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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preschool age children often experience marked anxiety and physical pain during laceration repair. Locally infiltrated anesthetics or topical tetracaine, adrenaline, and cocaine (TAC) usually control the physical pain but have little or no effect on anxiety. Midazolam is a short-acting benzodiazepine with anxiolytic, hypnotic, and antegrade amnestic effects. In a double-blind, randomized clinical trial, we evaluated the efficacy of midazolam in alleviating anxiety during laceration repair in children less than 6 years old. On admission to the emergency department, anxiety level was determined on a scale of 1 to 4 based on a predetermined behavior criteria. Patients with high anxiety level (3 or 4) received a single oral dose of either midazolam (0.2 mg/kg) or placebo. The anxiolytic effect of midazolam was considered adequate if the anxiety level decreased two or more points (from 4 to less than or equal to 2 or from 3 to 1) during laceration repair. In the midazolam group (30), 70% of the children had a two-point or more decrease in anxiety level compared with 12% in the placebo group (25) (P less than .0001). No respiratory depression or other complications were noted in the midazolam group. We conclude that a single oral dose of midazolam (0.2 mg/kg) is a safe and effective treatment for alleviating anxiety in children less than 6 years old during laceration repair in the ED.
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PMID:The effect of oral midazolam on anxiety of preschool children during laceration repair. 203 20

We have studied the effect of i.v. flumazenil 0.01 mg kg-1 on the amnesia and sedation caused by midazolam 2 mg and 5 mg i.v. in volunteers in order to determine the relationship between the actions of the antagonist on these two effects. Midazolam caused dose-dependent central neural depression as assessed by critical flicker fusion frequency, and dose-dependent amnesia for word cards. In subjects given flumazenil 5 min after administration of midazolam, fusion frequency readings and memory were restored to levels comparable to those before midazolam administration. These two effects of flumazenil were similar in time course and extent, suggesting that they share the same mechanism of action. Flumazenil given alone had no effect on memory. The study has demonstrated anterograde amnesia following benzodiazepine administration and antagonism by flumazenil. There was neither retrograde amnesia nor retrograde antagonism of amnesia.
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PMID:Effect of flumazenil on midazolam-induced amnesia. 222 35

Midazolam is the first water-soluble benzodiazepine. As with other benzodiazepines it has amnestic, sedative, hypnotic, anxiolytic, and anticonvulsant properties. Midazolam is about two to four times more potent than diazepam. Midazolam has been extensively used for a variety of outpatient procedures, but there has been no documentation of its safety in emergency department patients. The authors retrospectively reviewed all patients receiving midazolam during a 2-year period at the University of Cincinnati Center for Emergency Care. The study population consisted of 389 patients (men 56%; women 44%) with an average age of 33.3 years. Midazolam was used intravenously for sedation before a wide variety of painful procedures and for agitation control. The average dose was 3.86 mg, with a range of 0.5 mg to 20.0 mg. The majority of patients (79.2%) received narcotics or sedative/hypnotic agents in addition to midazolam. There was an overall complication rate of 1.0%. Two patients (0.5%) developed clinically significant respiratory depression after midazolam use. Both patients had also received fentanyl citrate and the respiratory depression was reversed with naloxone. Two patients (0.5%) receiving several other drugs developed short periods of hypotension. There were no apparent long term sequelae. The authors conclude that midazolam can be safely used in the emergency department setting. Careful dosing and titration to the desired clinical effects is mandatory. Patients should be closely monitored to maximize safety.
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PMID:Midazolam use in the emergency department. 230 91

