Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THIOPENTAL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

The concordance of early antipyrine and thiopental distribution kinetics.

Studies of factors affecting the initial disposition of drugs with a rapid onset of effect following i.v. administration have used antipyrine as a surrogate for lipophilic drugs because it lacks cardiovascular effects. The present study tested the assumption that antipyrine is a useful surrogate for the flow-dependent tissue distribution of the lipophilic drug thiopental by comparing the recirculatory pharmacokinetic models of antipyrine and thiopental disposition after concomitant administration to five dogs anesthetized with 1.5% halothane. The pharmacokinetics of indocyanine green, a marker of the intravascular behavior of antipyrine and thiopental, and antipyrine in these dogs was nearly identical to that described previously in dogs anesthetized with 1.5% halothane but not given thiopental. The total volume of distribution of the highly lipophilic drug thiopental was more than 60% larger than that of antipyrine, 53 versus 33 liters, respectively. Nonetheless, the initial distribution kinetics of the two drugs, including the pulmonary tissue volume and the volume of the nondistributive pathway as well as the clearance to it, were nearly identical. As a result, the fraction of cardiac output involved in distribution of the two drugs to peripheral tissues was similarly identical, although the distribution of cardiac output between clearance to the rapidly equilibrating tissues and clearance to the slowly equilibrating tissues differed slightly. This study validates the assumption that antipyrine is a useful surrogate for lipophilic drugs in pharmacokinetic studies in which physiologic stability is desirable to meet the assumption of system stationarity.

Animals↗

Propofol and thiopental attenuate adenosine triphosphate-sensitive potassium channel relaxation in pulmonary veins.

Pulmonary veins (PV) make a significant contribution to total pulmonary vascular resistance. We investigated the cellular mechanisms by which the intravenous anesthetics propofol and thiopental alter adenosine triphosphate-sensitive potassium (KATP+) channel relaxation in canine PV. The effects of KATP+ channel inhibition (glybenclamide), cyclooxygenase inhibition (indomethacin), nitric oxide synthase inhibition (L-NAME), and L-type voltage-gated Ca2+ channel inhibition (nifedipine) on vasorelaxation responses to levcromakalim (KATP+ channel activator) alone and in combination with the anesthetics were assessed. The maximal relaxation response to levcromakalim was attenuated by removing the endothelium and by L-NAME, but not by indomethacin. Propofol (10(-5), 3x10(-5), and 10(-4) M) and thiopental (10(-4) and 3x10(-4) M) each attenuated levcromakalim relaxation in endothelium-intact (E+) rings, whereas propofol (3x10(-5) and 10(-4) M) and thiopental (3x10(-4) M) attenuated levcromakalim relaxation in endothelium-denuded (E-) rings. In E+ rings, the anesthesia-induced attenuation of levcromakalim relaxation was decreased after pretreatment with L-NAME but not with indomethacin. In E-strips, propofol (10(-4) M) and thiopental (3x10(-4) M) inhibited decreases in tension and intracellular Ca2+ concentration ([Ca2+]i) in response to levcromakalim, and these changes were abolished by nifedipine. These findings indicate that propofol and thiopental attenuate the endothelium-dependent component of KATP+ channel-induced PV vasorelaxation via an inhibitory effect on the nitric oxide pathway. Both anesthetics also attenuate the PV smooth muscle component of KATP+ channel-induced relaxation by reducing the levcromakalim-induced decrease in [Ca2+]i via an inhibitory effect on L-type voltage-gated Ca2+ channels.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Thiopental in CSF and serum correlates with prolonged loss of cortical activity.

Barbiturate coma is initiated in brain-injured patients whenever elevated intracranial pressure remains unresponsive to other therapeutical strategies. However, barbiturates alter cortical activity resulting in difficulties in clinical evaluation. Therefore, we investigated the impact of long-term thiopental administration on responsiveness to exteroceptive stimuli in relation to pharmacokinetics of thiopental in CSF and serum. Long-term infusion increases thiopental levels which remain elevated for 6 and 9 days in CSF and serum, respectively, after termination of its administration. Prolonged unresponsiveness to exteroceptive stimuli correlates with persisting thiopental in CSF and serum. Thus, quantitative analysis of thiopental in serum becomes indispensable in predicting the length of drug-induced neurological impairment and in avoiding misinterpretation of the neurological status.

