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PubMed1992

Thiopental pharmacodynamics. II. Quantitation of clinical and electroencephalographic depth of anesthesia.

This study examined the relationship among pseudo-steady-state (constant) serum thiopental concentrations, clinical anesthetic depth as assessed by several perioperative stimuli, and the electroencephalogram (EEG). Twenty-six ASA physical status 1 or 2 patients participated in the study. Two constant serum thiopental concentrations were maintained in each patient using a computer-controlled infusion pump. The first randomly assigned target serum concentration of 10-30 micrograms/ml was maintained for 5 min to allow serum:brain equilibration. Then the following stimuli were applied at 1-min intervals: verbal command, tetanic nerve stimulation, trapezius muscle squeeze, and laryngoscopy. A second, higher, randomly assigned target serum concentration of 40-90 micrograms/ml was then achieved and maintained by the computer-controlled infusion pump. The previously described stimuli were reapplied, after which laryngoscopy and intubation was performed. A positive response was recorded if purposeful extremity movement or coughing was observed. Using the quantal movement or cough response and the measured constant serum thiopental concentration, the probability of no movement to each stimulus was characterized using logistic regression. The serum thiopental concentrations that produced a 50% probability of no movement response for the clinical stimuli were as follows: 15.6 micrograms/ml for verbal command, 30.3 micrograms/ml for tetanic nerve stimulation, 39.8 micrograms/ml for trapezius muscle squeeze, 50.7 micrograms/ml for laryngoscopy, and 78.8 micrograms/ml for laryngoscopy followed by intubation. The EEG was analyzed using aperiodic waveform analysis to derive the number of waves per second. A biphasic relationship between constant serum thiopental concentration and the EEG number of waves per second was observed. Loss of responsiveness to verbal stimulation occurred when the EEG was activated at 15-18 waves/s.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of propofol and thiopental on coronary blood flow and myocardial performance in an isolated rabbit heart.

BACKGROUND: Some clinical and experimental studies suggest that propofol decreases myocardial contractility and relaxation, whereas others report preserved cardiac function. To investigate the effects of propofol on intrinsic contractility and relaxation, increasing concentrations of propofol were infused in isolated blood-perfused rabbit hearts. Equimolar concentrations of thiopental were infused as a reference group. METHODS: Coronary blood flow, left ventricular contractility and relaxation (as maximal positive and negative left ventricular pressure derivatives [dP/dtmax and dP/dtmin], respectively), and myocardial oxygen consumption (MvO2) were measured during infusion of 10-1,000 microM propofol in blood-perfused hearts. To determine whether the effects of propofol depend on the heart's perfusate, propofol also was infused in isolated buffer-perfused rabbit hearts. In addition, the effects of propofol solvent were investigated in blood- and buffer-perfused preparations. RESULTS: In blood-perfused preparations, coronary blood flow increased with propofol concentrations greater than 30 microM and with 300 and 1,000 microM thiopental. Left ventricular dP/dtmax and dP/dtmin remained unchanged with propofol and decreased with concentrations of thiopental equal to or greater than 30 microM. MvO2 increased with 1,000 microM propofol, whereas coronary venous oxygen tension and content remained unchanged. MvO2 decreased with thiopental associated with a significant increase in coronary venous oxygen tension and content. In six buffer-perfused hearts, basal coronary blood flow was much greater and MvO2 less than in blood-perfused hearts. Left ventricular dP/dtmax and dP/dtmin decreased with 30, 100, and 300 microM propofol. Propofol vehicle did not change coronary blood flow, myocardial performance, or MvO2 of blood- or buffer-perfused hearts. CONCLUSIONS: When compared to a reference drug such as thiopental, propofol did not depress the myocardial performance of blood-perfused rabbit hearts. The type of the perfusate (blood vs. buffer), however, had a major influence on the myocardial effects of propofol.

Animals↗
PubMed1995

Faster recovery after anesthesia in infants after intravenous induction with methohexital instead of thiopental.

