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PubMed1990

Chronic alcohol intake does not change thiopental anesthetic requirement, pharmacokinetics, or pharmacodynamics.

The anesthetic requirements of chronic alcoholics for induction of anesthesia with thiopental were investigated using an electroencephalographic (EEG) measure of thiopental's CNS drug effect and pharmacodynamic modeling to relate thiopental serum concentrations to drug effect. Eleven patients with a history of excessive alcohol intake were studied from an inpatient alcohol rehabilitation program and compared with nine control patients or volunteers who were social drinkers. The alcoholic population had consumed ethanol 9-17 days prior to the study. They had no evidence of acute intoxication or acute withdrawal at the time of the study. Five of the 11 alcoholic patients were restudied after 1 month of abstinence from alcohol consumption. Each study consisted of a thiopental infusion until EEG burst suppression (1-3 s of isoelectric signal) was achieved. Timed arterial and then venous blood samples were obtained for measurement of thiopental serum concentrations for up to 36 h. Pharmacokinetic differences between groups were analyzed using a three-compartment model. Power spectral analysis of the EEG allowed determination of spectral edge frequency. An inhibitory sigmoid Emax pharmacodynamic model combined with an effect compartment was used to analyze concentration-response relationships and to provide an estimate of brain sensitivity to thiopental in the study populations. The thiopental anesthetic dose requirement using the EEG was not different between alcoholics and nonalcoholics. The mean dose requirement (+/- SD) of alcoholics was 823 +/- 246 mg and the mean dose requirement of nonalcoholics was 733 +/- 218 mg. There were no differences in thiopental pharmacokinetic and pharmacodynamic parameters between alcoholics and nonalcoholics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of thiopental on neurologic outcome following coronary artery bypass grafting.

To determine if thiopental reduces the incidence of neurologic sequelae after coronary artery surgery, we prospectively studied 300 patients undergoing coronary artery bypass grafting. Patients who had no history of neurologic or psychiatric illness were randomly assigned to receive either a thiopental infusion or a saline placebo infusion beginning with the administration of heparin and ending just after aortic decannulation. The patients received an opioid-relaxant anesthetic administered by an anesthesiologist who was not involved in this investigation and who was blinded to the test infusion. One of the investigators infused either saline or thiopental to produce an isoelectric electroencephalogram with 30-45 s between bursts. Standardized neurologic examinations were performed preoperatively and on the 2nd and 5th postoperative days by one of the blinded investigators. The group of patients receiving thiopental required a longer time for awakening (6.4 +/- 3.9 vs. 4.0 +/- 2.4 h, mean +/- SD, P less than 0.05) and for tracheal extubation (22.4 +/- 18.4 vs. 17.4 +/- 9.6 h, P less than 0.05), and a greater number of these patients were lethargic on the 2nd postoperative day. More patients receiving thiopental required vasoconstrictors during the thiopental loading and cardiopulmonary bypass (CPB) periods, while a greater number of patients receiving placebo required vasodilators. A greater number of patients receiving thiopental required inotropic drugs during separation from CPB. Despite the above differences, only 2 of the 151 patients in the placebo group (1.3%) and 5 of the 149 patients in the thiopental group (3.3%) experienced strokes (P = 0.2535).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Peripheral vascular effects of thiopental and propofol in humans with artificial hearts.