Adolescent↗

Torsade de pointes and sudden death induced by thiopental and isoflurane anesthesia in dogs with cardiac electrical remodeling.

BACKGROUND: Many anesthetic agents are known to have cardiac effects. The effects of pentobarbital, thiopental and isoflurane on dogs with electrical remodeling are lacking. METHODS AND RESULTS: We studied 12 dogs that underwent two anesthesias. First, anesthesia was induced (N=12) with intravenous thiopental (17 mg/kg) induction followed by isoflurane inhalation (1.5%-3% via endotracheal tube). For electrical remodeling, we created complete atrioventricular block (CAVB) and myocardial infarction (MI). In 6 of the 12 dogs we also infused nerve growth factor (NGF) to the right stellate ganglion. All dogs had an implantable cardioverter-defibrillator (ICD) implanted. A second anesthesia was done 66 +/- 20 days later. In 8 of the 12 dogs (6 without NGF), pentobarbital was used as the only anesthetic. In the remaining 4 dogs (all with NGF), 3 received thiopental and 1 received isoflurane. RESULTS: During the first anesthesia, none of 12 dogs had cardiac arrhythmia. During the second anesthesia, none of the 8 dogs that received pentobarbital developed ventricular fibrillation (VF). In contrast, all the dogs receiving either thiopental or isoflurane died of VF within 2 to 3 minutes. QT and P-P intervals before VF were 440 +/- 36 milliseconds and 298 +/- 28 milliseconds, longer and shorter (respectively) than those obtained the day prior to surgery (315 +/- 25 milliseconds, P < 0.001; 330 +/- 22 milliseconds, P < 0.01, respectively). CONCLUSION: Thiopental and isoflurane are not arrhythmogenic in normal dogs and dogs with acute MI and CAVB, but are extremely proarrhythmic in dogs with chronic MI and CAVB. Consistent with the results of in vitro studies, pentobarbital did not induce ventricular arrhythmia in dogs with cardiac electrical remodeling.

Anesthetics, Inhalation↗

Thiopental and succinylcholine: Action on intraocular pressure.

Intraocular pressure (IOP) measurements were made in a series of 92 male surgical patients, to assess the effects of timing and dosage of succinylcholine given after a standardized sleep dose of thiopental (3 mg./kg.). The major findings of this study were as follows: (1) thiopental alone lowered IOP; (2) a small (0.5 mg./kg.) dose of succinylcholine, given immediately after thiopental, returned IOP to normal; (3) a large (1 mg./kg.) dose of succinylcholine immediately after thiopental maintained the IOP at a low value; (4) if 2 minutes elapsed between thiopental and 1 mg./kg. of succinylcholine, the relaxant raised the IOP to slightly above preanesthetic control values; (5) tracheal intubation caused a significant rise in IOP, more than any effect from succinylcholine itself; (6) succinylcholine drip (0.1 percent), begun after establishment of satisfactory endotracheal halothane-nitrous oxide anesthesia, caused significant IOP elevation in 4 of 11 patients.

Adult↗

Naloxone fails to antagonize thiopental anesthesia.

A study was undertaken to determine the effect in man of naloxone on the central nervous system depression produced by IV thiopental. Eight normal volunteers were given 5 mg/kg thiopental IV. On a separate occasion the same 8 volunteers were given 50 microgram/kg naloxone IV 5 minutes prior to 5 mg/kg thiopental. Naloxone had no significant effect on the rate of return of consciousness following administration of thiopental. Naloxone also had no significant effect on the responses of blood pressure, heart rate, or respiratory rate to thiopental.

Adult↗

Depression of lung mucociliary dlearance by thiopental and halothane.

It has previously been demonstrated that an induction dose of thiopental, 25 mg/kg, without continuing anesthesia did not depress peripheral lung mucociliary clearance in the dog, whereas 2 hours of anesthesia with halothane, 1.2 MAC, did depress clearance. To determine whether this was because thiopental depresses the mucociliary apparatus less than halothane, this study compared mucociliary clearance after 2 hours of anesthesia with halothane with clearance after 2 hours of anesthesia with thiopental, 40 mg/kg. With thiopental, 40 mg/kg, 50% mucociliary clearance of tantalum from peripheral airways required 280 +/- 65 (SEM) minutes, which was comparable to clearance obtained with halothane, 1.2 MAC, 382 +/- 27 (SEM) minutes. Hence thiopental depresses mucociliary clearance as much as halothane does when both are administered in equivalent anesthetic doses for equal periods of time.

