Although drugs such as barbiturates and benzodiazepines are often used for the treatment of insomnia, they are associated with various side effects such as habituations, tolerance and addiction. Alternatively, natural products with minimal unwanted effects have been preferred for the treatment of acute and/or mild insomnia, with additional benefits of overall health-promotion. Basic and clinical researches on the mechanisms of action of natural products have been carried out so far in insomnia treatments. Recent studies have been focusing on diverse chemical components available in natural products, with an interest of developing drugs that can improve sleep duration and quality. In the last 15 years, our co-workers have been actively looking for candidate substances from natural products that can relieve insomnia. This review is, therefore, intended to bring pharmacological data regarding to the effects of natural products on sleep duration and quality, mainly through the activation of GABAA receptors. It is imperative that phytochemicals will provide useful information during electroencephalography (EEG) analysis and serve as an alternative medications for insomnia patients who are reluctant to use conventional drugs.
Barbiturates ; Benzodiazepines ; Biological Products* ; Electroencephalography ; Humans ; Phytochemicals ; Sleep Initiation and Maintenance Disorders

Many sedatives are used clinically and include benzodiazepines, barbiturates, antihistamines, propofol, and alpha-2-agonist. Benzodiazepines activate GABA neuronal receptors in the brain and present sedating, hypnotic, anxiolytic, amnestic, and anticonvulsant effects, but low analgesic effects. Propofol induce sedative, anxiolytic, and amnestic effects but no analgesic effects. However, risks such as cardiopulmonary instability and hypotension must be considered during administration. Dexmedetomidine is a high selective alpha-2 agonist and has many advantages as a sedative. Patients under dexmedetomidine sedation awaken easily and are more likely to be cooperative. Risk of respiratory depression and cardiopulmonary instability is low as well. Additionally, dexmedetomidine decreases amount of analgesic needed during and after surgery, presenting analgesic effects. Dexmedetomidine also decreases risk of delirium. However, bradycardia may occur and biphasic effects on blood pressure may be observed during beginning of administration. Because of lengthy symptom onset and offset time, physicians should carefully control administration at the beginning and end of dexmedetomidine administration. The purpose of this review is to evaluate the efficacy and availability of dexmedetomidine in various clinical fields including sedation for critically ill patients, regional anesthesia, monitored anesthesia care for some invasive procedures, stabilization of heart in cardiac surgery or endoscopic procedures.
Anesthesia* ; Anesthesia, Conduction ; Barbiturates ; Benzodiazepines ; Blood Pressure ; Bradycardia ; Brain ; Critical Illness ; Delirium ; Dexmedetomidine* ; GABAergic Neurons ; Heart ; Histamine Antagonists ; Humans ; Hypnotics and Sedatives ; Hypotension ; Propofol ; Respiratory Insufficiency ; Thoracic Surgery

Many sedatives are used clinically and include benzodiazepines, barbiturates, antihistamines, propofol, and alpha-2-agonist. Benzodiazepines activate GABA neuronal receptors in the brain and present sedating, hypnotic, anxiolytic, amnestic, and anticonvulsant effects, but low analgesic effects. Propofol induce sedative, anxiolytic, and amnestic effects but no analgesic effects. However, risks such as cardiopulmonary instability and hypotension must be considered during administration. Dexmedetomidine is a high selective alpha-2 agonist and has many advantages as a sedative. Patients under dexmedetomidine sedation awaken easily and are more likely to be cooperative. Risk of respiratory depression and cardiopulmonary instability is low as well. Additionally, dexmedetomidine decreases amount of analgesic needed during and after surgery, presenting analgesic effects. Dexmedetomidine also decreases risk of delirium. However, bradycardia may occur and biphasic effects on blood pressure may be observed during beginning of administration. Because of lengthy symptom onset and offset time, physicians should carefully control administration at the beginning and end of dexmedetomidine administration. The purpose of this review is to evaluate the efficacy and availability of dexmedetomidine in various clinical fields including sedation for critically ill patients, regional anesthesia, monitored anesthesia care for some invasive procedures, stabilization of heart in cardiac surgery or endoscopic procedures.
Anesthesia* ; Anesthesia, Conduction ; Barbiturates ; Benzodiazepines ; Blood Pressure ; Bradycardia ; Brain ; Critical Illness ; Delirium ; Dexmedetomidine* ; GABAergic Neurons ; Heart ; Histamine Antagonists ; Humans ; Hypnotics and Sedatives ; Hypotension ; Propofol ; Respiratory Insufficiency ; Thoracic Surgery

