Vascular resistance in the rat during baseline, chronic total sleep deprivation, and recovery from total sleep deprivation

Abstract

Rats subjected to total sleep deprivation (TSD) by the disk-over-water method exhibit an elevated temperature set point, increased energy expenditure (EE), and increased circulating norepinephrine - all of which should militate for an increase in body temperature. Instead, after a small rise early in TSD, intraperitoneal temperature (T(ip)) fell progressively, indicating a reduced ability to retain body heat. To evaluate whether vasoconstrictor defenses against heat loss in the regions of major heat dissipation in the rat (hindpaws and tail) were impaired, peripheral vascular resistance (PVR) was calculated from aortic blood pressure (BP) and blood flow (BF) (BP and BF were continuously recorded at the aortic-iliac junction). TSD rats and their yoked control (TSC) rats were subjected to TSD for 10 to 22 days. As in earlier studies, TSD rats showed excessive heat loss indicated by a falling T(ip) (after an initial rise) while EE was elevated. Temperature set point was presumably raised throughout deprivation as shown previously. Although a small decline in PVR early in deprivation could have increased heat loss, there was no evidence of a massive vasodilation in the region examined which could, in itself, account for the progressive inability to retain heat over the course of TSD. In fact, PVR was near baseline levels during the latter half of TSD. Nevertheless, there was evidence of impaired vasoconstrictive defenses in TSD rats inasmuch as they showed significantly lower PVR than TSC rats during most of the deprivation period in spite of indications that they were farther below set point. It is not yet clear whether this impairment was a major determinant of the heat loss in TSD rats. A rapid PVR rebound during recovery suggested a release from a TSD-linked blockage of vasomotor compensation for excessive heat loss.