The peripheral vascular effects of thiopental 5 mg/kg and propofol 2.5 mg/kg were compared in five patients whose lungs were being ventilated and in whom a Jarvik-7 artificial heart had been implanted. The patients were monitored, using catheters that had been surgically inserted into the radial artery, the right and left atria, and the pulmonary artery. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient received both drugs, with the interval between each drug ranging from 16 to 28 h. Hemodynamic parameters and catecholamine and atrial natriuretic peptide plasma concentrations were measured before drug administration and 5, 10, 15, 30, and 45 min later. Both drugs significantly decreased arterial pressure, systemic vascular resistance index, pulmonary arterial pressure (PAP), and right and left atrial pressures (RAP and LAP, respectively). However, propofol 2.5 mg/kg induced a significantly greater and more prolonged decrease in arterial pressure, systemic vascular resistance index, and RAP than that after administration of thiopental 5 mg/kg (P less than 0.05). Five minutes after drug injection, mean arterial pressure decreased by 21% after thiopental and by 39% after propofol (P less than 0.01); systemic vascular resistance index decreased by 21% after thiopental and by 44% after propofol (P less than 0.05); RAP decreased by 20% after thiopental and by 50% after propofol (P less than 0.05); mean PAP decreased by 18% after thiopental and by 32% after propofol (P less than 0.09); and LAP decreased by 40% after thiopental and by 46% after propofol (P less than 0.2). With both drugs, atrial natriuretic peptide, norepinephrine, and epinephrine plasma concentrations remained stable throughout the study period. Because cardiac output was maintained constant throughout the study, these results suggest that propofol 2.5 mg/kg is a more potent vasodilator of venous and arterial beds than is thiopental 5 mg/kg.

Adult↗
PubMed1993

Cardiac performance preserved despite thiopental loading.

BACKGROUND: Some cerebral artery aneurysms require cardiopulmonary bypass and deep hypothermic circulatory arrest to be clipped safely. During bypass these neurosurgical patients often are given large doses of thiopental in the hope that additional cerebral protection will be provided. However, thiopental loading during bypass has been associated with subsequent cardiac dysfunction in patients with heart disease. This study was undertaken to determine how patients without concomitant heart disease would respond to thiopental loading. METHODS: Twenty-four neurosurgical patients with giant cerebral aneurysms and little or no cardiac disease were anesthetized with fentanyl, nitrous oxide, and isoflurane. Thiopental was titrated to achieve electroencephalographic burst-suppression before bypass, and the infusion was continued until after separation. Prebypass hemodynamic and echocardiographic measurements were obtained during a stable baseline and 15 min after thiopental loading began. They were repeated after bypass. RESULTS: Prebypass thiopental loading increased heart rate from 61 +/- 11 to 72 +/- 13 beats/min and decreased stroke volume from 43 +/- 10 to 38 +/- 8 ml.beat-1.m-2, but arterial and filling pressures, vascular resistance, cardiac index, and ejection fraction remained the same. Before bypass, thiopental plasma concentration measured 28 +/- 8 micrograms/ml. Loading continued for 2-3 h until after bypass was terminated, and the overall infusion rate was 18 +/- 5 mg.kg-1.h-1. All patients were easily separated from bypass without inotropic support. Following bypass, vascular resistance was decreased; heart rate, filling pressures, and cardiac index were increased; stroke volume had returned to its baseline; and ejection fraction was unchanged. CONCLUSIONS: It was concluded that if preoperative ventricular function is good, thiopental loading to electroencephalographic burst-suppression causes negligible cardiac impairment and does not impede separation from cardiopulmonary bypass.

Adult↗
PubMed1995

Local cerebral glucose utilization in stimulated rats sedated with thiopental.

BACKGROUND: Recent studies have suggested that supraspinal structures are involved in barbiturate-induced enhancement of nociceptive processing. The goal of the study was to determine whether cortical and subcortical regions involved in nociception were relatively activated or depressed by noxious stimulation during infusion of small doses of thiopental. METHODS: Local cerebral glucose utilization (LCGU) was measured with the 14C-2-deoxyglucose radioautographic technique in 14 rats. During the LCGU experiment, pressure was applied to the tail every 2 min, and the somatic motor response threshold was recorded. Seven animals received thiopental infusions to produce a steady-state plasma concentration (target concentrations of 10 micrograms/ml), and seven untreated animals served as controls. RESULTS: A steady-state plasma thiopental concentration (11.1 +/- 1.8 to 13.0 +/- 2.1 micrograms/ml) was accompanied by a decrease in the somatic motor response threshold from 277 +/- 32 g (before thiopental) to 215 +/- 41 g (P < 0.001). The somatic motor response threshold remained unchanged in the control group. Average LCGU was 29% less in the thiopental-treated animals than in the untreated controls (P < 0.001). In cortical regions associated with nociception, LCGU was relatively increased (+3% +/- 14%) during the thiopental infusion in comparison to the visual and auditory cortices (-18% +/- 13%; P < 0.001). Individual structures that showed relative changes during thiopental infusion included the nucleus accumbens (+17%, P < 0.05) and the habenula (-17%, P < 0.05). Heterogenous relative changes (P < 0.05) in LCGU were observed in the auditory system: auditory cortex (-22%), medial geniculate (-16%), lateral lemniscus (+26%), superior olive (+38%). CONCLUSIONS: Noxious stimulation during low-dose thiopental infusions relatively increased LCGU in cortical regions postulated to be responsible for processing of noxious stimuli. Nuclei in the descending pain modulating system were not relatively depressed.

