Effects Of Barbiturates Research Articles

THE UNPREDICTABLE HISTORY OF THALIDOMIDE

The article reflects the history of thalidomide, synthesized by the West German pharmaceutical company Chemie Gr?nenthal in 1954. Initially the drug was promoted as an effective hypnotic, devoid of the adverse effects of barbiturates. The drug became very popular in Germany and beyond its borders, and had been used in more than 40 countries. At some point thalidomide began to be offered for the treatment of nausea in pregnancy. However with time a gradual increase in the incidence of congenital malformations in children whose mothers took thalidomide during pregnancy was noted. Two doctors – Widukind Lenz and William McBride – are known for drawing public attention to the dangerous consequences of the drug usage in pregnancy. Initially, thalidomide manufacturers denied their guilt, however a numerous number lawsuits obliged pharmaceutical companies to pay huge financial compensations to the victims of thalidomide. In the United States, FDA employee Francis Kelsey became famous for not giving permission for thalidomide for the US pharmaceutical market despite its unrestricted usage in European countries. The article provides information about some thalidomide victims who were able to live an active life and become famous. After the recognition of the thalidomide tragedy the therapeutic usage of the drug seemed to be irrevocably terminated. However, in 1964 the Israeli doctor Yakov Sheskin almost by occasion discovered the therapeutic effect of thalidomide on some types of leprosy. In subsequent years the effectiveness of the drug was reported in a number of other diseases. However, the “thalidomide tragedy” with its teratogenicity is still holding back the widespread use of the drug. The bad experience of thalidomide should be a painful lesson for the pharmaceutical industry, but unfortunately, the story can be repeated, that is exemplified by the obesity drug scandal this year.

Sedation-Induced Burst Suppression Predicts Positive Outcome Following Traumatic Brain Injury.

While electroencephalogram (EEG) burst-suppression is often induced therapeutically using sedatives in the intensive care unit (ICU), there is hitherto no evidence with respect to its association to outcome in moderate-to-severe neurological patients. We examined the relationship between sedation-induced burst-suppression (SIBS) and outcome at hospital discharge and at 6-month follow up in patients surviving moderate-to-severe traumatic brain injury (TBI). For each of 32 patients recovering from coma after moderate-to-severe TBI, we measured the EEG burst suppression ratio (BSR) during periods of low responsiveness as assessed with the Glasgow Coma Scale (GCS). The maximum BSR was then used to predict the Glasgow Outcome Scale extended (GOSe) at discharge and at 6 months post-injury. A multi-model inference approach was used to assess the combination of predictors that best fit the outcome data. We found that BSR was positively associated with outcomes at 6 months (P = 0.022) but did not predict outcomes at discharge. A mediation analysis found no evidence that BSR mediates the effects of barbiturates or propofol on outcomes. Our results provide initial observational evidence that burst suppression may be neuroprotective in acute patients with TBI etiologies. SIBS may thus be useful in the ICU as a prognostic biomarker.

What are the effects of prophylactic benzodiazepines, barbiturates, and anticonvulsants for management of febrile seizures in children?

What are the effects of prophylactic benzodiazepines, barbiturates, and anticonvulsants for management of febrile seizures in children?