BACKGROUND: To determine possible delays in recovery after intravenous anesthesia induction with thiopental, the drug was compared with methohexital in infants 1-12 months of age who were scheduled for hernia repair or circumcision. METHODS: The infants were given equipotent doses of methohexital (3.0 mg/kg, n = 21) or thiopental (7.3 mg/kg, n = 20), in random and blind fashion. After tracheal intubation, anesthesia was maintained with isoflurane in nitrous oxide/oxygen. All children received 0.75 ml/kg caudal bupivacaine (2.5 mg/ml). Isoflurane was discontinued at the beginning of skin closure, and nitrous oxide was terminated immediately after the last suture (end of surgery). RESULTS: There were no differences between the two groups with respect to age, weight, or duration of surgery, which lasted 19 min (14-23 min) in the methohexital group and 16 min (15-19 min) in the thiopental group (median and inner quartile range). Time from termination of nitrous oxide to extubation did not differ significantly between the groups. Time to spontaneous eye opening after end of surgery was 23 min (5-44 min) after methohexital induction and 55 min (25-74 min) after thiopental induction (P < 0.05). Recovery, assessed as postanesthetic recovery scores by a blinded observer, was significantly more rapid in the methohexital group at arrival in the recovery room and 5, 15, and 45 min after arrival. After 120 min, almost all infants of both groups were awake. CONCLUSIONS: Recovery after short surgical procedures in infants is faster after intravenous induction with methohexital than with thiopental.

Anesthesia Recovery Period↗
PubMed1995

Inhibitory effects of thiopental, ketamine, and propofol on voltage-dependent Ca2+ channels in porcine tracheal smooth muscle cells.

BACKGROUND: Intravenously administered anesthetics directly inhibit airway smooth muscle contraction. Because many anesthetic agents affect membrane ion channel function and sustained contraction of airway smooth muscle requires the influx of Ca2+ through voltage-dependent Ca2+ channels, it was hypothesized that intravenous anesthetics inhibit airway smooth muscle voltage-dependent Ca2+ channels. METHODS: Porcine tracheal smooth muscle cells were enzymatically dispersed and studied using whole-cell, patch-clamp techniques. The cells were exposed to thiopental (10(-7)-3 x 10(-4) M), ketamine (10(-6)-10(-3) M), or propofol (10(-7)-3 x 10(-4) M) while recording macroscopic voltage-activated Ca2+ currents (ICa). RESULTS: Each intravenous anesthetic tested significantly inhibited ICa in a dose-dependent manner with 3 x 10(-4) M thiopental, 10(-3) M ketamine, and 3 x 10(-4) M propofol each causing approximately 50% depression of peak ICa, but with no apparent shift in the voltage dependence of induced ICa. After pretreatment with the Ca2+ channel agonist Bay K 8644, thiopental, but not ketamine or propofol, shifted the maximum ICa to more positive potentials. All three anesthetics promoted the inactivated state of the channel at more negative potentials, but propofol was less effective than thiopental or ketamine in this regard. CONCLUSIONS: Three intravenous anesthetics evaluated in this study decreased the ICa of porcine tracheal smooth muscle cells but with subtle electrophysiologic differences. Hence, thiopental, ketamine, and propofol each inhibit L-type voltage-dependent Ca2+ channels of porcine tracheal smooth muscle cells but the molecular mechanisms involved may be agent specific. This inhibition may contribute to the airway smooth muscle relaxant effects of these agents observed in vitro at concentrations greater than those encountered clinically.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Inotropic effects of propofol, thiopental, midazolam, etomidate, and ketamine on isolated human atrial muscle.