Animals↗
PubMed1996

Synaptic mechanisms of thiopental-induced alterations in synchronized cortical activity.

BACKGROUND: Anesthetic depth after barbiturate administration has been correlated with distinct electroencephalogram (EEG) patterns. The current study used a rat neocortical brain slice micro-EEG preparation to investigate synaptic mechanisms underlying thiopental-induced transitions in synchronized neuronal activity. METHODS: Concentration-dependent cellular actions of thiopental were investigated in brain slices using specific pharmacologic probes, whole cell patch clamps, and extracellular field recordings. Theta-Like micro-EEG oscillations were elicited in neocortical slices by mimicking subcortical cholinergic and gamma-aminobutyric acid (GABA) afferent input with carbachol (100 microM), a cholinergic agonist, and bicuculline (10 microM) a GABAA antagonist. RESULTS: In the presence of 20 microM thiopental, micro-EEG slowing from theta (7.3 +/- 0.9 Hz, mean +/- SD, n = 19) to delta frequencies (2.5 +/- 0.5 Hz, n = 11) was associated with a threefold prolongation of inhibitory currents. Burst suppression activity occurred at 50 microM thiopental, and appeared to result from direct activation of GABAA-gated chloride currents, observed with voltage clamp recordings, and mimicked with a direct acting GABAA agonist, muscimol (1 microM). Isoelectric activity occurred at 100 microM thiopental, and likely resulted from reduced glutamatergic transmission, evidenced by depressed excitatory postsynaptic potentials. Glutamatergic excitation was required for burst suppression activity, because glutamate receptor antagonists blocked thiopental-induced bursts; forcing a transition to isoelectric activity. CONCLUSIONS: Thiopental produced a continuum of EEG-like states in brain slices similar to those observed in vivo. The progression of thiopental-induced effects appear to have resulted from specific cellular actions that were recruited in a concentration-dependent manner. Progressive enhancement of synaptic inhibition followed by depression of excitatory transmission led to micro-EEG frequency slowing, burst suppression, and isoelectric activity.

Anesthetics, Intravenous↗
PubMed1998

Thiopental alters contraction, intracellular Ca2+, and pH in rat ventricular myocytes.