Anesthesia, Inhalation↗

Inhibition of sympathetic neural outflow during thiopental anesthesia in humans.

The effects of sodium thiopental on postganglionic muscle sympathetic nerve activity (MSNA) and the reflex augmentation in MSNA produced by hypotension were examined in seven ASA physical status I and II patients, 34-65 yr old. Direct recordings of MSNA were obtained from a 5-micron-tipped, epoxy-coated needle percutaneously placed into the common peroneal nerve. Induction of anesthesia with sodium thiopental (4 mg/kg) significantly decreased R-R interval duration an average of 157 +/- 44 ms (mean +/- SEM) decreased systolic pressure (radial artery) an average of 11 +/- 4 mm Hg, and reduced tonic MSNA from 38 +/- 11 to 18 +/- 5 bursts/100 cardiac cycles (P less than 0.01). Baroreceptor reflex regulation of cardiac intervals and MSNA were determined by sequential boluses of nipride (100 micrograms) and phenylephrine (150 micrograms). Awake baroreceptor slopes relating R-R interval to systolic pressure were 9.5 +/- 2.9 ms/mm Hg and decreased 61% to 2.4 +/- 0.5 ms/mm Hg (P less than 0.01) during sodium thiopental infusions (0.25 mg.kg-1.min-1). Moreover baroreceptor slopes relating MSNA to diastolic pressure in awake patients were -4.0 +/- 0.9 bursts/mm Hg and were reduced by 95% to -0.3 +/- 0.18 bursts/mm Hg (P less than 0.01). Despite the fact that hypotension did not elicit increases in MSNA in anesthetized patients, laryngoscopy and tracheal intubation produced profound augmentations in MSNA. Thus, sodium thiopental reduces tonic levels of MSNA and markedly attenuates baroreceptor reflex control mechanisms. However, profound augmentations in sympathetic activity occurred in response to laryngoscopy and tracheal intubation during thiopental anesthesia.

Adult↗

A comparison of the cerebral protective effects of etomidate, thiopental, and isoflurane in a model of forebrain ischemia in the rat.

We evaluated the effect of etomidate, thiopental, and isoflurane on ischemic neuronal injury in rats. Control group animals received 1.2% isoflurane. The animals in the etomidate and thiopental groups received an infusion of either etomidate or thiopental until electroencephalographic (EEG) burst-suppression was attained. In the fourth group, the isoflurane concentration was increased to 3% (sufficient to produce EEG burst-suppression). Forebrain ischemia was induced by bilateral carotid artery occlusion with simultaneous hypotension for 10 min. Three days after ischemia, two blinded observers evaluated neuronal injury in coronal brain sections stained with hematoxylin and eosin. Injury to the ventral CA1 of the hippocampus was less in the etomidate group than in the control group. Injury to the entorhinal cortex was less in the thiopental group than in the control group. Histopathologic outcome in animals anesthetized with 1.2% isoflurane and 3% isoflurane was not different. Although these data indicate that etomidate and thiopental might reduce ischemic injury in some structures, the magnitude of the protective effects observed was small.

Animals↗

Remifentanil with thiopental for tracheal intubation without muscle relaxants.