BACKGROUND: Cardiovascular instability after intravenous induction of anesthesia may be explained partly by direct negative inotropic effects. The direct inotropic influence of etomidate, ketamine, midazolam, propofol, and thiopental on the contractility of isolated human atrial tissue was determined. Effective concentrations were compared with those reported clinically. METHODS: Atrial tissue was obtained from 16 patients undergoing coronary bypass surgery. Each fragment was divided into three strips, and one anesthetic was tested per strip in increasing concentrations (10(-6) to 10(-2) M). Strips were stimulated at 0.5 Hz, and maximum isometric force was measured. Induction agents were studied in two groups, group 1 (n = 7) containing thiopental, midazolam, and propofol, and group 2 (n = 9) consisting of etomidate, ketamine, and propofol. RESULTS: The tested anesthetics caused a concentration-dependent depression of contractility resulting in complete cessation of contractions at the highest concentrations. The IC50s (mean +/- SEM; microM) for inhibition of the contractility were: thiopental 43 +/- 7.6, propofol 235 +/- 48 (group 1), and 246 +/- 42 (group 2), midazolam 145 +/- 54, etomidate 133 +/- 13, and ketamine 303 +/- 54. CONCLUSIONS: This is the first study demonstrating a concentration-dependent negative inotropic effect of intravenous anesthetics in isolated human atrial muscle. No inhibition of myocardial contractility was found in the clinical concentration ranges of propofol, midazolam, and etomidate. In contrast, thiopental showed strong and ketamine showed slight negative inotropic properties. Thus, negative inotropic effects may explain in part the cardiovascular depression on induction of anesthesia with thiopental but not with propofol, midazolam, and etomidate. Improvement of hemodynamics after induction of anesthesia with ketamine cannot be explained by intrinsic cardiac stimulation.

Anesthetics, Intravenous↗
PubMed1996

Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation.

BACKGROUND: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS: Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS: Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate.

Adult↗
PubMed1997

Mild and moderate hypothermia provide better protection than a burst-suppression dose of thiopental against ischemic spinal cord injury in rabbits.

BACKGROUND: Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. METHODS: Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined. RESULTS: All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord. CONCLUSIONS: These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.

Anesthetics, Intravenous↗
PubMed1998

Thiopental and methohexital depress Ca2+ entry into and glutamate release from cultured neurons.

BACKGROUND: Although barbiturates activate alpha-aminobutyric acid type A receptors as part of their hypnotic effect, these drugs also inhibit voltage-gated calcium channels. The authors determined if barbiturates could decrease neuronal intracellular Ca2+ transients and the resulting glutamate release. METHODS: Neonatal rat cerebellar granule neurons were isolated and cultured on coverslips and studied at 37 degrees C. Spectrofluorometric assays were used during identical conditions to monitor intracellular Ca2+ with the Ca2+ -sensitive fluorophore fura-2 and glutamate release by a glutamate dehydrogenase-coupled assay, which produced the reduced form of nicotinamide-adenine dinucleotide phosphate in proportion to the amount of glutamate released. Neurons were depolarized by a rapid increase in external [K+] from 5 to 55 mM. Control responses were compared with those in the presence of 10, 30, and 100 microM thiopental; 3, 10, and 30 microM methohexital; decreased external [Ca2+]; or voltage-gated calcium channel blockers. RESULTS: Thiopental and methohexital depressed the intracellular Ca2+ transient peak and plateau in a dose-dependent manner, as did decreased Ca2+. The intermediate dose of either drug caused approximately 50% decrease in peak intracellular Ca2+ and 60% decrease in glutamate release. In the presence of specific L- and/or N-type voltage-gated calcium channel blockade by nicardipine or omega-conotoxin-GVIA, respectively, 30 microM thiopental further decreased the intracellular Ca2+ transient. Thiopental caused a dose-dependent decrease in glutamate release, which was proportional to the decreased peak intracellular Ca2+. CONCLUSIONS: Thiopental and methohexital depress the depolarization-induced increase in intracellular Ca2+ and the accompanying glutamate release, actions which can contribute to the anesthetic and neuronal protective effects of these drugs.

Anesthetics, Intravenous↗
PubMed2000

Absence of bronchodilation during desflurane anesthesia: a comparison to sevoflurane and thiopental.