BACKGROUND: Myocardial contractility is regulated by intracellular concentration of free Ca2+ ([Ca2'],) and myofilament Ca2+ sensitivity. The objective of this study was to elucidate the direct effects of thiopental on cardiac excitation-contraction coupling using individual, field-stimulated ventricular myocytes. METHODS: Freshly isolated rat ventricular myocytes were loaded with the Ca2+ indicator, fura-2, and placed on the stage of an inverted fluorescence microscope in a temperature-regulated bath. [Ca2+], (340/380 ratio) and myocyte shortening (video-edge detection) were monitored simultaneously in individual cells field-stimulated at 0.3 Hz. Amplitude and timing of myocyte shortening and [Ca2+l, were compared before and after addition of thiopental. Intracellular pH was measured with the pH indicator, BCECF (500/440 ratio). Real-time uptake of Ca2+ into isolated sarcoplasmic reticulum vesicles was measured using fura-2 free acid in the extravesicular compartment. One hundred thirty-two cells were studied. RESULTS: Field stimulation increased [Ca2+]i from 85 + 10 nM to 355 + 22 nM (mean + SEM). Myocytes shortened by 10% of resting cell length (127 + 5 tlm). Times to peak [Ca2+], and shortening were 139 + 6 and 173 + 7 msec, respectively. Times to 50% recovery for [Ca2+], and shortening were 296 + 6 and 290 + 6 ms, respectively. Addition of thiopental (30-1,000 /lM) resulted in dose-dependent decreases in peak [Ca2+]i and myocyte shortening. Thiopental altered time to peak and time to 50% recovery for [Ca2+], and myocyte shortening and inhibited the rate of uptake of Ca2+ into isolated sarcoplasmic reticulum vesicles. Thiopental did not, however, alter the amount of Ca2+ released in response to caffeine in sarcoplasmic reticulum vesicles or intact cells. Thiopental (100 uM) increased intracellular pH and caused an upward shift in the dose-response curve to extracellular Ca2+ for shortening, with no concomitant effect on peak [Ca2+],. These effects were abolished by ethylisopropyl amiloride, an inhibitor of Na+-H+ exchange. CONCLUSION: Thiopental has a direct negative inotropic effect on cardiac excitation-contraction coupling at the cellular level, which is mediated by a decrease in [Ca2+],. Thiopental also increases myofilament Ca2+ sensitivity via alkalinization of the cell, which may partially offset its negative inotropic effect.

Anesthetics, Intravenous↗
PubMed1999

Ionic mechanisms mediating the differential effects of methohexital and thiopental on action potential duration in guinea pig and rabbit isolated ventricular myocytes.

BACKGROUND: Commonly used barbiturate anesthetics may significantly influence cardiac electrophysiologic characteristics. The authors evaluated thiopental (a thiobarbiturate) and methohexital (an oxybarbiturate), two compounds with similar physicochemical properties but different structures, to determine whether they have distinct effects on the major ionic currents that determine action potential duration (APD) in ventricular myocytes. METHODS: The effects of thiopental and methohexital (50 microM) on APD at 50% (APD50) and 90% (APD90) repolarization were studied in guinea pig and rabbit single ventricular myocytes using the patch-clamp technique in a whole-cell configuration. The ionic mechanisms underlying the APD changes were evaluated by measuring the anesthetics' effects on the L-type calcium inward current, the inward rectifier potassium current, and the delayed rectifier potassium current in guinea pig cells and on the transient outward potassium current in rabbit cells. RESULTS: Thiopental and methohexital caused opposite effects on APD. Whereas thiopental prolonged APD50 and APD90 in guinea pig and rabbit ventricular myocytes, methohexital shortened them. Thiopental markedly depressed both the inward and outward components of the inward rectifier potassium current, whereas methohexital caused minimal inhibition of the inward component and no change in the outward component. The delayed rectifier potassium current was inhibited by thiopental but significantly potentiated by methohexital. Neither thiopental nor methohexital significantly affected the transient outward potassium current or the L-type calcium inward current. CONCLUSIONS: Despite their similar lipid solubilities, molecular weights, and pKa values, thiopental increased and methohexital decreased the APD in ventricular myocytes by predominantly inhibiting the inward rectifier potassium current and the delayed rectifier potassium current and by increasing the delayed rectifier potassium current, respectively. These characteristics suggest distinct structure-specific actions of barbiturates on the function of myocardial ionic channels.

Action Potentials↗
PubMed2002

Selective synaptic actions of thiopental and its enantiomers.

