Quantified human sleep after pentobarbital

Kay, David C.; Jasinski, Donald R.; Eisenstein, Richard B.; Kelly, O.A.

doi:10.1002/cpt1972132221

Cited by 30 publications

(8 citation statements)

References 6 publications

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“…Spindle density is a very sensitive indicator of activity for some hypnotics (Hirschkowitz, Thomby & Karacan, 1981), and its failure to respond may be a distinct characteristic of phenobarbitone; this may also be seen in the results of Feinberg et al (1969). The lack of a phenobarbitone effect on sleep spindles in this study is in contrast to the increase in spindling obtained from pentobarbitone (Kay et al, 1972) and the decrease in spindling obtained from secobarbitone (Lester et al, 1968 (Baekeland, 1967;Haider & Oswald, 1971;Hartmann, 1968;Kales et al, 1975;Kay et al, 1972;Lehmann & Ban, 1968;Lester et al 1968;Risberg, Risberg & Ingvar, 1975). This has not, however, been true in all studies reported in the literature.…”

Section: Dinmentioning

confidence: 49%

Dose‐related effects of phenobarbitone on human sleep‐waking patterns.

Karacan¹,

Orr²,

Roth³

et al. 1981

Brit J Clinical Pharma

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I Twenty-four healthy male subjects had two consecutive drug nights at 2-week intervals using placebo and 80, 140 and 240 mg doses of phenobarbitone in a double-blind cross-over design. 2 Phenobarbitone produced significant dose-related decreases in sleep latency and number of awakenings, along with increased total sleep time. 3 Both subjective and objective measures of sleep indicated the presence of cumulative (first v second night) effects of phenobarbitone, especially decreases in the number of awakenings and in delta waveform activity. 4 Measures of REM sleep were highly sensitive to phenobarbitone. The high dose decreased REM density to 30% of baseline on the first night and to 18% on the second night.5 EEG a activity was decreased, f8 activity was increased and sigma spindle activity was unaffected by phenobarbitone during sleep. 6 Subjects experienced some impairment of cognitive performance along with residual sedation the following morning.

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Section: Dinmentioning

confidence: 49%

Dose‐related effects of phenobarbitone on human sleep‐waking patterns.

Karacan¹,

Orr²,

Roth³

et al. 1981

Brit J Clinical Pharma

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“…The scoring of the paper strip chart was blind to drug condition, and used techniques described by Kay, Jasinski, Eisenstein & Kelly (1972 (Kay et al, 1972). REM sleep disruptions were divided into waking state disruptions and non-REM sleep (NREM sleep) disruptions; these were calculated only for SN.…”

Section: Scoringmentioning

confidence: 99%

“…The scoring of the paper strip chart was blind to drug condition, and used techniques described by Kay, Jasinski, Eisenstein & Kelly (1972). Briefly, each sleep-waking state was defined to the nearest 2-s epoch, and had to persist for at least 10 s to be so identified, although drowsiness prior to spindle sleep might persist for less than 10 s. Waking state (stage 0), drowsiness (stage 1), spindle sleep (stage 2), delta sleep (stages 3 + 4), and REM sleep were all identified and tabulated for two durations: 360 min after the first sleep spindle (standard sleep time: ST) and 450 min after lights out (standard night: SN).…”

Section: Scoringmentioning

confidence: 99%

Morphine‐like insomnia from heroin in nondependent human addicts.

Dc¹,

Pickworth²,

Neider³

1981

Brit J Clinical Pharma

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1 This study was performed because dose-related effects of heroin on human sleep had not been described previously, and to discover if heroin produces a morphine-like insomnia. 2 After three adaptation nights, the sleep of seven male nondependent opiate addicts was studied following i.m. doses of heroin (3, 6, 12 mg/70 kg), morphine (10, 20 mg/70 kg) or placebo at weekly intervals in a randomized double-blind crossover design. 3 Heroin produces a dose-related increase in wakefulness, drowsiness episodes, muscle tension, and shifts in sleep-waking states.I 4 Heroin produces a dose-related decrease in total sleep, sleep efficiency, delta sleep and REM sleep (REMS). 5 Heroin is about twice as potent as morphine in producing this type of insomnia. 6 'Morphine insomnia' appears to be a characteristic initial effect of several opioids, at least in nondependent opiate addicts, and might serve as a model insomnia for evaluation of hypnotics.

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“…Sleep requires the inhibition of multiple pathways in the arousal system and available evidence suggests that the VLPO is a major source of sleep-active neurons that provide GABAergic, inhibitory input to many elements of the arousal system (Sherin et al, 1996), including the tuberomammillary nucleus (TMN), locus coeruleus, and orexinergic neurons (Saper et al, 2010). In addition, many compounds that enhance GABAergic transmission promote sleep at low doses (Kales et al, 1968; Kay et al, 1972), but induce anesthesia at high doses (Eikermann et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

The ventrolateral preoptic nucleus is not required for isoflurane general anesthesia

et al. 2011

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Neurons of the ventrolateral preoptic nucleus (VLPO) promote sleep and VLPO loss produces insomnia. Previous studies show that general anesthetics including isoflurane activate VLPO neurons, and may contribute to their sedative effects. However, it is not clear to what extent the activation of VLPO neurons contributes to general anesthesia. We tested whether destruction of the VLPO neurons would affect the onset, depth, or recovery from isoflurane's general anesthetic effects. The VLPO was ablated in 25 rats by bilateral local injection of orexin-saporin, and polysomnography was performed to measure baseline sleep loss and responses to isoflurane anesthesia at 1% and 2%. Eight rats received sham (saline) injections. We measured isoflurane effects on time to loss of righting reflex, onset of continuous slow wave activity, and burst suppression; burst-suppression ratio; and time to recovery of righting reflex and desynchronized EEG. VLPO neuron cell loss was quantified by post hoc histology. Loss of VLPO neurons as well as lesion size were associated with cumulative sleep loss (r=0.77 and r=0.62, respectively), and cumulative sleep loss was the strongest predictor of high sensitivity to anesthesia, expressed as decreased time to loss of righting reflex (−0.59), increased burst-suppression ratio (r=0.52), and increased emergence time (r=0.54); an interaction-effect of isoflurane dose was observed (burst-suppression ratio: p<0.001). We conclude that the sleep loss caused by ablation of VLPO neurons sensitizes animals to the general anesthetic effects of isoflurane, but that the sedation produced by VLPO neurons themselves is not required for deep isoflurane anesthesia.

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Quantified human sleep after pentobarbital

Abstract: Quantified human sleep after pentobarbitalIntramuscular doses of pentobarbital (75, 150, 300 mg. per 70 Kg.)

Cited by 30 publications

References 6 publications

Dose‐related effects of phenobarbitone on human sleep‐waking patterns.

Dose‐related effects of phenobarbitone on human sleep‐waking patterns.

Morphine‐like insomnia from heroin in nondependent human addicts.

The ventrolateral preoptic nucleus is not required for isoflurane general anesthesia

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