Studies were carried out in chloralose-anesthetized cats while monitoring respiratory (tidal volume and respiratory rate) and cardiovascular (arterial pressure and heart rate) activity. Midazolam applied bilaterally to the intermediate area of the ventral surface of the medulla in doses of 0.75, 7.5 and 75 micrograms/side reduced tidal volume by -6 +/- 3, -10 +/- 1 and -11 +/- 1 ml, respectively. A dose of 250 micrograms/side produced apnea in each animal tested. Corresponding changes in arterial pressure were -35 +/- 9, -44 +/- 6, -43 +/- 9 and -64 +/- 17 mm Hg, respectively. Larger doses of chlordiazepoxide (e.g., 1000 micrograms/side) were required to produce similar effects. Intravenous administration of midazolam in doses of 1.5 to 150 micrograms had no significant effect on cardiorespiratory activity. However, larger doses of midazolam given i.v. produced cardiorespiratory depression that was similar to that observed with centrally applied drug. Pretreatment or treatment with centrally applied flumazenil or bicuculline counteracted the cardiorespiratory effects of centrally applied midazolam. Most importantly, ventral surface application of flumazenil counteracted the cardiorespiratory depressant effects of i.v. midazolam. Central administration of ethyl-beta-carboline-3-carboxylate produced cardiorespiratory effects opposite to those seen with midazolam, and these stimulatory effects were also counteracted by centrally applied flumazenil. These results indicate that alterations in cardiorespiratory activity can be produced by drugs interacting with gamma-aminobutyric acid/benzodiazepine receptors at the ventral surface of the medulla.
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PMID:Drug interaction with gamma-aminobutyric acid/benzodiazepine receptors at the ventral surface of the medulla results in pronounced changes in cardiorespiratory activity. 253 19

A study was carried out on the effects of midazolam 15 mg in conjunction with ethanol 0.5 g/kg on objective and subjective sleep parameters and psychomotor performance in normal subjects. Midazolam significantly decreased total wake time. Total sleep time (TST) increase was related to larger amounts of stage 2 NREM sleep. Ethanol showed similar effects on sleep, although TST increase was associated with nonsignificant increments of NREM sleep and REM sleep. Ethanol slightly potentiated midazolam effects on sleep. Accordingly, total wake time, REM sleep time and number of wakes showed further depression than with midazolam alone. Subjective evaluations showed relatively good correlation with sleep laboratory findings. In addition, the different treatments did not impair subject's psychomotor performance the morning after their administration.
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PMID:Combined effects of midazolam and ethanol on sleep and on psychomotor performance in normal subjects. 261 61

Twelve systemically healthy patients each (ASA risk groups 1-2) who required oral surgery under local anesthesia received the short-acting benzodiazepin Midazolam for analgosedation as well as the analgesics Pentazocin or Piritramid. Both i.v. medications are suitable as adjuvants for local anesthesia since neither clinically relevant respiratory and circular depression nor major sleepiness were observed.
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PMID:[Analgosedation as an adjuvant during surgery under local anesthesia]. 263 69

Midazolam is a short-acting benzodiazepine with anxiolytic, sedative-hypnotic and marked amnestic properties. Due to an excellent local tolerability, its slight reduction in blood pressure and minor dose-related respiratory depression, midazolam is useful for anaesthetic induction and postoperative (long-term) sedation especially for intensive care patients. Compared to other benzodiazepines, midazolam exhibits a rapid onset of action and a fast hepatic elimination (t1/2 2 to 4h; CL 400 to 600 ml/min). In patients with liver cirrhosis and critically ill patients, an impaired elimination and longer duration of action has to be taken into consideration. Likewise, in the elderly an amplified response will be noted, because of the increased sensitivity of the central nervous system to benzodiazepines during aging. In such populations at risk, "normal" dosage of midazolam has to be reduced at least by factor 2.
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PMID:[Clinical pharmacology of midazolam]. 269 Aug 43