BACKGROUND: There is conflicting evidence concerning the extent to which the intravenous general anesthetic thiopental acts by enhancing inhibitory gamma-aminobutyric acid-mediated (GABAergic) synaptic transmission or by inhibiting excitatory glutamatergic transmission. Yet there are remarkably few studies on the effects of thiopental on functional synapses. In addition, the degree of stereoselectivity of thiopental acting at synapses has yet to be tested. METHODS: The actions of thiopental and its enantiomers on GABAergic and glutamatergic synapses were investigated using voltage clamp techniques on microisland cultures of rat hippocampal neurons, a preparation that avoids the confounding effects of complex neuronal networks. RESULTS: Racemic thiopental markedly enhanced the charge transfer at GABAergic synapses without significantly affecting the peak of the postsynaptic current. At a surgically relevant concentration (25 microm), charge transfer was increased by approximately 230%. However, even at twice this concentration there were no significant effects on glutamatergic postsynaptic currents. At GABAergic synapses, thiopental acted stereoselectively, with the S(-) enantiomer being approximately twice as effective as the R(+) enantiomer at enhancing charge transfer. CONCLUSIONS: Thiopental stereoselectively enhances inhibitory GABAergic synaptic transmission in a way that reflects animal potencies, supporting the idea that this is a principal mode of action for this drug. The absence of any effect on glutamatergic synapses at surgically relevant concentrations suggests that the inhibition of these excitatory synapses is not an important factor in producing thiopental general anesthesia.

Anesthetics, Intravenous↗
PubMed1992

Deleterious effect of urokinase used to treat experimental intra-arterial thiopental injection injuries.

UNLABELLED: Inadvertent arterial drug injections continue to be an important source of morbidity. Although the clinical picture of thiopental injection has been well defined over the past 50 years, there is still much controversy concerning pathophysiology and treatment regimen. Recently, a case report showed the efficacy of urokinase in treating this problem. The current study used the reliable ear model to study more closely this phenomenon. Rabbits were divided into four groups. Ears in Group 1 rabbits (n = 10) received an intra-arterial thiopental (15 mg/kg) injection. Group 2 rabbits (n = 10) received thiopental followed by a 1-ml saline injection 15 minutes later. Group 3 rabbits (n = 10) received thiopental followed by 50,000 U of urokinase. Finally, Group 4 rabbits (n = 4) received an intra-arterial injection of saline alone. Necrosis was evaluated 2 weeks later and expressed as a percentage. Student's t tests were used to evaluate data significance. RESULTS: Group 1 (thiopental alone) and Group 2 (thiopental and saline) rabbits had significantly more necrosis than Group 4 (saline alone) rabbits, 21.2% and 17.5% versus 0% (p less than 0.001 for both). Group 3 (thiopental and urokinase) rabbits had significantly more necrosis (46.5%) than Groups 1 and 2 rabbits (p less than 0.001 for both). CONCLUSION: From this study, we found that treatment of intra-arterial thiopental injection injuries with urokinase was of no benefit, but more importantly, it increased tissue necrosis by approximately 100%. Clinical use of this treatment is to be discouraged until underlying mechanisms are better defined.

Animals↗
PubMed1980

The role of thiopental and fentanyl in the production of balanced anaesthesia.

In order to clarify the interactions between various doses of thiopental and fentanyl in producing "balanced anaesthesia", their effects on consciousness, superficial nociception, and respiration and circulation were studied during N2O+O2 inhalation in connection with the induction of anaesthesia. Altogether 60 patients were studied; the drug combinations used were thiopental 5 mg/kg (TP5), thipental 3 mg/kg (TP3), thiopental 3 mg/kg and fentanyl 0.5 micrograms/kg (TP3F0.5), thiopental 2 mg/kg and fentanyl 1 micrograms/kg (TP2F1), thiopental 1 mg/kg and fentanyl 2 micrograms/kg (TP1F2), and fentanyl 3 micrograms/kg (F3). Five minutes after the i.v. supplementation of N2O+O2 anaesthesia, the depth of anaesthesia and analgesia (antinociception) were evaluated from the eyelid reflex and by pinching an inguinal skin fold. Cardiorespiratory parameters were measured during this study period at 1-min intervals. The balance between antinociception and anaesthesia was closest to optimum in groups TP2F1 and TP2F0.5. In pure thiopental groups, the analgesia was poor; only four patients did not respond to the nociceptive stimulus, whereas in group F3 anaesthesia (disappearance of the eyelid reflex) was obtained in only two patients. The respiratory depression was most pronounced in groups receiving 3, 2 and 1 micrograms/kg fentanyl and weakest in groups where only thiopental was used. Blood pressure decreased in all groups but no statistically significant differences were noted. On the basis of the results it seems obvious that attempts to achieve what is called "balanced anaesthesia" by the supplementation of an N2O+O2 mixture with fentanyl only leads to an unnecessarily prnounced respiratory depression, whereas supplementation with thiopental alone does not offer adequate antinociception.