UNLABELLED: Tracheal intubation may be accomplished with remifentanil and a non-opioid IV anesthetic without a muscle relaxant. In this study, we evaluated in double-blinded, prospective, randomized manner the dose requirements for remifentanil with thiopental without muscle relaxant administration to obtain clinically acceptable intubation conditions and cardiovascular responses. After premedication with midazolam 0.03 mg/kg IV, 105 patients were randomized equally to one of three study groups, each receiving the following: remifentanil 2 micro g/kg (Group I), 3 micro g/kg (Group II), and 4 micro g/kg (Group III). Remifentanil was administered over 30 s, and anesthesia was induced with thiopental 5 mg/kg. Tracheal intubation conditions were assessed by the anesthesiologist performing the intubation as: (a) excellent, (b) satisfactory, (c) fair, and (d) unsatisfactory. There were no statistically significant differences among groups regarding to demographic data. Blood pressure and heart rate did not increase in any group after accomplishing intubation. There was a significant improvement in intubation conditions between Groups I and II, I and III, and II and III (P < 0.001). We conclude that remifentanil 4 micro g/kg administered before thiopental 5 mg/kg provided excellent or satisfactory intubation conditions in 94% of patients and prevented cardiovascular responses to intubation. IMPLICATIONS: We evaluated in a double-blinded manner the dose requirements for remifentanil with thiopental without muscle relaxants for obtaining acceptable intubation condition. Our results show that remifentanil 4 micro g/kg administered before thiopental provided excellent or satisfactory intubation condition in 94% of patients.

Adolescent↗

Electroencephalographic burst suppression versus loss of reflexes anesthesia with propofol or thiopental: differences of variance in the catecholamine and cardiovascular response to tracheal intubation.

UNLABELLED: The electroencephalographic burst suppression pattern (BSP) might indicate the brain's effect-site concentration of anesthetics more precisely than clinical signs and thus eliminate bias from studies on the reaction to tracheal intubation after different induction drugs. To test this hypothesis, we compared the catecholamine and cardiovascular responses and their variances to tracheal intubation when either BSP was induced by infusion of propofol (30 mg x kg(-1) x h(-1); n = 14) or thiopental (75 mg x kg(-1) x h(-1); n = 14) or anesthesia by repeated bolus doses until loss of reflexes (LR), initially of propofol 2.5 mg/kg (n = 15) or thiopental 5 mg/kg (n = 15). The standard deviations were more often smaller in the BSP than in the LR groups, but the results of Levene's test for differences of variance were insignificant. At the LR level, propofol attenuated catecholamine, arterial blood pressure, and heart rate responses to intubation better than thiopental, but at the BSP level, only the norepinephrine response was better attenuated. Cp50 concentrations of propofol and thiopental at the onset of BSP were 9.65 and 31.60 micro g/mL, respectively. IMPLICATIONS: Our results did not support the hypothesis that the responses to tracheal intubation can be more accurately predicted when unconsciousness is controlled with the aid of an electroencephalographic burst suppression pattern. Significant differences were found in the reactions between propofol and thiopental. At the burst suppression level, the catecholamine response was abolished with propofol.

Adult↗

The effects of melatonin premedication on propofol and thiopental induction dose-response curves: a prospective, randomized, double-blind study.

BACKGROUND: The effect of melatonin on the intraoperative requirements for i.v.anesthetics has not been documented. We studied the effect of melatonin premedication on the propofol and thiopental dose-response curves for abolition of responses to verbal commands and eyelash stimulation. METHODS: This prospective, randomized, double-blind study included 200 adults with ASA physical status I. Patients received either 0.2 mg/kg melatonin or a placebo orally for premedication (n = 100 per group). Approximately 50 min later, subgroups of 10 melatonin and 10 placebo patients were administered various doses of propofol (0.5, 1.0, 1.5, 2.0, or 2.4 mg/kg) or thiopental (2.0, 3.0, 4.0, 5.0, or 6.0 mg/kg) for anesthetic induction. The ability of each patient to respond to the command, "open your eyes," and the disappearance of the eyelash reflex were assessed 60 s after the end of the injection of propofol or thiopental. Dose-response curves were determined by probit analysis. RESULTS: Melatonin premedication decreased thiopental ED50 values for loss of response to verbal command and eyelash reflex from 3.4 mg/kg (95% confidence interval, 3.2-3.5 mg/kg) and 3.7 mg/kg (3.5-3.9 mg/kg) to 2.7 mg/kg (2.6-2.9 mg/kg) and 2.6 mg/kg (2.5-2.7 mg/kg), respectively (P < 0.05). Corresponding propofol ED50 values decreased from 1.5 mg/kg (1.4-1.6 mg/kg) and 1.6 mg/kg (1.5-1.7 mg/kg) to 0.9 mg/kg (0.8-0.96 mg/kg) and 0.9 mg/kg (0.8-0.95 mg/kg), respectively (P < 0.05). CONCLUSIONS: Melatonin premedication significantly decreased the doses of both propofol and thiopental required to induce anesthesia.