Uses and Side Effects of Barbiturate

Uses and Side Effects of Barbiturate

Sedative-Hypnotics: Addiction and Current Research Status

Central nervous system depressants, e.g. alcohol, barbiturates, and benzodiazepines, have a wide spectrum of activity in human and animals. These depressants produce varying degrees of CNS depression, depending mainly upon the dose used. In small doses, they can alleviate anxiety and/or reduce spontaneous activity; in moderate doses, they induce sleep; with large doses, severe CNS depression progresses to anesthesia, coma or even death. This graded, dose-dependent CNS depression is a common feature of these agents. In addition to causing CNS depression, these agents also possess other pharmacological properties, e. g. muscle relaxation, Anticonvulsant activity, respiratory depression, hypothermia, etc. Tolerance-dependence developing to sedative-hypnotics is a common feature following continuous administration of sedative-hypnotics. Tolerance is defined as a decreasing response to repeated administration of the same dose of a sedative-hypnotic or as a necessary increase of the dosage to obtain the initial response. There are two types of tolerance-one dispositional (pharmacokinetic), the other functional (pharmacodynamic). Dependence is defined as a modification of physiological functions that require continuous drug adiministration to prevent the appearance of withdrawal symptoms. Abrupt withdrawal from long-term usage of these drugs may produce anxiety, dizziness, nausea and vomiting, insomnia, muscular twitching, hyperthermia, delirium, tremors, convulsions, and death. Evidence accumulated suggests that some of the pharmacological actions exerted by sedative-hypnotics, e.g benzodiazepines, barbiturates and alcohol, may be mediated through the GABA system by mimicking GABAergic transmission. However, the mechanisms of the actions of these agents on the GABA system remain to be elucidated. Benzodiazepines have been demonstrated to have receptors which are parts of the GABAA receptors (GABA benzodiazepine receptor chloride ionophore complexes). Although a definitive barbiturate binding site has not yet been identified, the available evidence strongly suggests that barbiturate binding sites and convulsant binding sites are separate but allosterically affect each other. As far as ethanol is concerned, it is likely that multiple neurotransmitter systems are affected. Therefore, it is still unclear how alcohol, barbiturates, and benzodiazepines are functionally associated with the GABA system. The evidence summarized demonstrates that the GABA synapse plays an important role in the pharmacologic effects of barbiturates, alcohol and benzodiazepines. There are similarities and differences in the effects of these CNS depressants on the pharmacology and biochemistry of the GABA synapse. The effects of alcohol, barbiturates and benzodiazepines on GABA synapses are different in different brain regions. Furthermore, the results which have been reported in the literature are inconsistent. This may be due

What are the effects of prophylactic benzodiazepines, barbiturates, and anticonvulsants for management of febrile seizures in children?

What are the effects of prophylactic benzodiazepines, barbiturates, and anticonvulsants for management of febrile seizures in children?

Effect of Intravenous Phenobarbital on Left Ventricular Myocardial Contractility Determined by Echocardiography in Children

Animal studies and rare human studies have suggested a negative effect of barbiturates on cardiac function. Although intravenous (IV) phenobarbital is used routinely in children in the clinical setting, studies in children are lacking. We performed a study to evaluate effect of IV phenobarbital loading on myocardial systolic function of children. In a prospective pilot study in children without congenital heart defects, the effect of IV phenobarbital was evaluated on the left ventricular systolic function measured by ejection fraction (EF) by Simpson's method via an echocardiogram. Any child less than 18 years of age who received IV loading dose of at least 20 mg/kg of phenobarbital given as an infusion over 20 - 30 minutes for various medical indications was eligible to take part in the study. Three measurements of EF by an echocardiogram were made: before loading dose, 30 minutes after completion of the loading dose, and prior to the first maintenance dose. Relevant clinical data were recorded, including vital signs, immediately prior to each echocardiogram. Change of function as measured by EF over time was analyzed using linear mixed modeling methods. For this study, significant change in blood pressure was defined as a drop of at least 20 mmHg in systolic blood pressure. Ten children (70% female, age range two days to 8.2 years) were enrolled. Three had hypotension with a drop of systolic blood pressure greater than 20 mmHg from baseline. On examining the trajectory of EF on each individual graphically, the left ventricular EF tended to fall immediately following phenobarbital therapy and return to baseline on re-evaluation. These trajectories were statistically significant for EF. Phenobarbital had a direct and transient depressant effect on systolic function of the myocardium in one third of the cases. The depression in EF appeared to be transient with return to baseline in less than 24 hours. We recommend close monitoring with anticipation of decreased function in children when using IV phenobarbital.

The Second Anesthetists' Travel Club Meeting: Bootleggers, Madison and Ralph Waters!

The second annual meeting of any organization is almost as critical as the first. A second meeting begins to assure the viability and importance of the organization. After the very successful first meeting of the Anesthetists' Travel Club in Rochester, Minnesota, in December of 1929, Ralph Waters (1883-1979) was charged with hosting the 1930 meeting at the University of Wisconsin in Madison. The meeting was held Thursday December 18th through Saturday December 20th. Dr. Waters started the meeting at 8:00 am with a tour of the operating rooms of the Wisconsin General Hospital. Lunch followed at the Memorial Union with the afternoon split between experimental surgery, and the anatomy, and physiology laboratories. There was an early dinner before the group took in the basketball game between the University of Pennsylvania and the University of Wisconsin. Friday's meeting was very similar; starting in the operating rooms at 8:00 am followed by a Union Club lunch. The afternoon was spent in the Pharmacology laboratory with a 4:00 pm lecture entitled “Demonstration Clinical Effects of Barbiturates in Neuropsychiatry”. Dinner was held at the University Club. Saturday's program followed the same lines, but with an afternoon tea and a dinner at the Waters' home. In February1931, almost a year to the date from his first note, Waters wrote to those who had attended the meeting. He followed up on the clinical cases the group had seen, and commented upon the Guedel-Waters balloons for endotracheal tubes and the spinal he had performed. He even commented upon the use of cyclopropane in obstetrics. Thus, the Anesthetists' Travel Club meeting in 1930 successfully concluded.