Adult↗
PubMed1991

Effects of thiopental and halothane on spontaneous contractile activity induced in isolated ventricular muscles of the rabbit.

To see if the known properties of thiopental of reducing Ca2+ and K+ fluxes across the myocardial sarcolemma account for its arrhythmogenic action, we have evaluated the effect of the anesthetic on spontaneous contractile activity induced in isolated rabbit papillary muscles. Thiopental (20 mg/l) prolonged the duration of sustained automaticity induced by stimulation at 1-2 Hz in the presence of 1 mumol/l isoproterenol. Thiopental (10, 20 mg/l) shortened the delay before the onset of Ba(2+)-induced automaticity, which involves a decrease in a K+ current. The minimum concentration of Ba2+ required to induce automaticity was lowered by thiopental. Whether spontaneous activities were induced by high frequency stimulation in the presence of isoproterenol or by Ba2+, thiopental lowered the frequency of spontaneous beats. Thus, thiopental appears to have both arrhythmogenic and antiarrhythmic actions, and the former may be unmasked when catecholamines counteract the latter by increasing Ca2+ influx. Like thiopental, halothane (1.0%) decreased the frequency and force of Ba(2+)-induced automatic beats but, unlike thiopental, prolonged the delay before the onset of Ba(2+)-induced automaticity, indicating that halothane acts as a purely antiarrhythmic agent in this type of automaticity.

Animals↗
PubMed1996

In vitro myocardial depression by ketamine or thiopental is dependent on the underlying beta-adrenergic tone.

BACKGROUND: Depression of myocardial contractility by muscarinic stimulation is dependent on the underlying beta-adrenergic tone. Prior beta-adrenergic stimulation enhances muscarinic negative inotropic responses, an effect that has been termed accentuated antagonism. The purpose of this study was to determine whether accentuated antagonism occurs with myocardial depression caused by thiopental or ketamine. METHODS: Using an isolated, electrically stimulated rat left afrium model, the dose-response curves to the muscarinic agonist carbachol and the anesthetics ketamine and thiopental were compared under conditions of high (10(-6)M isoproterenol bath concentration) or low (10(-6)M propranolol) beta-adrenergic tone. RESULTS: As expected, depression by carbachol was accentuated in preparations stimulated with isoproterenol compared with atria treated with propranolol. The decrease in tension by high doses (> 400 muM thiopental, > 200 muM ketamine) of thiopental or ketamine was attenuated in isoproterenol-stimulated tissue when compared with beta-adrenergic blocked muscle. Low concentrations (200 muM thiopental, 100 muM ketamine) of anesthetic caused either no change in contractility (thiopental) or small positive inotropic responses (ketamine) in pro-pranolol-treated but not isoproterenol-stimulated tissue. CONCLUSIONS. In contrast to muscarinic agonists, myocardial depression by high concentrations of ketamine or thiopental is attenuated by prior beta-adrenergic stimulation. Positive inotropic responses may be seen with low concentrations of ketamine in muscle with low beta-adrenergic tone. The results of this study demonstrate that the underlying beta-adrenergic tone greatly influences the in vitro response of cardiac tissue to ketamine or thiopental.

Adrenergic beta-Agonists↗
PubMed2005

Comparison of two thiopental infusion rates for the induction of anaesthesia in dogs.

