doi: 10.1093/sleep/16.6.511pmid: N/A
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Yamashiro,, Yoshihiro;Kryger, Meir, H.
doi: 10.1093/sleep/16.6.513pmid: 8235235
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Guilleminault,, Christian;Clerk,, Alex;Labanowski,, Michael;Simmons,, Jerald;Stoohs,, Riccardo
doi: 10.1093/sleep/16.6.524pmid: N/A
Summary: Nine patients with stable cardiac failure and mean left ventricular ejection fraction of 30% were investigated. All had previously been prescribed a benzodiazepine hypnotic by their home physicians, but the medication had been discontinued for at least 1 month. Subjects were monitored under three conditions: 1) without any sleeping medication, 2) during nasal CPAP administration and 3) at two points during a month-long administration of the benzodiazepine that had initially been prescribed to them. Overall, the benzodiazepine hypnotic improved the sleep fragmentation noted in these patients by decreasing the arousal index from a mean of 18 ± 6 per hour at baseline to a mean of 9 ± 6.5 per hour after one month of benzodiazepine therapy. Total nocturnal sleep time was consequently improved [baseline mean nocturnal total sleep time: 313 ± 27.3 minutes; benzodiazepine mean nocturnal total sleep time: 350 ± 17.3 minutes (p < 0.0003)], as was sleep efficiency. However, the benzodiazepine hypnotic had no significant effect on central hypopneas or apneas [baseline mean respiratory disturbance index (RDI): 20.5 ± 5.85 events/hour; mean RDI after 1 month of drug intake: 21.3 ± 2.5 events/ hour]. Nasal CPAP was also ineffective on the disordered breathing. In this group of subjects, respiration was even significantly worsened with nasal CPAP compared to baseline, as indicated by RDI(p < 0.0001), lowest Sa02 (p < 0.0001) and total nocturnal sleep time (p < 0.0001) measurements. Cardiac failure, Benzodiazepines, Nasal CPAP, Cheyne-Stokes breathing, Central apnea, Sleep disturbances This content is only available as a PDF.
Biberdorf, D., J.;Steens,, R.;Millar, T., W.;Kryger, M., H.
doi: 10.1093/sleep/16.6.529pmid: 8235237
Summary: We studied seven male patients with moderate to severe congestive heart failure (CHF) [left ventricular ejection fraction (LVEF) = 22.4 ± 6.7; mean ± SD] in a double-blind crossover trial to determine the effects of temazepam 15 mg on arousability, sleep architecture, Cheyne-Stokes respiration (CSR) and nighttime oxygen saturation. Sleep architecture was not markedly improved with temazepam. There was no significant change in total sleep time (TST) (383.1 ± 14.1 minutes to 396.6 ± 15.4 minutes, p = ns) (mean ± SE, placebo vs. temazepam) or total wake time (TWT) (96.9 ± 14.0 vs. 81.4 ± 14.0 minutes, p = ns). Sleep stage proportions did not change appreciably except for a reduction in stage 1 sleep (6.7 ± 1.2% vs. 4.0 ± 1.0%, p < 0.05). Microarousals per hour of sleep decreased with temazepam (21.1 ± 2.7/hour vs. 13.9 ± 2.1/hour placebo, p < 0.05), with the largest change occurring in stage 2 (24.9 ± 5.4/hour vs. 15.0 ± 3.1/hour, p < 0.05). Wake time during sleep (WDS) was reduced from 82.5 ± 11.7 minutes to 54.5 ±9.4 minutes, p< 0.03. Daytime alertness was improved with temazepam as was indicated by an increase in mean latency to sleep [multiple sleep latency test (MSLT) = 7.1 ± 2.4 vs. 5.7 ± 2.0 minutes, p < 0.04) on days following treatment with temazepam. There was no significant change in CSR as a percentage of TST (38.7 ± 13.6% vs. 32.5 ± 11.8%, p = ns). However, the apnea/hypopnea index (AHI) (10% filter) was decreased in stage 1 (28.1 ± 9.7/hour vs. 15.6 ± 8.2/hour). Overnight oxygen saturation did not change with temazepam (95.1 ± 0.6% both nights) and the percentage of TST spent below 90% oxygen saturation was minimal for both conditions (1.5 ± 1.1% vs. 2.2 ± 1.7%, p = ns). We conclude that CHF patients with CSR experience frequent arousals and that these arousals can be reduced with temazepam. There was an improvement in daytime somnolence. There was no worsening of nighttime oxygen saturation. Congestive heart failure, Left ventricular ejection fraction, Cheyne-Stokes respiration, Temazepam This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Wilcox,, Ian;Grunstein, Ronald, R.;Hedner, Jan, A.;Doyle,, Jean;Collins, Fiona, L.;Fletcher, Peter, J.;Kelly, David, T.;Sullivan, Colin, E.
