Summary

A survey of the literature on a large number of vertebrate animals shows that sleep is associated with profound cardiovascular and respiratory adjustments which are very similar in each species. A hypothesis is advanced that these adjustments are 'goal directed' by neural structures in the brainstem, to ensure an adequate O2 and CO2 transport to and from the brain whilst at the same time reducing energy cost. During synchronised sleep there is a vagal bradycardia leading to reduced cardiac output and a fall in blood pressure; despite this cerebral blood flow increases. During desynchronized sleep there is a tonic fall in blood pressure and heart rate resulting from a unique repatterning of sympathetic discharge, that to heart, kidney, splanchnic and pelvic vascular beds decreasing whilst that to skeletal muscle increasing; cerebral blood flow shows a further increase. This differential pattern is probably initiated by neurones located in the caudal raphe nucleus obscurus. Phasic increases in blood pressure and heart rate also occur during desynchronized sleep mainly as a consequence of increases in sympathetic activity. Ventilation decreases during synchronized sleep accompanied by an increase in partial pressure of arterial CO2, which vasodilates cerebral blood vessels, indicating that the influence of CO2 on the level of ventilation has changed. During desynchronized sleep ventilation increases and becomes very irregular but the partial pressure of O2 and CO2 in arterial blood is little changed from wakefulness. Control of respiration is shifted to a central generator which apparently is different to the automatic/metabolic one which is normally dominant during wakefulness. Reflex control of the circulation and respiration is mainly governed by peripheral chemoreceptors, the threshold of most other afferent inputs being significantly raised during sleep.