OBJECTIVE: To compare the induction dose requirements of thiopental using two different infusion rates for induction of anaesthesia in dogs. STUDY DESIGN: Prospective, randomized study. ANIMALS: Fifty, healthy (ASA I or II) client-owned dogs with a mean age of 4.1 years and a mean mass of 20.4 kg undergoing elective surgery. MATERIALS AND METHODS: Animals were randomly assigned to receive an infusion of 2.5% thiopental at a rate of either 0.1 ml kg(-1) minute(-1) or 0.4 ml kg(-1)minute(-1), 30-40 minutes after pre-anaesthetic medication with intramuscular acepromazine (0.025 mg kg(-1)) and pethidine (3.5 mg kg(-1)). Thiopental administration was controlled by a precision syringe driver. Statistical analyses of the results, using the outcome 'mg kg(-1) required for induction' (log-transformed) included unpaired t-tests for all categorical data (thiopental infusion rate, breed, sex, obesity, sedation quality) and univariable linear regression for continuous variables (mass, age). All variables were then considered in a multivariable linear regression model. The quality of induction with the two different infusion rates was also assessed. RESULTS: After controlling for quality of sedation, the thiopental induction dose requirement was significantly less (p < 0.001) with the slower infusion rate (median = 7.5 mg kg(-1); range 4.9-13.7) compared with the faster infusion rate (median =11.0 mg kg(-1); range 6.6-18.0). The quality of sedation also affected the dose required (p = 0.03). The slower infusion rate was associated with a significantly poorer induction quality (p = 0.03) [corrected] CONCLUSIONS: Slow thiopental infusion (0.1 ml kg(-1) minute(-1)) for anaesthesia induction after acepromazine/pethidine pre-anaesthetic medication reduced the induction dose requirement, although the quality of induction was inferior. CLINICAL RELEVANCE: The induction dose of thiopental was reduced with a slower administration rate and so slow administration is recommended in thiopental-sensitive animals.

Anesthesia↗
PubMed1992

Effect of intravenous clonidine on the dose of thiopental required to induce anesthesia.

A randomized, double-blind, controlled trial was conducted to investigate the influence of intravenous clonidine on thiopental dose requirements when used for induction of anesthesia and associated hemodynamic effects. Sixty ASA physical status I or II patients were randomly allocated to one of three treatment groups: normal saline solution (control, n = 20); clonidine (2.5 micrograms/kg, n = 20); or clonidine (5 micrograms/kg, n = 20). The test drug was administered 15 min before induction of anesthesia with intravenous thiopental. The dose of thiopental to produce loss of lash reflex was recorded as well as mean arterial blood pressure and heart rate at 3-min intervals up to induction of anesthesia and then at 1-min intervals for 5 min. Significant decreases in thiopental dose were observed in both groups receiving clonidine compared with the control group, but there was no significant difference between clonidine groups. With dosage calculated according to total body mass, the control group required 5.50 +/- 1.15 mg/kg (mean +/- SD) of thiopental, whereas those who received 2.5 micrograms/kg of clonidine required 4.15 +/- 1.46 mg/kg of thiopental (a reduction of 25%), and those who received 5.0 micrograms/kg of clonidine required 3.48 +/- 1.06 mg/kg of thiopental (a reduction of 37%). When thiopental dose was adjusted for lean body mass, similar reductions were obtained. Clonidine, in both doses, produced more sedation than control, and the 2.5-mg/kg dose produced less sedation than the larger dose. Mean arterial blood pressure was lower in the groups receiving clonidine. There were no significant differences in heart rate among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Pretreatment with thiopental for prevention of pain associated with propofol injection.