doi: 10.1093/sleep/16.6.539pmid: 8235238
Summary: Ambulatory blood pressure (BP) was measured noninvasively (Oxford Medilog ABP) at 15-minute intervals for 24 hours before and after 8 weeks of treatment with nasal continuous positive airway pressure (nCPAP) in 19 men with obstructive sleep apnea (OSA). We included both normotensive and hypertensive patients, but hypertensives were studied after withdrawal of antihypertensive drugs. Ambulatory BP before and after treatment was compared using patients as their own controls. Treatment with nCPAP was successfully established in 14 of the 19 patients (74%). Blood pressure fell significantly in patients who were successfully treated: 24-hour mean BP (systolic/diastolic) decreased from 141 ± 18/89 ± 11 mm Hg to 134 ± 19/85 ± 13 mm Hg (p < 0.05). The reduction in 24-hour mean systolic BP occurred during both day and night, but a significant fall in mean diastolic BP was only observed during the day. The mean blood pressure fell in both normotensive and hypertensive patients. Patients who were inadequately treated with nCPAP had no reduction in mean 24-hour BP. Effective treatment of sleep apnea with nCPAP was associated with a significant fall in both systolic and diastolic BP independent of changes in body weight or alcohol consumption, suggesting that sleep apnea was an independent factor contributing to elevated nighttime and daytime BP in these patients. Sleep apnea, Hypertension, Obesity This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Suzuki,, Mayumi;Otsuka,, Kuniaki;Guilleminault,, Christian
doi: 10.1093/sleep/16.6.545pmid: 8235239
Summary: We investigated the way in which nasal continuous positive airway pressure (CPAP) affects the circadian profiles of blood pressure (BP) and heart rate (HR) in obstructive sleep apnea syndrome (OSAS) patients. Nine patients with OSAS, confirmed by nocturnal polysomnography, were studied with ambulatory blood pressure monitoring (Colin ABPM-630) during two 48-hour periods, before and during nasal CPAP treatment, at the Stanford University Sleep Disorders Clinic. During each 48-hour monitoring period, blood pressure measurements were taken by the ambulatory device every 30 minutes. During the ambulatory blood pressure recordings, nocturnal sleep time was defined as the period between 0000 hours to 0600 hours and active daytime was defined as the period between 1000 hours and 2000 hours. An average systolic blood pressure >135 mm Hg during the 48-hour baseline recording was defined as hypertensive. Using these criteria, we selected four hypertensive and five normotensive patients. Average BP (systolic/diastolic) and HR during the 48-hour periods decreased significantly from 148.6/88.2 mm Hg to 138.7/81.4 mm Hg, and from 77.9 beats per minute (bpm) to 67.2 bpm in hypertensives during CPAP treatment (p = 0.04), but there were no significant changes observed in normotensives. Average BP, during the day and at night, decreased from 152.3/ 91.8 mm Hg to 141.2/85.1 mm Hg and from 133.9/76.8 mm Hg to 125.9/73.7 mm Hg, respectively, in the hypertensives during CPAP, but such changes were not observed in normotensives. Average HR during the day and at night decreased significantly from 85.2 bpm to 72.6 bpm and from 69.8 bpm to 56.5 bpm in the hypertensives (p = 0.04), but not in normotensives. In conclusion, nasal CPAP is effective in improving circadian BP profiles and in normalizing daytime hypertension in some hypertensive OSAS patients. Obstructive sleep apnea syndrome, Nasal continuous positive airway pressure, Ambulatory blood pressure monitoring This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Dickerson, Linda, W.;Huang, Alice, H.;Thumher, Marian, M.;Nearing, Bruce, D.;Verrier, Richard, L.