BACKGROUND: Bronchospasm is a potential complication in anyone undergoing general anesthesia. Because volatile anesthetics relax bronchial smooth muscle, the effects of two newer volatile anesthetics, desflurane and sevoflurane, on respiratory resistance were evaluated. The authors hypothesized that desflurane would have greater bronchodilating effects because of its ability to increase sympathetic nervous system activity. METHODS: Informed consent was obtained from patients undergoing elective surgery with general anesthesia. We recorded airway flow and pressure after thiopental induction and tracheal intubation (baseline) and for 10 min after beginning volatile anesthesia ( approximately 1 minimum alveolar concentration inspired). Respiratory system resistance was determined using the isovolume technique. RESULTS: Fifty subjects were randomized to receive sevoflurane (n = 20), desflurane (n = 20), or thiopental infusion (n = 10, 0.25 mg. kg-1. h-1). There were no differences between groups for age, height, weight, smoking history, and American Society of Anesthesiologists physical class. On average, sevoflurane reduced respiratory resistance 15% below baseline, whereas both desflurane (+5%) and thiopental (+10%) did not decrease respiratory resistance. The respiratory resistance changes did not differ in patients with and without a history of smoking during sevoflurane or thiopental. In contrast, administration of desflurane to smokers resulted in the greatest increase in respiratory resistance. CONCLUSIONS: Sevoflurane causes moderate bronchodilation that is not observed with desflurane or sodium thiopental. The bronchoconstriction produced by desflurane was primarily noted in patients who currently smoked. (Key words: Bronchospasm; respiratory resistance; volatile anesthetics.)

Anesthesia, General↗
PubMed2004

Effects of imposed acid-base derangement on the cardiovascular effects and pharmacokinetics of bupivacaine and thiopental.

BACKGROUND: By changing physicochemical properties such as effective lipophilicity, changes in blood pH could alter the distribution, elimination, and effects of weakly ionizing drugs. The authors examined the outcome of imposed acid-base derangement on cardiovascular effects and myocardial and whole body pharmacokinetics of bupivacaine, a weak base, and thiopental, a weak acid. METHODS: Intravenous infusions of rac-bupivacaine HCl (37.5 mg) or rac-thiopental sodium (250 mg, subanesthetic dose) were administered over 3 min to previously instrumented conscious ewes with normal blood pH, acidemia imposed by lactic acid infusion, or alkalemia imposed by bicarbonate infusion. Hemodynamic and electrocardiographic effects were recorded; arterial and coronary sinus drug blood concentrations were analyzed by chiral high-performance liquid chromatography. RESULTS: Bupivacaine decreased myocardial contractility, coronary perfusion, heart rate, and cardiac output; however, cardiac output and stroke volume were not as affected by bupivacaine with acidemia. Thiopental decreased myocardial contractility and stroke volume and increased heart rate; acidemia enhanced the tachycardia and produced a greater decrease in stroke volume than with alkalemia. Taken as a whole, the cardiovascular changes were not systematically modified by acid-base derangement. Overall, the tissue distribution of bupivacaine was favored by alkalemia, but thiopental pharmacokinetics were essentially unaffected by acid-base derangement. Acid-base derangement did not influence the kinetics of either drug enantioselectively. CONCLUSIONS: At the doses used, the hemodynamic and electrocardiographic effects of bupivacaine and thiopental were not systematically modified by acid-base derangement, nor were there changes in regional or whole body pharmacokinetics of either drug that were clearly related to acid-base status.

Acid-Base Imbalance↗
PubMed2005

Seizure length and clinical outcome in electroconvulsive therapy using methohexital or thiopental.

Seizure duration is an extensively studied and controversial indicator of treatment quality in electroconvulsive therapy. Previous research comparing the effect of the barbiturate anesthetics methohexital and thiopental on seizure duration has yielded conflicting results. A recent period of unavailability of methohexital in the United States allowed for retrospective comparison of seizure length as well as clinical improvement in treatment using each agent. Retrospective review was made of 837 treatments administered to 97 patients between January 2, 2002, and May 31, 2003, examining anesthetic, seizure duration, and Global Assessment of Functioning (GAF) scores of inpatients at hospital admission and discharge. Analysis of variance of treatments 2-5 showed no significant effect for anesthetic on seizure duration. Analysis on a treatment-by-treatment basis revealed a marginally significant trend toward shorter EEG seizures in the thiopental group at the second treatment (50.5 +/- 23.6 s vs. 61.1 +/- 27.9 s; P = 0.07) and fifth treatment (41.7 +/- 16.9 s vs. 51.8 +/- 24.0 s; P = 0.07). A difference approaching statistical significance revealed shorter convulsion length in the thiopental group at treatment 5 (29.0 +/- 12.3 s vs. 34.8 +/- 12.3 s; P = 0.07). Comparison of GAF score improvement at hospital discharge revealed no significant difference (GAF increase 26.4 +/- 9.4 for methohexital-treated patients vs. 24.8 +/- 12.0 for thiopental-treated patients; t = 1.00, df = 82, P > 0.1). Trends approaching significance in treatments 2 and 5 revealed shorter seizures in the thiopental group. However, data on clinical recovery reveals no greater improvement in the methohexital group. Thus, this study calls further into question the premise that choice of barbiturate anesthetic may affect clinical efficacy.

