Cardiopulmonary regulation after rapid-eye-movement sleep deprivation.

Arterial blood pressure, chest movement, electroencephalogram, and electromyogram were monitored in six normotensive Sprague-Dawley rats for 4 h/day 3 days before and 4 days after 114 h of rapid-eye-movement (REM) sleep deprivation. During recovery sleep immediately after REM sleep deprivation (RD), there was a significant increase in the amount of time spent in REM sleep. During this rebound in REM sleep, there was a significant rise (26%) in heart rate in wakefulness, non-REM sleep, and REM sleep during the first 4 h after RD. Systolic blood pressure was also significantly elevated (14%) but only during wakefulness before recovery sleep. Rats with the greatest waking systolic blood pressure after RD had the lowest REM sleep rebound in the 4 h immediately after RD (r = -0.885, P less than 0.05). The rise in heart rate, systolic blood pressure, and REM sleep time evident on day 1 immediately after RD was absent on recovery days 2-4. The respiratory rate tended to be higher throughout the recovery period in every state of consciousness; however, these values never reached the level of significance. In the initial recovery sleep period, regulation of heart rate was more disrupted by REM sleep deprivation than either arterial blood pressure or respiratory rate.     

Moderate glucose deprivation preconditions myocardium against infarction.

Glucose-free perfusion preconditions myocardium against the consequences of subsequent ischemia. We investigated whether mitochondrial ATP-sensitive potassium (mK (ATP)) channels are involved in preconditioning by glucose deprivation, and whether moderate glucose deprivation also preconditions myocardium. Isolated rat hearts underwent 30 min of no-flow ischemia followed by 1 h reperfusion. Controls were not further treated. Three groups were preconditioned by perfusion with 0, 40 or 80 mg/dl (0, 2.22, 4.44 mmol/l) glucose (correction of osmotic pressure by addition of urea) for 10 min followed by 10 min perfusion with normal buffer (150 mg/dl, or 8.33 mmol/l glucose) before the ischemia reperfusion protocol. In one group, 100 micromol/l of the mK (ATP) channel blocker 5-HD was added to the glucose-free perfusate. Two groups were treated with 5-HD or urea before ischemia without preconditioning. Left ventricular developed pressure and maximum ischemic contracture (82 +/- 21 mmHg) were similar in all groups. Mean left ventricular developed pressure was 100 +/- 16 mm Hg under baseline conditions, and poorly recovered to 8 +/- 11 mm Hg during reperfusion. Preconditioning with 0 and 40 mg/dl glucose containing buffer reduced infarct size from 41 +/- 10% (control) to 23 +/- 12% (p = 0.02) and 26 +/- 8% (p = 0.011). The 5-HD blocked preconditioning by glucose deprivation (38 +/- 9%, p = 0.04) while 80 mg/dl glucose, 5-HD and urea had no effect on infarct size (39 +/- 9%; 38 +/- 13%; 37 +/- 8%; p = 1.0 each). We conclude that transient severe glucose deprivation and moderate glucose deprivation preconditions the isolated rat heart. Preconditioning by complete glucose deprivation depends on the opening of mK (ATP) channels.     

Effects of nutrient deprivation on Vibrio cholerae.

Environmental and clinical strains of Vibrio cholerae were exposed to nutrient-free artificial seawater and filtered natural seawater microcosms for selected time intervals and examined for changes in cell morphology and number. Cells observed by transmission electron and epifluorescence microscopy were found to undergo gross alterations in cell morphology with time of exposure. The vibroid cells decreased in volume by 85% and developed into small coccoid forms surrounded by remnant cell walls. The initial number of cells inoculated into nutrient-free microcosms (culturable count and direct viable count) increased 2.5 log10 within 3 days, and even after 75 days the number of viable cells was still 1 to 2 log10 higher than the initial inoculum size. Nutrient-depleted coccoid-shaped cells were restored to normal size and assumed a bacillary shape within 3 h and began to divide within 5 h after nutrient supplementation. The increase in cell number and decrease in cell volume under nutrient-depleted conditions, as well as the rapid growth response after nutrient supplementation, may describe some of the survival mechanisms of V. cholerae in the aquatic environment.     

Grommets,tonsillectomies, and deprivation in Scotland.

OBJECTIVE--To see whether there is a relation between grommet insertion operation and tonsillectomy rates, otolaryngology services, and deprivation scores in Scotland. DESIGN--Analysis of routine 1990 NHS data on grommet insertions and tonsillectomies in Scottish children aged 0-15 years compared with data on general practitioner and otolaryngology services and Carstairs deprivation scores. SETTING--All 15 Scottish health boards. SUBJECTS--All children aged 0-15 (1,021,933). RESULTS--Tonsillectomy was more common than grommet insertion operations in Scotland (6182:4850). Health boards with high grommet insertion rates were more likely to have low tonsillectomy rates (Spearman''s rank correlation -0.59; 95% confidence interval -0.87 to -0.03). Grommet insertion rates varied fourfold (from 2.4/1000 to 9.2/1000) and tonsillectomy rates twofold (from 3.6/1000 to 8.0/1000) across Scottish health boards. Variation between health boards had changed over the 15 years 1975-90. Variation in grommet insertion rates did not reflect variation in the supply of otolaryngology consultants (Spearman''s rank correlation -0.25). There was a non-significant tendency for high general practitioner referral rates to be associated with high grommet insertion rates, low tonsillectomy rates, and less deprived areas (Spearman''s rank correlation coefficients 0.50, -0.53, and -0.43). Deprivation (measured by Carstairs scoring for each health board) was associated with higher tonsillectomy rates (Spearman''s rank correlation 0.41; 95% confidence interval -0.22 to 0.80) and significantly lower grommet insertion rates (-0.73; -0.92 to -0.28). CONCLUSION--Social factors as well as differences in disease prevalence and medical practice need to be considered when studying variation in childhood grommet insertion and tonsillectomy rates.     

Paradoxical sleep deprivation increases glutamine synthetase in rat brain.

The modifications of glutamine synthetase (GS) level, an enzyme mainly located in astrocytes, were investigated in rat after paradoxical sleep deprivation and during recovery. An immunotitration method was used to evaluate the relative level of GS in brain tissue. At the end of a 24 hrs. paradoxical sleep deprivation, a significant increase in GS level was observed both in the frontoparietal cortex and the locus coeruleus area. 4 hrs. later, during recovery, the GS level returned to control level in the cortex but was lower in the locus coeruleus area.