doi: 10.1093/sleep/16.6.550pmid: 8235240
Summary: Previous studies in dogs showed dramatic increases in coronary blood flow associated with episodes of sinus tachycardia during rapid eye movement (REM) sleep. The present study demonstrates that 90% of these surges in heart rate and coronary flow are concentrated during periods of phasic REM sleep and only 10% in tonic REM sleep. Intensely phasic REM was distinguished from moderately phasic REM sleep by the degree of phasic eye movement. The surges were three times more frequent during intensely phasic REM than in moderately phasic REM sleep. However, the magnitudes of heart rate (37% ± 3%) and coronary flow (25% ± 3%) surges were unaffected by the specific substage of REM sleep. The incidence of surge events was almost eleven times greater in epochs of phasic REM that also contained a muscle twitch than in those that did not. During REM sleep, muscle twitches accompanying surges were not associated with any additional elevations in coronary flow or myocardial demand. Our data indicate that the sinus tachycardia-associated surges in coronary flow represent integrated autonomic responses intrinsic to phasic periods of REM sleep in dogs. Coronary flow, Sinus tachycardia, Canine, REM sleep, Phasic activity This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Philip,, Pierre;Guilleminault,, Christian
doi: 10.1093/sleep/16.6.558pmid: 8235241
Article PDF first page preview Close This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Allen, Richard, P.;McCann, Una, D.;Ricaurte, George, A.
doi: 10.1093/sleep/16.6.560pmid: 7901886
Summary: (±)3,4-methylenedioxymethamphetamine (MDMA) is a recreational drug of abuse which damages serotonin neurons in animals. It is not known whether MDMA is also neurotoxic in humans, and if so, whether there are functional consequences. Given the putative role of serotonin in sleep, it was hypothesized that one manifestation of serotonin neurotoxicity in humans might be disturbances of sleep. To determine whether MDMA use has effects on sleep, all-night polysomnograms of 23 MDMA users were compared to those of 22 age- and sex-matched controls. On average, MDMA users had 19 minutes less total sleep and 23.2 minutes less non-REM (NREM) sleep than controls. These statistically significant differences in NREM sleep were due primarily to an average of 37 minutes less stage 2 sleep, with no significant differences noted in stages 1, 3 or 4. Although it is not known whether the alterations in sleep observed in MDMA users are due to serotonin neurotoxicity, the present findings suggest that MDMA use can lead to persistent changes in CNS structures involved in human sleep generation. MDMA, Serotonin, Neurotoxicity, Amphetamines, Sleep This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
Kronholm,, Erkki;Alanen,, Erkki;Hyyppä, Markku, T.
doi: 10.1093/sleep/16.6.565pmid: 8235242
Summary: The relationships between nocturnal motor activity and daytime psychophysiological activation were investigated in a random community sample of 199 subjects aged 35–55 years. Nocturnal motor activity was recorded with the static charge sensitive bed (SCSB, Bio-Matt®). The association of nocturnal motor activity with demographic features, health status, laboratory blood values, afternoon electrodermal activity (EDA) and psychological distress was studied. A model for nocturnal motor activity was constructed and statistically analyzed. The analysis revealed that psychological distress, breathing disturbance, plasma glucose level and sympathetic activity were related significantly and independently to nocturnal motor activity. Their relations and the associations of sex, age, body mass index (BMI), sleep latency and health status with nocturnal motor activity were discussed in the context of the arousal theory of poor sleep. Sleep, Motor activity, Community study, Laboratory tests, Electrodermal activity, Distress This content is only available as a PDF. © 1993 American Sleep Disorders Association and Sleep Research Society
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