Nocturnal peaks in core body temperature of rats during the estrous cycle were highest during the night of ovulation (2300-0200 h, proestrus-estrus) and lowest during the night before (diestrus 2-proestrus). Less dramatic diurnal secondary peaks, absent only during estrus, occurred 3-4 h after the onset of daylight. After induction of pseudopregnancy, mean temperature declined, but both daily peaks persisted until the first postluteal estrus, when the secondary peak was again absent transiently. Ovariectomy reduced mean core temperature and abolished all secondary peaks. In contrast, castration during pseudopregnancy did not abolish the secondary peaks. When cyclic rats were gonadectomized (abolishing the secondary rhythm) it was possible to re-establish this rhythm by stimulating the uterine cervix (as if to induce pseudopregnancy). However, in animals exposed to darkness (which also abolishes the secondary rhythm) reinduction by cervical stimulation was ineffective. These results indicated that the integrity of the secondary peak, though dependent on photoperiod, nevertheless was influenced by a neuroendocrine reflex arc.
Radiotelemetry of core temperature in unrestrained, mature female rats revealed the existence of a 24-h rhythm that was bimodal. The principal peak occurred during the night under control conditions of 14 h light and 10 h darkness, and a less pronounced, secondary peak occurred 3-4 h after the onset of the light phase. Shifts in the phase of the photoperiod or alteration of the proportion of light per day revealed that the temperature rhythm was entrained by light, but that the two component peaks were governed by different aspects of the lighting regimen. Exposure of rats to continuous darkness, continuous light, or to a 20-h photoperiod revealed that the primary rhythm was endogenous, entrained by circadian photoperiods only, whereas the secondary rhythm was exogenous, requiring a circadian light/dark rhythm. A relationship between mean core temperature and ttion pressure, end-systolic L was constant, despite variations in filling and therefore independent of initial L and delta L; moreover, the L to which the ventricle shortened was determined by the course of the systolic force L-relation. Thus, irrespective of loading, delta L occurs within the confines of the contractile state-depdendent isovolumic force-L relation and where the latter is equivalent to the end-systolic force-length relation.
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