Tijana Bojic

Sleep-Dependent Changes in the Coupling Between Heart Period and Arterial Pressure in Newborn Lambs

This study assessed whether sleep-dependent changes in the relationship between heart period (HP) and mean arterial pressure (MAP) occur in newborn life. Electrodes for electrocorticographic, electromyographic, and electrooculographic monitoring and an arterial catheter for blood pressure recordings were implanted in 11 newborn lambs. HP and MAP beat-to-beat values were computed from 120-s blood pressure recordings during quiet wakefulness, active sleep, and quiet sleep. For each recording, the time shift at which the maximum of the HP versus MAP cross-correlation function was attained was identified. For each lamb and wake-sleep state, an average correlation coefficient was then computed corresponding to the median value of such time shifts. The maximum of the cross-correlation function was attained with HP lagging behind MAP. The corresponding mean correlation coefficient was significantly higher in quiet sleep (0.51 ± 0.05) than either in quiet wakefulness (0.31 ± 0.05) or in active sleep (0.29 ± 0.03). Sleep-related differences in the correlation between HP and MAP were maintained after HP and MAP data were low-pass filtered at 0.3 Hz to remove their fast ventilatory oscillations. In conclusion, data indicate that the relationship between spontaneous fluctuations in HP and those in MAP is sleep-state dependent in newborn lambs. A positive HP versus MAP correlation with HP lagging behind MAP is consistent with baroreflex control of HP. Heart rhythm thus may be more tightly controlled by the baroreceptor reflex and less dependent on central autonomic commands in quiet sleep than either in quiet wakefulness or in active sleep.

Sleep-Related Brain Activation Does Not Increase the Permeability of the Blood-Brain Barrier to Glucose

We compared blood-brain barrier (BBB) permeability to glucose between quiet wakefulness and rapid-eye-movement (REM) sleep to assess whether changes in BBB permeability play a role in coupling glucose supply to the physiologic metabolic needs of the brain. Male Sprague-Dawley rats were prepared with electrodes for wake-sleep state scoring and with arterial and venous catheters. Using the single-pass, dual-label indicator method, unidirectional glucose extraction by the brain and cerebral blood flow (CBF) were simultaneously measured during states of quiet wakefulness (n = 12) or REM sleep (n = 7). The product of BBB surface area and permeability to glucose (PS product) was computed in each state. During REM sleep, CBF significantly exceeded that during quiet wakefulness in all regions but the cerebellum, whereas the difference in the PS product between quiet wakefulness and REM sleep was not statistically significant in any brain region. In the brain as a whole, CBF significantly increased 29% from quiet wakefulness to REM sleep, while a nonsignificant 0.8% increase occurred in the PS product. During REM sleep, the increase in CBF indicates a higher rate of brain glucose consumption than in quiet wakefulness, given the tight flow-metabolism coupling in the brain. Therefore, these data show that modulation of BBB permeability to glucose is not a mechanism that provides ‘energy on demand’ during the physiologic brain activation characterising REM sleep.

Brain capillary perfusion in the spontaneously hypertensive rat during the wake-sleep cycle.

Hypertension is accompanied by circulatory changes in the brain and in other vascular districts; at disease onset, these changes may be largely functional and dependent on metabolic and vegetative drives. The wake-sleep cycle is a major physiological source of ultradian variability in autonomic function and in cerebral blood flow and metabolism. Aim of the study was to investigate whether sleep induces functional changes in the brain microcirculation in the developing hypertensive state. The fraction of brain capillaries perfused by plasma (perfused/anatomical capillaries) was assessed in young (8–10xa0weeks) spontaneously hypertensive rats (SHR) during quiet wakefulness, quiet sleep and active sleep. The density of anatomical capillaries was assessed in two groups of animals using both a histochemical method (alkaline phosphatase, AP, for morphometric measurements) and an immunofluorescence method (anti-fibronectin antibodies, FN, to detect all existing capillaries). The density of perfused capillaries was determined by intravascular injection of a fluorescent marker. The fraction of anatomical capillaries perfused by plasma was always close to maximal (0.96–0.97), without significant variations among the states of the wake-sleep cycle, and was the same for AP-stained and FN-stained sections. Data thus indicate that in this model of essential hypertension no functional changes in plasma perfusion of cerebral capillaries occur in the early stages of the disease.