Excitatory synaptic transmission, induced by electrical stimulation of optic nerve fibres on relay neurones, was recorded from in vitro preparations of the optic tectum of the frog. Bath-applied glutamate (the putative excitatory transmitter of the optic nerve) produced transient enhancement of tectal field potentials, followed by a depression, presumably caused by sustained neuronal depolarization. Pentobarbitone potently antagonized the depressant effect of glutamate, producing an approximate 50% reduction in the response of the tectum to glutamate at 25 microM. Midazolam also decreased the effect of glutamate with an IC50 value of 5 nM. Since, in the optic tectum of the frog, neither pentobarbitone nor midazolam enhance responses to bath-applied GABA, it is suggested that this area of the brain is a useful preparation in which to investigate the interaction of barbiturates and benzodiazepines with glutamate receptor mechanisms, without concurrent interactions with GABAergic processes.
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PMID:Antagonism of the actions of glutamate by pentobarbitone or midazolam in the frog optic tectum in vitro. 281 83

ICU patients often require sedation. Midazolam (M), a new imidazobenzodiazepine, features rapid onset and rapid elimination time. Flumazenil (Ro 15-1788) is a new benzodiazepine antagonist. We studied the efficacy and safety of M by continuous infusion in 28 ICU patients: 16 post major surgery, and 12 medical patients, aged 20-77 years. M was administered as a loading dose of 0.05-0.15 mg/kg per min followed by continuous infusion of 0.05-0.1 mg/kg per h titrated to maintain patients asleep but arousable. M was administered for up to 14 days in doses of 1-15 mg/h and cumulative doses of up to 1915 mg. No untoward effects were noted except for slight decreases in blood pressure following the loading dose. ACTH challenge tests performed before and 24 h or more following the start of M showed no depression of adrenal responsivity. All patients meeting weaning criteria were weaned off mechanical ventilation while still on M. In 13 patients extubation was performed immediately after M was stopped, and flumazenil (0.38 +/- 0.27 mg, i.v.) given until full awakening. Patients remained awake yet calm. Vital signs remained stable after flumazenil. Midazolam by continuous infusion appears to be a safe and effective mode of sedation in ICU patients. Flumazenil may increase the flexibility and safety of this mode of sedation.
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PMID:Midazolam infusion and the benzodiazepine antagonist flumazenil for sedation of intensive care patients. 284 76

The purpose of these experiments was to analyze the cerebrovascular and cerebral metabolic effects of midazolam, a short-acting water-soluble benzodiazepine, and to investigate its interaction with alcohol in rats. A benzodiazepine antagonist, 3-carbo-t-butoxy-beta-carboline (beta-CCT), was used to test the role of the benzodiazepine receptor in midazolam-alcohol effects. Experiments were carried out under 70% N2O, 30% O2 anesthesia. Rats were tested with intraperitoneal injections of 0.75-5 mg/g ethanol, intravenous infusions of 0.57, 5.75 mg/kg midazolam, and 1.15 mg/kg beta-CCT separately and in combination. Cortical cerebral blood flow (CBF) was measured with radioactive microspheres, and cerebral oxygen consumption (CMRO2) was determined from cortical CBF and arterial-sagittal sinus blood samples 20 min after ethanol treatment and/or after a 15-min drug infusion. Alcohol alone produced dose-related increases in plasma ethanol concentrations but no depression in CMRO2 except at the highest dose (5 mg/g). Midazolam infusions alone decreased cortical CBF and CMRO2 35-40%, while 2.5 mg/g alcohol (which did not depress CMRO2 alone) combined with midazolam produced a 70% depression of cortical CBF and metabolism. An infusion of beta-CCT given alone increased CMRO2 alone and reversed the depression in both cortical CBF and CMRO2 produced by midazolam plus alcohol. These results indicate that the ability of alcohol to potentiate benzodiazepine-induced sedation is not simply an additive effect but may be related to the facilitation by alcohol of benzodiazepine receptor binding. The fact that beta-CCT reversed midazolam-ethanol-induced depression suggests that the effect may be mediated through the benzodiazepine receptor.
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PMID:Midazolam-ethanol interactions and reversal with a benzodiazepine antagonist. 285 40


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