Benzylidene Barbituric Acid Derivatives Shown Anticonvulsant Activity on Pentylenetetrazole-Induced Seizures in Mice: Involvement of Nitric Oxide Pathway

ABSTRACT Background: Barbituric acid derivatives have long been used as central nervous system (CNS) suppressants, such as sedatives, hypnotics and anticonvulsants. In addition, previous studies have implicated the involvement of nitric oxide (NO) in the anticonvulsive effects of barbiturates in CNS. Therefore, the purpose of this study was to figure out the effects of a novel class of barbituric acid derivatives on pentylenetetrazole (PTZ)-induced seizures in male mice. Methods: Thirteen synthesized barbituric acid derivatives (a-m) and phenobarbital were administered intraperitoneally (i.p.) 30 min before induction of seizures by PTZ administration. The mechanisms of PTZ-induced seizures in the mice was evaluated using a non-selective nitric oxide synthase (NOS) inhibitor, selective inducible NOS (iNOS) inhibitor, a selective neuronal NOS (nNOS) inhibitor, and NO substrate. Results: Administration of most of the above mentioned derivatives significantly increased the seizures threshold (P<0.001). The most potent derivative (compound a), was chosen in order to investigate the mechanism of action involving in anticonvulsant activity. Administration of a non-selective NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) and a selective nNOS inhibitor, 7-nitroindazole (7-NI) reversed anticonvulsant activity of compound a. However, injection of the nitric oxide precursor, L-arginine (L-Arg) and a selective iNOS inhibitor, aminoguanidine (AG), did not change anticonvulsant activity of the mentioned compound. Conclusion: These results indicated that the NO system, specifically nNOS may contribute to the anticonvulsant activity of benzylidene barbituric acid derivative a. Therefore, this compound is a good candidate in order to designing new anticonvulsant medications

Thiamylal sodium increased inflammation and the proliferation of vascular smooth muscle cells.

BackgroundThiamylal sodium is a common anesthetic barbiturate prepared in alkaline solution for clinical use. There is no previously reported study on the effects of barbiturates on the inflammation and proliferation of vascular smooth muscle cells (VSMCs). Here, we examined the effects of clinical-grade thiamylal sodium solution (TSS) on the inflammation and proliferation of rat VSMCs.MethodsExpression levels of interleukin (IL)-1α, IL-1β, IL-6, and toll-like receptors in rat VSMCs were detected by quantitative reverse transcription-polymerase chain reaction and microarray analyses. The production of IL-6 by cultured VSMCs or ex vivo-cultured rat aortic segments was detected in supernatants by enzyme-linked immunosorbent assay. VSMC proliferation and viability were determined by the water-soluble tetrazolium-1 assay and trypan blue staining, respectively.ResultsTSS increased expression of IL-1α, IL-6, and TLR4 in VSMCs in a dose-dependent manner, and reduced IL-1β expression. Ex vivo TSS stimulation of rat aorta also increased IL-6. Low concentrations of TSS enhanced VSMC proliferation, while high concentrations reduced both cell proliferation and viability. Expression of IL-1 receptor antagonist, which regulates cell proliferation, was not increased by TSS stimulation. Exposure of cells to the TSS additive, sodium carbonate, resulted in significant upregulation of IL-1α and IL-6 mRNA levels, to a greater extent than TSS.ConclusionsTSS-induced proinflammatory cytokine production by VSMCs is caused by sodium carbonate. However, pure thiamylal sodium has an anti-inflammatory effect in VSMCs. TSS exposure to VSMCs may promote vascular inflammation, leading to the progression of atherosclerosis or in-stent restenosis, resulting in vessel bypass graft failure.

Plurality of anxiety and depression alteration mechanism by oleanolic acid.

