA, NE and 5-HT after the administration of barbitone sodium and thiopental sodium may be due either to inhibition of transmitter release by an action at the monoamine nerve terminal or to effects causing a decrease in nerve impulse flow. On the other hand, the decrease in 5-HIAA may be due to the decrease in the turnover of 5-HT.

Animals↗