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Contribution of thermal and nonthermal factors to the regulation of body temperature in humans.

The set point has been used to define the regulated level of body temperature, suggesting that displacements of core temperature from the set point initiate heat production (HP) and heat loss (HL) responses. Human and animal experiments have demonstrated that the responses of sweating and shivering do not coincide at a set point but rather establish a thermoeffector threshold zone. Neurophysiological studies have demonstrated that the sensor-to-effector pathways for HP and HL overlap and, in fact, mutually inhibit each other. This reciprocal inhibition theory, presumably reflecting the manner in which thermal factors contribute to homeothermy in humans, does not incorporate the effect of nonthermal factors on temperature regulation. The present review examines the actions of these nonthermal factors within the context of neuronal models of temperature regulation, suggesting that examination of these factors may provide further insights into the nature of temperature regulation. It is concluded that, although there is no evidence to doubt the existence of the HP and HL pathways reciprocally inhibiting one another, it appears that such a mechanism is of little consequence when comparing the effects of nonthermal factors on the thermoregulatory system, since most of these factors seem to exert their influence in the region after the reciprocal cross-inhibition. At any given moment, both thermal and several nonthermal factors will be acting on the thermoregulatory system. It may, therefore, not be appropriate to dismiss the contribution of either when discussing the regulation of body temperature in humans.

Autonomic Nervous System↗

Evidence for regulation of body temperature in rats by dopamine D2 receptor and possible influence of D1 but not D3 and D4 receptors.

The dopamine D(3) receptor agonist PD 128907 decreased body temperature in the rat. The selective dopamine D(3) and D(4) receptor antagonists, A-437203 and L-745,870, respectively, did not prevent this effect. In contrast, PD 128907-induced hypothermia was antagonized by SCH 23390, a selective D(1) receptor antagonist, and by L-741,626, a selective D(2) receptor antagonist. Moreover, the selective D(2) receptor agonist trihydroxy-N-n-propylnoraporphine (TNPA) elicited a robust hypothermia which was prevented by pretreatment with L-741,626 but not by A-437203. In agreement with previous data obtained in D(3) knock-out mice, present results suggest that D(2) rather than D(3) receptors mediate dopamine receptor agonist-induced hypothermia in rats. In addition, it appears that both D(1) and D(2) receptors may be involved in a cooperative manner.

Animals↗

Central nervous regulation of body temperature during sleep.

The relationship between hypothalamic temperature and metabolic heat production was measured during wakefulness, slow-wave sleep, and paradoxical sleep in unrestrained kangaroo rats (Dipodomys). Hypothalamic temperature was manipulated with chronically implanted, water-perfused thermodes while cortical electroencephalogram, electromyogram, metabolic rate, and body movement were continuously recorded. During slow-wave sleep, in comparison to wakefulness, there is a lowered threshold hypothalamic temperature for the metabolic heat production response and a lowered proportionality constant relating rate of metabolic heat production to hypothalamic temperature. During paradoxical sleep no increase in metabolic heat production could be elicited by lowering hypothalamic temperature, which indicates that the thermoregulatory system is inoperative. These results provide a basis for explaining the changes in various body temperatures, metabolic rate, and other thermoregulatory responses during sleep in a variety of mammals.

Animals↗

Observations on the effect of salicylate in fever and the regulation of body temperature against cold.

Prostaglandins appear to be mediators, within the hypothalamus, of heat production and conservation during fever. We have investigated a possible role of prostaglandins in the nonfebrile rabbit during thermoregulation in the cold. Shorn rabbits were placed in an environment of 20 degrees C, and rectal and ear skin temperatures, shivering and respiratory rates were measured. A continuous intravenous infusion of leucocyte pyrogen was given to establish a constant fever of approximately 1 degree C, and after observation of a stable febrile temperature for 90 min, a single injection of 300 mg of sodium salicylate, followed by a 1.5 mg/min infusion was then given. After the salicylate infusion was begun, rectal temperature began to fall, and reached nonfebrile levels within 90 min. Shivering activity ceased, respiratory rates increased, and in two animals, ear skin temperature increased. When these same rabbits were placed in an environment of 10 degrees C, at a time they were not febrile, and an identical amount of salicylate was given, rectal and ear skin temperatures, shivering and respiratory rates did not change. These results indicate that prostagladins do not appear to be involved in heat production and conservation in the nonfebrile rabbit.

Animals↗

Intravascular volume and tonicity as factors in the regulation of body temperature.

The effect of alterations in intravascular volume and tonicity on thermoregulatory and cardiovascular responses to heat and exercise have been compared in four subjects. Core temperatures were found to be significantly higher during dehydration, and when dehydration was prevented by administration of 1% saline, than when dehydration was prevented by water administration. These higher temperatures were associated with elevated levels of plasma [Na] and osmolarity, but no consistent relationship between temperature and changes in intravascular volume could be demonstrated. Relationships observed between core temperature and plasma tonicity were consistent with the hypothesis that the adverse effects of dehydration on thermoregulation can be attributed to an inhibition of sweating mediated by an increase in either plasma osmotic pressure or plasma [Na]. In separate experiments the heart rate response to exercise was shown to be reduced by saline, compared with water and dehydration, and this may be explained by the smaller reduction in intravascular volume which occurs during exercise following administration of hypertonic saline. It is concluded that the effects of reduced intravascular volume, and increased intravascular tonicity on physical work capacity may be distinguished by the adverse effect on the cardiovascular system of the former, and on the thermoregulatory system of the latter.

Adult↗