Our study sought to evaluate the anxiolytic and antidepressant activities of oleanolic acid as well as the neural mechanisms involved. Animal models such as barbiturate sleep-induction, light-dark box, elevated plus maze, forced swimming test, tail suspension test and open field test were conducted. Male Albino Swiss mice were treated orally with vehicle 10 mL/kg, fluoxetine 20 mg/kg, imipramine 15 mg/kg, diazepam 1 mg/kg or oleanolic acid 5-40 mg/kg. Pretreatment (intraperitoneal) of animals with pentylenetetrazole (PTZ) 20 mg/kg, 1-(2-methoxyphenyl)-4-[4- (2-phthalimido) butyl]piperazine hydrobromide (NAN-190) 0.5 mg/kg, p-chlorophenylalanine methyl ester (PCPA) 100 mg/kg or α-methyl-p-tyrosine (AMPT) 100 mg/kg, WAY100635 (WAY) 0.3 mg/kg, prazosin (PRAZ) 1 mg/kg, yohimbine 2 mg/kg as well as monoamine oxidase assay and hippocampal brain-derived neurotrophic factor (BDNF) quantification were carried out. Oleanolic acid potentiated the hypnotic effect of barbiturate and demonstrated an anxiolytic effect in both the light-dark box and elevated plus maze. This effect was not reversed by PTZ. Acute and/or chronic oral treatment of mice with oleanolic acid (5-20 mg/kg) elicited an antidepressant effect in the forced swimming test and the tail suspension test without interfering with the locomotor activity. The antidepressant effect of oleanolic acid was attenuated by NAN-190, AMPT, PCPA, WAY and PRAZ. Although monoamine oxidase activity remained unaltered by oleanolic acid, chronic administration of oleanolic acid augmented hippocampal BDNF level. These findings demonstrate multiple mechanisms of the anxiolytic and antidepressant effect of oleanolic acid.

Barbiturates for acute traumatic brain injury.

Raised intracranial pressure (ICP) is an important complication of severe brain injury, and is associated with high mortality. Barbiturates are believed to reduce ICP by suppressing cerebral metabolism, thus reducing cerebral metabolic demands and cerebral blood volume. However, barbiturates also reduce blood pressure and may, therefore, adversely effect cerebral perfusion pressure. To assess the effects of barbiturates in reducing mortality, disability and raised ICP in people with acute traumatic brain injury. To quantify any side effects resulting from the use of barbiturates. The following electronic databases were searched on 26 September 2012: CENTRAL (The Cochrane Library), MEDLINE (Ovid SP), PubMed, EMBASE (Ovid SP), PsycINFO (Ovid SP), PsycEXTRA (Ovid SP), ISI Web of Science: Science Citation Index and Conference Proceedings Citation Index-Science. Searching was not restricted by date, language or publication status. We also searched the reference lists of the included trials and review articles. We contacted researchers for information on ongoing studies. Randomised controlled trials of one or more of the barbiturate class of drugs, where study participants had clinically diagnosed acute traumatic brain injury of any severity. Two review authors screened the search results, extracted data and assessed the risk of bias in the trials. Data from seven trials involving 341 people are included in this review.For barbiturates versus no barbiturate, the pooled risk ratio (RR) of death from three trials was 1.09 (95% confidence interval (CI) 0.81 to 1.47). Death or disability, measured using the Glasgow Outcome Scale was assessed in two trials, the RR with barbiturates was 1.15 (95% CI 0.81 to 1.64). Two trials examined the effect of barbiturate therapy on ICP. In one, a smaller proportion of patients in the barbiturate group had uncontrolled ICP (68% versus 83%); the RR for uncontrolled ICP was 0.81 (95% CI 0.62 to 1.06). In the other, mean ICP was also lower in the barbiturate group. Barbiturate therapy results in an increased occurrence of hypotension (RR 1.80; 95% CI 1.19 to 2.70). For every four patients treated, one developed clinically significant hypotension. Mean body temperature was significantly lower in the barbiturate group.In one study of pentobarbital versus mannitol there was no difference in death between the two study groups (RR 1.21; 95% CI 0.75 to 1.94). Pentobarbital was less effective than mannitol for control of raised ICP (RR 1.75; 95% CI 1.05 to 2.92).In one study the RR of death with pentobarbital versus thiopental was 1.78 (95% CI 1.03 to 3.08) in favour of thiopental. Fewer people had uncontrollable ICP with thiopental (RR 1.64; 95% CI 1.03 to 2.60). There was no significant difference in the effects of pentobarbital versus thiopental for death or disability, measured using the Glasgow Outcome Scale (RR 1.31; 95% CI 0.88 to 1.94), or hypotension (RR 0.95; 95% CI 0.81 to 1.12). There is no evidence that barbiturate therapy in patients with acute severe head injury improves outcome. Barbiturate therapy results in a fall in blood pressure in one in four patients. This hypotensive effect will offset any ICP lowering effect on cerebral perfusion pressure.