Aged↗
PubMed2006

Brain stem death testing after thiopental use:A survey of UK neuro critical care practice.

A postal survey was conducted to determine how thiopental is used in UK neurosurgery critical care units. Thirty units were contacted and 26 replied. Thiopental is used in 23 units. The majority (60%) of these units govern the use of thiopental with protocols or guidelines and 74% use cerebral monitoring to guide dosage. When patients have had thiopental, 20 units delay brain stem testing, two will not perform tests and one unit incorporates cerebral angiography into their protocol. Twelve units use serum thiopental assays in their brain stem testing procedures, but there is wide variation in the interpretation of the results. We found inconsistency and confusion surrounding brain stem testing in this patient group, raising the possibility of misdiagnosis of brain stem death.

Brain Death↗
PubMed1984

Thiopental loading during controlled hypotension for intracranial aneurysm surgery.

In this study we report our clinical experience with supplementary thiopental loading, based on 30 patients undergoing surgery for intracranial aneurysm after a recent episode of subarachnoid haemorrhage. As standard procedure we used pentobarbitone induction, pancuronium relaxation, endotracheal intubation, maintenance with halothane 0.5%, N2O 66% in oxygen, fentanyl, and moderate hypocapnia. A thiopental load of up to 20 mg X kg-1 was supplied while the aneurysm was approached. Satisfactory and well-controlled hypotension was obtained in five cases after thiopental alone, and after thiopental and sodium nitroprusside (SNP) (means +/- s.d.) 1.3 +/- 0.9 microgram X kg-1 X min-1 in the remaining 25 patients. No ECG sign of myocardial ischaemia was observed. One disadvantage was a prolonged recovery period, which in some cases necessitated controlled ventilation for some hours. We conclude that thiopental loading can be used safely as a supplement to neuroanaesthesia for aneurysm surgery.

Adult↗
PubMed1989

The influence of halothane and thiopental on respiratory-related nerve activities in decerebrate cats.

The effects of halothane and thiopental on the respiratory efferent activities in the phrenic, recurrent laryngeal and hypoglossal nerves were studied in decerebrate, paralyzed and artificially ventilated cats. Inhalation of halothane (2%, 90 s) and intravenous injection of thiopental (2-3 mg/kg) produced a similar change in the breathing pattern, characterized by an increase in respiratory frequency and a decrease in the respiratory burst discharge in the three nerves studied. Depression of the respiratory activity was greatest in the hypoglossal nerve, intermediate in the recurrent laryngeal nerve, and least in the phrenic nerve. Both drugs diminished the whole power spectral densities of the three nerves. Thiopental selectively attenuated the high frequency peaks of these spectra and shifted the peak frequencies to lower values. Bilateral section of the vagus and carotid sinus nerves had no effect on the action of thiopental on the respiratory neural activities, whereas it decreased, but did not eliminate, the action of halothane. The present results demonstrate that both halothane and thiopental produce a selective depression of the upper airway motor activities, with stronger effects on the hypoglossal nerve. Effects on the peripheral receptors and the central respiratory drives differ between the two drugs.

Administration, Inhalation↗
PubMed1995

Autogenous production of hydroxyl radicals from thiopental.

It is generally believed that barbiturates can protect neural tissues from the damage induced by cerebral hypoxia. One of the mechanisms for protecting neurons is through the inhibition of lipid peroxidation (LPO). We therefore examined LPO in rat brain, liver and kidney by measuring the accumulation of thiobarbituric acid-reactive substances (TBAR) after thiopental administration under 21% O2. We also designed an in vitro study to gain insight into free radical generation leading to the formation of LPO from thiopental by electron spin resonance (ESR). An accumulation of TBAR in the rat liver was observed after the administration of a large dose of thiopental (70 mg/kg intraperitoneally). However, no change in LPO in the brain and kidney was observed. In the in vitro study, thiopental could scavenge superoxide (O2-.) radicals, while it spontaneously generated hydroxyl radicals (.OH) in solution. We conclude that thiopental can scavenge O2-., while producing .OH, subsequently resulting in membrane lipid peroxidation under physiologic O2 conditions. This formation of .OH may damage cell membrane lipids.