UNLABELLED: Propofol causes pain on IV injection in 28%-90% of patients. A number of techniques have been tried to minimize propofol-induced pain, with variable results. We compared the efficacy of pretreatment with thiopental 0.25 mg/kg and 0.5 mg/kg and lidocaine 40 mg after venous occlusion for prevention of propofol-induced pain. One-hundred-twenty-four adult patients, ASA physical status I-II, undergoing elective surgery were randomly assigned into 4 groups of 31 each. Group I received normal saline, group II received lidocaine 2% (40 mg), and groups III and IV received thiopental 0.25 mg/kg and 0.5 mg/kg, respectively. All pretreatment drugs were made in 2 mL and were accompanied by manual venous occlusion for 1 min. Propofol was administered after release of venous occlusion. Pain was assessed with a four-point scale: 0 = no pain, 1 = mild pain, 2 = moderate pain, and 3 = severe pain at the time of propofol injection. Twenty-four patients (77%) complained of pain in the group pretreated with normal saline as compared with 12 (39%), 10 (32%), and 1 (3%) in the groups pretreated with lidocaine 40 mg, thiopental 0.25 mg/kg, and thiopental 0.5 mg/kg, respectively (P < 0.05). Thiopental 0.5 mg/kg was the most effective treatment. We therefore suggest routine pretreatment with thiopental 0.5 mg/kg along with venous occlusion for 1 min for prevention of pain associated with propofol injection. IMPLICATIONS: Pain associated with IV injection of propofol is seen in 28%-90% patients. Pretreatment with thiopental 0.25 mg/kg and 0.5 mg/kg after manual venous occlusion for 1 min effectively attenuated pain associated with propofol injection. Thiopental 0.5 mg/kg was the most effective in prevention of propofol pain and can be used routinely.

Adult↗
PubMed2006

Modulation of gamma-aminobutyric acid A receptor function by thiopental in the rat spinal dorsal horn neurons.

To assess the actions of thiopental at the spinal dorsal horn level, we examined the effects of thiopental using the whole cell patch-clamp technique on mechanically dissociated rat spinal dorsal horn neurons. Thiopental, at large concentrations, elicited a current (I(Thio)) through activation of chloride conductance, and its threshold concentration was approximately 50 microM. I(Thio) was sensitive to bicuculline, a gamma-aminobutyric acid (GABA)A receptor antagonist, but not to strychnine, a glycine receptor antagonist. At a clinically relevant concentration (30 muM), thiopental markedly enhanced the peak amplitude of a subsaturating GABA-induced current (I(GABA)) but not that of a saturating GABA-induced current. Furthermore, thiopental prolonged the time constants of both desensitization and deactivation of I(GABA). At a large concentration (300 muM), it inhibited the peak amplitude of I(GABA), which may be the result of open-channel blockade. In addition, at 30 microM, thiopental increased the duration and decreased the frequency of GABAergic miniature inhibitory postsynaptic currents. These results indicate that thiopental enhances GABAergic inhibitory transmission and suggest that GABA(A) receptors in the spinal cord are a potential target through which thiopental causes immobility and depresses the response to noxious stimuli.

Animals↗
PubMed2005

Membrane sensors for the selective determination of thiopental.

Novel miniaturized polyurethane (PU) membrane sensors in an all-solid state graphite support were developed, electrochemically evaluated and used for the assay of thiopental drug. The thiopental (T) sensors are based on the formation of ion-association complexes of thiopental with copper(II) and cobalt(II)-bathophenanthroline (bphen) counter anions as electroactive materials dispersed in a polyurethane matrix. The sensors show a linear response for thiopental over the range of 1 x 10(-1) - 5 x 10(-5) M thiopental at 25 degrees C over the pH range 6 - 11 with anionic slopes of -28.7 and -28.3 mV decade(-1) with Cu- and Co-bphen thiopental membrane sensors, respectively. These sensors exhibit a fast response time (25 - 45 s), a low detection limit (5 x 10(-6) M), a long lifetime (7 weeks) and good stability. The selectivity coefficients for thiopental sensors relative to the number of interfering anions, were investigated. These sensors were used for the direct potentiometry of thiopental in a pharmaceutical formulation and human serum. Results with mean accuracy of 99.8 +/- 0.5% of nominal were obtained, which compare well with data obtained using spectrophotometric (UV-Vis) and British Pharmacopoeia (BP) methods.

Humans↗