Barbiturates Use and Its Effects in Patients with Severe Traumatic Brain Injury in Five European Countries

The guidelines for management of traumatic brain injury (TBI) recommend that high-dose barbiturate therapy may be considered to lower intracranial pressure (ICP) that is refractory to other therapeutic options. Lower doses of barbiturates may be used for sedation of patients with TBI, although there is no mention of this in the published guidelines. The goal of this study was to analyze the use of barbiturates in patients with severe TBI in the European centers where the International Neurotrauma Research Organization introduced guideline-based TBI management and to analyze the effects of barbiturates on ICP, use of vasopressors, and short- and long-term outcome of these patients. Data on 1172 patients with severe TBI were collected in 13 centers located in five European countries. Patients were categorized into three groups based on doses of barbiturates administered during treatment. Univariate and multivariate statistical methods were used to analyze the effects of barbiturates on the outcome of patients. Fewer than 20% of all patients with severe TBI were given barbiturates overall, and only 6% was given high doses. High-dose barbiturate treatment caused a decrease in ICP in 69% of patients but also caused hemodynamic instability leading to longer periods of mean arterial pressure <70 mm Hg despite increased use of high doses of vasopressors. The adjusted analysis showed no significant effect on outcome on any stage after injury.Thiopental and methohexital were equally effective. Low doses of thiopental and methohexital were used for sedation of patients without side effects. Phenobarbital was probably used for prophylaxis of post-traumatic seizures.

Neuro protective effect of barbiturates leading to successful cerebral recovery after drug induced cardiac arrest and following severe multi organ fail

Neuro protective effect of barbiturates leading to successful cerebral recovery after drug induced cardiac arrest and following severe multi organ fail

Neuro protective effect of barbiturates leading to successful cerebral recovery after drug induced cardiac arrest and following severe multi organ fail

Results 23 year old woman suffered cardiac arrest due to a combined drug overdose with high doses of barbiturates, benzodiazepines and opioids. The patient was found unconscious and after 8 minutes of successful resuscitation transferred to the ICU where she rapidly developed multi organ failure due to the hypoxia and hypo perfusion during the time of cardiac arrest. The organ failure included lever, kidney, lung, pancreas and coagulation, but due to the neuron protective effect of barbiturates, there were no symptoms of cerebral damage. After weeks of stabilizing organ functions the patient was discharged with sustained damage to the kidneys, but no sign of cerebral damage.

AP039 Neuroprotective effect of barbiturates cause successful cerebral recovery after drug induced cardiac arrest and severe multiorganfailure

AP039 Neuroprotective effect of barbiturates cause successful cerebral recovery after drug induced cardiac arrest and severe multiorganfailure

Pilot study of the efficacy and safety of lettuce seed oil in patients with sleep disorders

Background:Lactuca sativa (garden lettuce) is a popular salad herb. It has been in use in folk medicine since ancient times as both an appetite stimulant and as an aid to sleep. L. sativa seed oil (Sedan®) has demonstrated a pronounced sedative effect and potentiated the hypnotic effect of barbiturates in animal models. It also exhibited significant analgesic and anti-inflammatory activities. In this study, we evaluated the sedative and hypnotic effects of L. sativa in patients suffering from insomnia.Methods:Sixty patients suffering from insomnia with or without anxiety were randomized to receive capsules containing L. sativa seed oil 1000 mg (n = 30) or placebo (n = 30). All patients were asked to complete a verbal questionnaire before the start of the trial and 1 week after starting treatment.Results:Improvements in the modified State-Trait Anxiety Inventory and the Sleep rating scale scores were significantly greater in patients receiving L. sativa seed oil compared with those on placebo (P < 0.05). No side effects were found to be attributable to L. sativa seed oil at the given dosage.Conclusion:L. sativa seed oil was found to be a useful sleeping aid and may be a hazard-free line of treatment, especially in geriatric patients suffering from mild-to-moderate forms of anxiety and sleeping difficulties.