Animals↗
PubMed1997

Analgesic and psychomotor effects of thiopental at subanesthetic concentrations in human volunteers.

BACKGROUND: Studies of the effects of barbiturates on the modulation of pain have produced mixed results. In a prospective, double-blind, randomized, placebo-controlled trial, we studied the effects of thiopental at presumed steady-state, "conscious sedation" levels on cold-pressor-induced pain in 12 healthy volunteers. METHODS: Five drug conditions were used, each condition consisting of an injection (either drug or placebo) with a 20-min infusion and a 160-min recovery period. The conditions were placebo (saline), thiopental targeted to three effect-site concentrations, and fentanyl (1.4 micrograms/kg), as a positive control to verify test sensitivity to analgesic drugs. The three thiopental concentrations were modeled (STANPUMP) to achieve effect-site concentrations of 5, 7.5, and 10 micrograms/ml using a bolus and a three-step continuous infusion. Five minutes into the infusion period and 115 min after the infusion period was terminated, subjects immersed their forearms in ice cold water for 3 min while pain and behavioral assessments were recorded. RESULTS: Thiopental at the highest dose produced a significant reduction (P < 0.05) in self-reported pain intensity both at 5 min into the infusion period and at 115 min after termination of the infusion. Fentanyl reduced pain intensity during the first immersion only. Thiopental changed subjects' moods and psychomotor performance in a dose-related fashion. CONCLUSIONS: Our laboratory results do not support the long-held belief that barbiturates are "antanalgesic" or hyperalgesic, at least for cold-pressor-induced pain.

Adult↗
PubMed1983

The binding of thiopental to human serum albumin at variable pH and temperature.

The binding of thiopental was studied in vitro by equilibrium dialysis over the concentration range 0.8-80 micrograms/ml in solutions with 45 g albumin (HSA) per litre. The binding at 37 degrees was from 79% to 67.6% at pH 6 while it was 94.5% to 93.0% at pH 9. At intermediate values of pH the observed values for binding were compatible with the assumption of a gradual transition of an N-form of HSA present exclusively at pH 6 to a B-form present exclusively at pH 9. The variation in binding could not be explained by changes in the balance between ionised and nonionized drug (pKa = 7.6). An increase in r (number of thiopental molecules bound per HSA molecule) was demonstrated when the temperature was lowered to 2 degrees. Graphs showing the relation between drug concentrations and percentual binding all showed a very modest slope and it was concluded that a traditional binding model with calculation of the number of binding sites and association constants was of little use in the evaluation of our binding studies of thiopental. The binding between thiopental and albumin may be characterized best by the solubility of thiopental in hydrophobic areas in the albumin solutions.

Humans↗
PubMed1986

Interactions between hexobarbital and thiopental in male rats evaluated with an anaesthesia threshold.

The anaesthetic interaction between hexobarbital and thiopental in different combinations were investigated in male rats by using the isobolografic method. Data on dose, serum or brain concentrations at an EEG-criterion induced with a threshold method were utilized. The criterion was defined by a burst suppression in the EEG of 1 sec. or more (the "silent second"). With rats more than 115 days of age a synergistic interaction (potentiation) was obtained when a low dose of hexobarbital and a high dose of thiopental were used. The relationship between serum and brain concentrations of hexobarbital and thiopental in the different tested combinations gave no evidence for a pharmacokinetic interaction. Thus the synergistic interaction was located in the brain and probably related to the mechanisms of action. The same tests performed on rats at an age of approximately 90 days gave not only a potentiation when a low dose of hexobarbital and a high dose of thiopental were used, but also a potentiation when a high dose of hexobarbital and a low dose of thiopental were used. These results indicate an age-related change in sensitivity in the CNS between 90 and 115 days of age. Further investigations of this age-related change showed that this change from a potentiation to an additive interaction occurred between the age of 85 and 96 days.

Anesthesia↗