Key result
Tail vasoactivity in rats acts as an abrupt on-off control mechanism for heat dissipation, driving a 20-min cycle of hypothalamic temperature changes between 29-33 degrees C.
Tail vasoactivity in rats operates as an on-off control mechanism for heat dissipation, driven by hypothalamic temperature changes.
Does not support clinical thermoregulation changes; leaves open extension of rodent tail vasoactivity mechanisms to humans.
Anterior hypothalamic temperature, tail vasoactivity, and tail heat loss were observed in unanaesthetised rats resting at an ambient temperature that was varied between 25 and 35 degrees C between experiments, but was held constant within an experiment. Vasodilation and vasoconstriction at the tail were qualitatively detectable by the appearance and disappearance of temperature differences between the tail surface overlying the ventral arterial supply, and the lateral venous drainage. Vasodilation detected this way was an abrupt singular event (being either on or off), and preceded subsequent exponential changes in tail surface temperature and heat loss. Within the ambient temperature range of 29--33 degrees C, the following sequence occurred in a 20-min cycle, despite the noncycling constant environmental and metabolic heat loads: tail vasodilation - 0.2 to 0.4 degrees C fall in hypothalamic temperature - tail vasoconstriction - 0.2 to 0.4 degrees C rise in hypothalamic temperature. This behaviour, consistent with the limit-cyclic behaviour of some nonlinear controllers, as well as the abrupt two-state nature of vasoactivity at the rat tail, provides evidence that the mechanism can be described by an on-off control model. In addition, angiography suggests that vasoconstriction rather than countercurrent heat exchange provides the major barrier to core to tail heat flow during the "off" phase.
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Young et al. (1982) studied this question. Ambient temperature variation (25-35 degrees C) was evaluated on Anterior hypothalamic temperature, tail vasoactivity, and tail heat loss. Tail vasoactivity in rats acts as an abrupt on-off control mechanism for heat dissipation, driving a 20-min cycle of hypothalamic temperature changes between 29-33 degrees C.
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