Barbiturates Require the N Terminus and First Transmembrane Domain of the δ Subunit for Enhancement of α1β3δ GABAA Receptor Currents

GABA(A) receptors are composed predominantly of alphabetagamma receptors, which mediate primarily synaptic inhibition, and alphabetadelta receptors, which mediate primarily extrasynaptic inhibition. At saturating GABA concentrations, the barbiturate pentobarbital substantially increased the amplitude and desensitization of the alpha1beta3delta receptor but not the alpha1beta3gamma2L receptor currents. To explore the structural domains of the delta subunit that are involved in pentobarbital potentiation and increased desensitization of alpha1beta3delta currents, chimeric cDNAs were constructed by progressive replacement of gamma2L subunit sequence with a delta subunit sequence or a delta subunit sequence with a gamma2L subunit sequence, and HEK293T cells were co-transfected with alpha1 and beta3 subunits or alpha1 and beta3 subunits and a gamma2L, delta, or chimeric subunit. Currents evoked by a saturating concentration of GABA or by co-application of GABA and pentobarbital were recorded using the patch clamp technique. By comparing the extent of enhancement and changes in kinetic properties produced by pentobarbital among chimeric and wild type receptors, we concluded that although potentiation of alpha1beta3delta currents by pentobarbital required the delta subunit sequence from the N terminus to proline 241 in the first transmembrane domain (M1), increasing desensitization of alpha1beta3delta currents required a delta subunit sequence from the N terminus to isoleucine 235 in M1. These findings suggest that the delta subunit N terminus and N-terminal portion of the M1 domain are, at least in part, involved in transduction of the allosteric effect of pentobarbital to enhance alpha1beta3delta currents and that this effect involves a distinct but overlapping structural domain from that involved in altering desensitization.

The intravenous anesthetics barbiturates inhibit hypoxia-inducible factor 1 activation

Hypoxia-inducible factor 1 (HIF-1) is a master transcription factor of hypoxia-induced gene expression. Anesthetics and perioperative drugs have been reported to affect HIF-1 activity. However, the effect of barbiturates on HIF-1 activity has not been reported. In this study, we investigated the effect of thiopental and thiamylal on HIF-1 activity using the neuronal SH-SY5Y cells, the non-neuronal HEK293 cells, and the macrophage-differentiated THP-1 cells. Cells were exposed to 20% or 1% O 2 conditions with or without thiopental or thiamylal treatment. The cell lysate were subjected to Western blot analysis using anti-HIF-1α and -HIF-1β antibodies. HIF-1-dependent gene expression was investigated by semi-quantitative real-time RT-PCR and luciferase assay. Hydroxylation of HIF-1α protein was evaluated by in vitro pulldown assay using recombinant protein. Both thiopental and thiamylal reversibly suppressed hypoxia-induced HIF-1 activation in the neuronal and the non-neuronal cells in a dose-dependent manner. Moreover, the barbiturates inhibited lipopolysaccharide-induced HIF-1α expression in THP-1 cells. The HIF-1-downstream gene expression was also inhibited by the barbiturates. HIFα-hydroxylases activity and HIF-1α stability were not affected but the HIF-1α protein neosynthesis was inhibited by the barbiturates. Our experimental results indicate that barbiturates inhibit induced HIF-1 activation and downstream genes expression.

Fatal Fluctuation of Serum Potassium Level during Barbiturate Coma Therapy

Severe hypokalemia and rebound hyperkalemia is rare side effect of barbiturate. The authors report an experience of lifethreatening fluctuation of serum potassium level from barbiturate coma therapy (BCT) in severe brain injury patient. A 54year-old man falling from a golf-cart suffered multiple hemorrhagic contusion and traumatic subarachnoid hemorrhage. He was treated with barbiturate coma therapy conservatively for 20 hours. One hour after cessation of barbiturate infusion, cardiac arrest happened. Meanwhile serum potassium level was 1.5 mmol/L. 24 hours after discontinuation of barbiturate, another asystole occurred, and the serum potassium level was 8.5 mmol/L. This rare side effect of barbiturate is mediated by transcellular shift of potassium. Clinicians should monitor closely the electrolyte balance during barbiturate infusion, and possibility of rebound hyperkalemia after the cessation must be borne in mind. (J Kor Neurotraumatol Soc 2009;5:99-102)