BACKGROUND: Thiamylal 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. METHODS: Expression 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. RESULTS: TSS 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. CONCLUSIONS: TSS-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.
Animals ; Aorta ; Atherosclerosis ; Barbiturates ; Carbon ; Cell Proliferation ; Enzyme-Linked Immunosorbent Assay ; Inflammation* ; Interleukin-1 ; Interleukin-6 ; Interleukins ; Muscle, Smooth, Vascular* ; Rats ; RNA, Messenger ; Sodium ; Thiamylal* ; Toll-Like Receptors ; Transplants ; Trypan Blue ; Up-Regulation

Erythema multiforme is an acute cutaneous reaction which manifests as macular patches and edematous papules commonly involving the hands, feet, forearm and mucous membranes. It is thought to be caused by viral and bacterial infections, neoplasms, autoimmune diseases such as rheumatoid arthritis, and also by pharmaceuticals such as sulfonamides, phenytoin, barbiturates, penicillins, carbamazepines. Nonsteroidal antiinflammatory drugs (NSAIDs) have been also reported as a possible cause. However, meloxicam that is a kind of cyclooxygenase-2 selective inhibitor has not been rarely reported as a cause of erythema multiforme. Therefore, we report a case with a review of the literature.
Anti-Inflammatory Agents, Non-Steroidal ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Bacterial Infections ; Barbiturates ; Cyclooxygenase 2 ; Erythema Multiforme* ; Erythema* ; Foot ; Forearm ; Hand ; Mucous Membrane ; Penicillins ; Phenytoin ; Sulfonamides

OBJECTIVE: Decompressive craniectomy is widely used in cases of uncontrolled intracranial hypertension, including traumatic brain injury or acute stroke. Physiological monitorings, such as intracranial pressure or electroenecephalography (EEG) are critical for patients in the acute phase. We retrospectively reviewed our experience of continuous electrocorticography (ECoG) monitoring by subdural strip electrode in patients who performed decompressive craniectomy and assessed its clinical efficacy. METHODS: Patients who underwent decompressive craniectomy because of severe intracranial hypertension were included. 4 Channel strip electrodes were inserted on the frontal cortex before closure. 24-hour continuous monitoring of ECoG was done to identify abnormal electrical activity. The level of consciousness was assessed according to Glasgow Coma Scale (GCS). In patients with malignant intracranial hypertension, barbiturate coma therapy was considered. RESULTS: Fifteen patients (9 men and 6 women) were included and the mean age was 55.7 years (from 17 to 80). The initial mean GCS score was 7.9 (from 3 to 14). In six out of fifteen patients, abnormal spike activities were identified, and one of these six patients was diagnosed as nonconvulsive status epilepticus (NCSE). Cortical spreading depression (CSD) was suspected in five. Three patients underwent barbiturate coma therapy and ECoG monitoring of these patients showed typical burst suppression pattern, which was used for indicator of therapeutic level. The mean duration of strip electrode and ECoG monitoring was 3.5 days, and there was no complication. CONCLUSION: Continuous ECoG monitoring using subdural strip electrode was useful to detect abnormal brain activity in the acute period after decompressive craniectomy.
Barbiturates ; Brain ; Brain Injuries ; Coma ; Consciousness ; Cortical Spreading Depression ; Decompressive Craniectomy* ; Electrodes* ; Glasgow Coma Scale ; Humans ; Intracranial Hypertension ; Intracranial Pressure ; Male ; Retrospective Studies ; Status Epilepticus ; Stroke

Medication errors remain an unsolved problem in medicine. Some factors have been found to contribute to drug errors, and among them, the incorrect administration of drugs is a major factor. In this case report, 2 ml of dobutamine was inadvertently injected intrathecally instead of bupivacaine owing to ampoule confusion during spinal anesthesia, followed by the induction of general anesthesia with sodium thiopental-sevoflurane. It was uneventful during perioperative period, however, nystagmus was observed in post anesthesia care unit (PACU), about 1 h after induction of general anesthesia. There were no other neurologic abnormalities except nystagmus and vital sign were stable during PACU stay. Nystagmus subsided spontaneously and it was confirmed there was no evidence of any central nervous system lesion on imaging study. The patient was discharged 5 days later without any complications.
Anesthesia ; Anesthesia, General ; Anesthesia, Spinal ; Barbiturates ; Bupivacaine ; Central Nervous System ; Dobutamine ; Humans ; Medication Errors ; Perioperative Period ; Sodium ; Vital Signs

Animals ; Barbiturates ; Coloring Agents ; Fallopian Tubes ; cytology ; embryology ; physiology ; Female ; Isoxazoles ; Male ; Membrane Potentials ; Mice ; Mice, Inbred Strains

BACKGROUNDAdipose-derived stromal cell (ADSC) differentiation into neural cells in vitro is becoming widely studied. However, there are few reports on astrocytes following differentiation, and particularly on maturation and electrophysiology. In this study, we used various methods to determine ADSC-derived astrocyte maturity.

