Anaesthesia techniques for midazolam and flumazenil ‐ an overview

Lauven, P. M.; Kulka, P. J.

doi:10.1111/j.1399-6576.1990.tb03192.x

Cited by 16 publications

(7 citation statements)

References 30 publications

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“…Midazolam might have an influence in patients with elevated IL-6 levels in the CNS; however, the exact clinical effects are not clear. It has been reported that blood concentrations of midazolam reach as much as 1.9 μM after a bolus injection [39]. The suppressive effect of midazolam on IL-6 release that we find in the present study was observed at concentrations over 0.3 μM.…”

Section: Discussionsupporting

confidence: 67%

Midazolam suppresses interleukin-1β-induced interleukin-6 release from rat glial cells

Tanabe

Kozawa

Iida

2011

Journal of Neuroinflammation

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BackgroundPeripheral-type benzodiazepine receptor (PBR) expression levels are low in normal human brain, but their levels increase in inflammation, brain injury, neurodegenerative states and gliomas. It has been reported that PBR functions as an immunomodulator. The mechanisms of action of midazolam, a benzodiazepine, in the immune system in the CNS remain to be fully elucidated. We previously reported that interleukin (IL)-1β stimulates IL-6 synthesis from rat C6 glioma cells and that IL-1β induces phosphorylation of inhibitory kappa B (IκB), p38 mitogen-activated protein (MAP) kinase, stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2, and signal transducer and activator of transcription (STAT)3. It has been shown that p38 MAP kinase is involved in IL-1β-induced IL-6 release from these cells. In the present study, we investigated the effect of midazolam on IL-1β-induced IL-6 release from C6 cells, and the mechanisms of this effect.MethodsCultured C6 cells were stimulated by IL-1β. IL-6 release from C6 cells was measured using an enzyme-linked immunosorbent assay, and phosphorylation of IκB, the MAP kinase superfamily, and STAT3 was analyzed by Western blotting.ResultsMidazolam, but not propofol, inhibited IL-1β-stimulated IL-6 release from C6 cells. The IL-1β-stimulated levels of IL-6 were suppressed by wedelolactone (an inhibitor of IκB kinase), SP600125 (an inhibitor of SAPK/JNK), and JAK inhibitor I (an inhibitor of JAK 1, 2 and 3). However, IL-6 levels were not affected by PD98059 (an inhibitor of MEK1/2). Midazolam markedly suppressed IL-1β-stimulated STAT3 phosphorylation without affecting the phosphorylation of p38 MAP kinase, SAPK/JNK or IκB.ConclusionThese results strongly suggest that midazolam inhibits IL-1β-induced IL-6 release in rat C6 glioma cells via suppression of STAT3 activation. Midazolam may affect immune system function in the CNS.

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Section: Discussionsupporting

confidence: 67%

Midazolam suppresses interleukin-1β-induced interleukin-6 release from rat glial cells

Tanabe

Kozawa

Iida

2011

Journal of Neuroinflammation

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“…The remaining children were frightened of either pain and needles, going to sleep and dying, strangers, or being separated from their mother (Table 1). The mean fastest preoperative postbox toy completion time for the 30 children was 18.1 seconds (SD 5.9, range 11-37) and the mean highest preoperative WISC-R scale performance was 17.1 (SD 2.4, range [11][12][13][14][15][16][17][18][19]. The preoperative PBTR and WISC-R ratio at different times after premedication are shown in Table 2 and the relationship between midazolam concentrations, PBTR and WISC-R scale ratio are shown in Figure 3.…”

Section: Resultsmentioning

confidence: 99%

Premedication with Oral Midazolam in Children—an Assessment of Psychomotor Function, Anxiolysis, Sedation and Pharmacokinetics

Jones

Visram

Kornberg

et al. 1994

Anaesth Intensive Care

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We studied 30 children, aged 4 to 12 years, undergoing elective circumcision, premedicated with midazolam 0.5 mg.kg-I and atropine 0.02 mg.kg-I by mouth. A modified postbox test and the coding component of the Wechsler intelligence scale (WISC-R) was used to assess the preoperative effect of premedication on psychomotor function. Mood and sedation were also scored and related to serum midazolam concentrations. The children showed a significant decline in psychomotor performance 30 and 60 minutes after premedication when compared with their best un medicated performance recorded the previous evening. This decline in psychomotor performance was only weakly associated with serum midazolam concentrations (r = 0.1). The postbox toy ratio is a suitable measurement of psychomotor performance in children because of its simplicity and ease of use in the clinical environment, although it may suffer the "test-retest" limitations of similar types of assessment. The sedative and anxiolytic effects of midazolam provide a quiet environment for a smooth induction of anaesthesia.

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“…Differential ability of benzodiazepines to induce this withdrawal excitability might be related to the biological half-lives of the drugs. In contrast to clonazepam, where biological half-life (T 1/2 ) in man ranges between 19 and 60 h (Berlin and Dahlstrom 1975), midazolam belongs to short-acting benzodiazepines (T 1/2 =150-180 min in man; Lauven and Kulka 1990). No data are available on developmental changes of biological half-life of these two benzodiazepines, but our previous study on the time-course of protection against PTZ-induced seizures demonstrated that clonazepam suppressed seizure activity for nearly 24 h (Kubová and Mareš 1989) whereas midazolam did so only for 30 min in animals 12 days old .…”

Section: Discussionmentioning

confidence: 99%

The benzodiazepine receptor partial agonist Ro 19-8022 suppresses generalized seizures without impairing motor functions in developing rats

Kubová

Mikulecká

Haugvicová

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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The action of a partial benzodiazepine receptor agonist Ro 19-8022 [(R)-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)carbo nyl] -2-pyrrolidine-methanol] in doses from 0.01 to 150 mg/kg was studied using motor seizures induced by pentylenetetrazol (PTZ) in rats 7, 12, 18, 25 and 90 days old. Generalized tonic-clonic seizures were suppressed in all age groups, the three youngest groups being more sensitive than older animals. The highest dose of Ro 19-8022 did not exhibit anticonvulsant action in the 25-day-old rats. The other types of seizures (minimal clonic) induced by PTZ were suppressed by Ro 19-8022 only in 18-day-old and older rats in which PTZ reliably elicited these types of seizures. The doses of 50, 100 and 150 mg/kg were ineffective against minimal seizures. On the contrary, incidence of minimal seizures was significantly increased by Ro 19-8022 in 7-and 12-day-old rat pups. Motor performance of rat pups was not compromised by Ro 19-8022 (0.5 and 50 mg/kg) in contrast to the full agonist midazolam (1 and/or 2 mg/kg). The duration of anticonvulsant effects studied with a dose of 0.5 mg/kg was longer in 12-day-old than in adult rats. This dose of Ro 19-8022 resulted in a rebound proconvulsant effect 24 and 48 h after the administration in 12-day-old rats only. Ro 19-8022 exhibited an excellent anticonvulsant action especially against generalized tonic-clonic seizures; this action was lost with very high doses. It did not compromise the motor system, but in some tests motivation was probably lost.

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Anaesthesia techniques for midazolam and flumazenil ‐ an overview

Cited by 16 publications

References 30 publications

Midazolam suppresses interleukin-1β-induced interleukin-6 release from rat glial cells

Midazolam suppresses interleukin-1β-induced interleukin-6 release from rat glial cells

Premedication with Oral Midazolam in Children—an Assessment of Psychomotor Function, Anxiolysis, Sedation and Pharmacokinetics

The benzodiazepine receptor partial agonist Ro 19-8022 suppresses generalized seizures without impairing motor functions in developing rats

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