Adolescent↗

Effects of intravenous anesthetics, thiopental, fentanyl, and morphine on ventricular delayed activation in a canine myocardial infarction model.

We examined the effects of intravenous anesthetics (thiopental, fentanyl and morphine) on the ventricular activation in a canine myocardial infarction model. Thiopental at 5 and 10 mg/kg delayed or abolished the delayed activation in the infarcted zones with slight delay of activation of the normal zones. Fentanyl at 30 micrograms/kg slightly but significantly prolonged the activation time in both normal and infarcted zones. Morphine at 1 mg/kg did not produce any significant effect. Thiopental, but neither fentanyl nor morphine, inhibited ventricular stimulation-induced arrhythmias. Thus, thiopental, but not fentanyl nor morphine, markedly depressed the delayed activation in myocardial infarction, which may affect and probably inhibits the ventricular arrhythmias in myocardial infarction. It also should be kept in mind that thiopental may have arrhythmogenic effects in myocardial infarction.

Action Potentials↗

Pharmacokinetic and pharmacodynamic consequences of thiopental in renal dysfunction rats: evaluation with electroencephalography.

The purpose of this work was to investigate the disposition characteristics and pharmacodynamics of a barbiturate, thiopental, in renal dysfunction rats. Normal and renal dysfunction rats were infused with 40 and 20 mg/kg of thiopental, respectively. The quantitative electroencephalographic (EEG) method was used as the surrogate measure of pharmacological response. Signals from two electrodes fitted on the skull of rats were continuously measured, recorded and subjected to off-line analysis. Total amplitude (0.5-29.9Hz) from aperiodic analysis was taken as the EEG parameter. Thiopental concentration in plasma and cerebrospinal fluid (CSF) was assayed by an HPLC method. Steady-state volume of distribution was increased in renal dysfunction rats due to decreased plasma protein binding, while no change in clearance or volume of distribution based on the plasma unbound concentration was observed. Amplitude changes induced by thiopental in both normal and renal dysfunction rats were characterized by the sigmoidal Emax model. The unbound plasma concentration at half maximal effect was lowered by 30% in renal dysfunction rats as compared to the normal rats. In addition to considerable alteration in the pharmacokinetics of thiopental, it was also evident that renal impairment is associated with an increase in apparent pharmacological sensitivity, which is related to affinity.

Analysis of Variance↗

Anesthetic induction agents, sympathetic nerve activity and baroreflex sensitivity: a study in rabbits comparing thiopental, propofol and etomidate.

The mechanisms of arterial hypotension following intravenous anesthetic induction agents are multifactorial. The purpose of this study was to evaluate and compare the effects of thiopental, propofol and etomidate on hemodynamics, sympathetic outflow and arterial baroreflex sensitivity using not only neuraxis-intact but also totally baro-denervated rabbits. A total of 60 rabbits was anesthetized with urethane, tracheotomized, and mechanically ventilated with oxygen in nitrogen (FiO2 0.5). The left renal sympathetic nerve was isolated and placed on a bipolar electrode to record renal sympathetic nerve activity (RSNA). Thirty animals underwent a surgical preparation of total baroreceptor denervation. Bolus injections of an anesthesia induction dose of thiopental 4 mg/kg and twice the induction dose of propofol 4 mg/kg significantly decreased RSNA to the same extent (19.4+/-6.7 and 19.7+/-5.2% reduction, mean +/- SEM) and mean arterial pressure (MAP) also to the same extent (19.5+/-4.6 and 22.1+/-3.1% reduction) in the neuraxis-intact animals. RSNA was increased (34.5+/-6%) without reduction of MAP by an induction dose of etomidate, 0.3 mg/kg. Sympathetic barosensitivity was attenuated even 10 min after thiopental at 4 mg/kg or propofol at 4 mg/kg (68% and 54% of control, respectively). Propofol at 2 mg/kg (induction dose) and etomidate at 0.6 mg/kg decreased RSNA and MAP only in the baro-denervated animals. It was found from the barosensitivity study that patients can be hemodynamically unstable even though blood pressure has returned to normal after thiopental and propofol administration. Data suggest that etomidate can even stimulate the sympathetic nervous system and increase sympathetic outflow. It was also clearly found from the baro-denervated animal study that thiopental was stronger than propofol in directly suppressing sympathetic outflow at the induction dose.