METHODSChemical induction with isobutylmethylxanthine (IBMX) was used to differentiate adult ADSCs into astrocytes followed by hematoxylin-eosin (HE) staining to observe morphology and transmission electron microscopy for cellular ultrastructure assessment. Immunofluorescence was used to detect expression of neural stem cell marker nestin as well as glial markers glial fibrillary acidic protein (GFAP) and S-100. In addition, we measured membrane potentials in bis-(1,3-dibarbituric acid) trimethine oxanol-labeled ADSCs and astrocytes by stimulation with a high potassium solution under an inverted fluorescence microscope. Finally, cell cycle distribution was detected by flow cytometry.

RESULTSTypical astrocyte morphology was shown by HE staining after 48-hour differentiation. Glial fibril was observed with transmission electron microscopy. GFAP and S-100 were not expressed in the control group, but were expressed within 24-hour differentiation and reached a maximum at day 14 with no change up to day 28. Nestin was weakly expressed in control cells and also reached a maximum at day 14 with the percentage of positive cells constant until day 21 followed by a decrease. Differentiated cell membrane potentials after stimulation with potassium were slightly increased, and then gradually declined over time. There was no significant membrane potential change in the control group. Flow cytometry showed that the percentage of cells in G0/G1 phase was 93% and only 5% in S phase.

CONCLUSIONADSCs were differentiated into mature astrocytes with typical characteristics including morphology, ultrastructure, marker protein expression, mature potassium channels and mitotic capacity.

1-Methyl-3-isobutylxanthine ; pharmacology ; Adipose Tissue ; cytology ; Adult ; Astrocytes ; cytology ; Barbiturates ; pharmacology ; Cell Differentiation ; drug effects ; Cells, Cultured ; Electrophysiology ; methods ; Female ; Flow Cytometry ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Male ; Membrane Potentials ; drug effects ; Microscopy, Fluorescence ; S100 Proteins ; metabolism ; Stromal Cells ; cytology ; Young Adult

OBJECTIVE: This study was conducted to compare the effect of etomidate with that of thiopental on brain protection during temporary vessel occlusion, which was measured by burst suppression rate (BSR) with the Bispectral Index (BIS) monitor. METHODS: Temporary parent artery occlusion was performed in forty one patients during cerebral aneurysm surgery. They were randomly assigned to one of two groups. General anesthesia was induced and maintained with 1.5-2.5 vol% sevoflurane and 50% N2O. The pharmacological burst suppression (BS) was induced by a bolus injection of thiopental (5 mg/kg, group T) or etomidate (0.3 mg/kg, group E) according to randomization prior to surgery. After administration of drugs, the hemodynamic variables, the onset time of BS, the numerical values of BIS and BSR were recorded at every minutes. RESULTS: There were no significant differences of the demographics, the BIS numbers and the hemodynamic variables prior to injection of drugs. The durations of burst suppression in group E (11.1+/-6.8 min) were not statistically different from that of group T (11.1+/-5.6 min) and nearly same pattern of burst suppression were shown in both groups. More phenylephrine was required to maintain normal blood pressure in the group T. CONCLUSION: Thiopental and etomidate have same duration and a similar magnitude of burst suppression with conventional doses during temporary arterial occlusion. These findings suggest that additional administration of either drug is needed to ensure the BS when the temporary occlusion time exceed more than 11 minutes. Etomidate can be a safer substitute for thiopental in aneurysm surgery.
Anesthesia, General ; Aneurysm ; Arteries ; Barbiturates ; Blood Pressure ; Brain ; Demography ; Dietary Sucrose ; Etomidate ; Glycosaminoglycans ; Hemodynamics ; Humans ; Intracranial Aneurysm ; Methyl Ethers ; Parents ; Phenylephrine ; Random Allocation ; Thiopental