Anesthetics, Intravenous↗

Effects of thiopental, ketamine, etomidate, propofol and midazolam on the production of adrenomedullin and endothelin-1 in vascular smooth muscle cells.

Endothelin-1 (ET-1) and adrenomedullin (AM) are potent vasoconstrictive and vasodilative peptides. Vascular smooth muscle cells are one of the major producing tissues of these peptides. We investigated effect of thiopental, ketamine, etomidate, midazolam and propofol on the production of ET-1 and AM in cultured rat aorta vascular smooth muscle cells. Rat cultured vascular smooth muscle cells are used and the dose-dependent effect (10(-8)-10(-4) M) of thiopental, ketamine, etomidate, midazolam, and propofol on the production of ET-1 and AM was examined. The concentration of these peptides in the culture medium were measured by radioimmunoassay. Ketamine, etomidate, propofol and midazolam, but not thiopental, decreased the production of ET-1 at a concentration of 10(-4) M and the effect of midazolam is the most potent. Thiopental and etomidate produced small but significant increases in the production of AM at a concentration of 10(-4) M. Ketamine did not affect the production, but propofol and midazolam decreased the production at 10(-4) M and 10(-5) M, respectively. These results suggest that thiopental, ketamine, etomidate, propofol and midazolam differentially affect the production of ET-1 and AM in rat vascular smooth muscle cells.

Adrenomedullin↗

The depressant effect of halothane and sodium thiopental on the spontaneous and evoked activity of dorsal horn cells: lamina specificity, time course and dose dependence.

The effects of halothane and sodium thiopental on dorsal horn cell unit activity were studied in the lumbar spinal cord of decerebrate, low thoracic spinal cats. Both halothane (0.5, 1 and 1.5%) and sodium thiopental (2.5, 5 and 10 mg/kg) depressed, in a dose-dependent manner, the spontaneous firing frequency of cells in Rexed laminae I, V and VI and the evoked firing frequency of cells in laminae I and V. They, however, had no effect on cells in lamina IV. The maximum depression of cell activity occurred 5 to 8 minutes after inhalation of halothane and 2 to 3 minutes after the intravenous administration of sodium thiopental. The recovery of cell activity occurred within 15 to 30 minutes after discontinuation of halothane and within 10 to 30 minutes after intravenous administration of sodium thiopental. The depressive effect of halothane and sodium thiopental, both primarily hypnotic anesthetics, on lamina VI cells is in contrast to our previous finding that morphine sulfate, nitrous oxide and ketamine hydrochloride, primarily analgesic agents, had no significant effect on this lamina.

Animals↗

Comparative benefit of preemptively applied thiopental for propofol injection pain: the advantage over lidocaine.

Propofol is one of the most frequently applied intravenous anesthetics for the induction of general anesthesia. However, pain on injection of this agent is a considerable problem in daily anesthesia practice because of its severity. Administration of lidocaine prior to propofol injection is a standard technique for reducing the pain on injection. However, this method provides insufficient pain relief. To evaluate whether pretreatment with an ultra-short acting barbiturate, thiopental, is more effective than with lidocaine, a randomized and single-blinded trial was conducted. Patients (20-65 years old, n = 137) were allocated into six groups, and applied with physiological saline, thiopental (25, 50, 75, or 100 mg), or lidocaine (40 mg) at 30 second prior to propofol injection (1 mg/kg, 1200 ml/h). The patient was interviewed about the degree of pain just after propofol was totally injected. Both thiopental (> or =25 mg) and lidocaine decreased the severity of pain in comparison with physiological saline as evaluated by a six-graded pain score. Lidocaine failed to influence the incidence of pain (from 86% to 55%), although thiopental significantly decreased it to 40% (25 mg), 21% (50 mg), 12% (50 mg), and 0% (100 mg), respectively. Thiopental (> or =50 mg) decreased both the severity and incidence of pain more effectively than lidocaine. A Hill plot analysis of these data, after rearrangement by patient's body weight, estimated that the half-effective dose (ED50) and the ED99 of this drug to block pain on injection of propofol were 0.6 and 1.4 mg/kg, respectively.

Adult↗