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At least 271 records · Page 15Linked to original sources
PubMed2000

Influence of hormone replacement therapy and aspirin on temperature regulation in postmenopausal women.

Postmenopausal women receiving estrogen-replacement therapy (ERT) regulate body temperature (T(b)) at a lower level than women not receiving hormone replacement therapy (untreated) and women using estrogen plus progesterone therapy (E + P), but it is not clear if reproductive hormones alter T(b) by directly acting on central thermoregulatory centers or indirectly via a secondary mediator(s). The purpose of the present investigation was to examine the possible involvement of pyrogenic cytokines and cyclooxygenase (COX) products (e.g., prostaglandins) in the regulation of T(b) in three groups of postmenopausal women (8 ERT, 7 E + P, and 8 untreated). We measured ex vivo secretion of cytokine agonists [tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta and -6] and modifiers (IL-2 soluble receptor, IL-1 receptor antagonist, soluble TNF receptor type I, soluble TNF receptor type II, soluble IL-6 receptor, and soluble glycoprotein 130) from peripheral blood mononuclear cells and thermoregulatory responses at rest and during 1 h of passive whole body heating in the postmenopausal women before and after 3 days of placebo or aspirin (50 mg. day(-1). kg(-1)). With and without aspirin, the ERT group had a lower baseline rectal temperature (T(re); 0.44 degrees C, P < 0.004) and a reduced T(b) threshold for cutaneous vasodilation (0.29 degrees C and 0.38 degrees C, P < 0.01) compared with the untreated and E + P groups, respectively. In the placebo condition, waking morning oral temperature (T(or)) correlated with ex vivo secretion of the proteins associated with IL-6 bioactivity. Aspirin caused significant reductions in waking T(or) in the E + P group and in baseline T(re) in the untreated group. However, the difference in thermoregulation brought about by steroid hormone treatment could not be explained by these relatively modest apparent influences by cytokines and COX products. Therefore, the altered thermoregulation induced by reproductive steroid therapy appears to occur via a mechanism distinct from a classic infection-induced fever.

Aged↗
PubMed2006

Central mechanisms for thermoregulation in a hot environment.

Homeothermic animals regulate body temperature by autonomic and behavioral thermoeffector responses. The regulation is conducted mainly in the brain. Especially, the preoptic area (PO) in the hypothalamus plays a key role. The PO has abundant warm-sensitive neurons, sending excitatory signals to the brain regions involved in heat loss mechanisms, and inhibitory signals to those involved in heat production mechanisms. The sympathetic fibers determine tail blood flow in rats, which is an effective heat loss process. Some areas in the midbrain and medulla are involved in the control of tail blood flow. Recent study also showed that the hypothalamus is involved in heat escape behavior in rats. However, our knowledge about behavioral regulation is limited. The central mechanism for thermal comfort and discomfort, which induce various behavioral responses, should be clarified. In the heat, dehydration affects both autonomic and behavioral thermoregulation by non-thermoregulatory factors such as high Na+ concentration. The PO seems to be closely involved in these responses. The knowledge about the central mechanisms involved in thermoregulation is important to improve industrial health, e.g. preventing accidents associated with the heat or organizing more comfortable working environment.

Animals↗
PubMedDate not supplied

Immune cytokines and regulation of body temperature, food intake and cellular immunity.

Interleukin-1 (IL-1) and interferon alpha (IFN alpha), cytokines originally detected in immunological cells, now have been shown to produce nonimmunological host defense responses of central and peripheral origins. These cytokines are released from glial cells in the brain in pathological states. Local application of IL-1 beta and IFN alpha to thermosensitive neurons in the preoptic and anterior hypothalamus and glucose responsive neurons in the ventromedial hypothalamus in vivo and in vitro, altered the activity in appropriate ways to explain the cytokines-induced fever and anorexia, respectively. The responses to IL-1 beta, but not to IFN alpha, were blocked by sodium salicylate, suggesting the involvement of synthesis of prostaglandins. alpha MSH, an endogenous antipyretic and a possible antagonist of IL-1 beta at lymphocytes, specifically depressed the responses to IL-1 beta, but not those to IFN alpha. In contrast, the action of IFN alpha was reversibly blocked by naloxone, suggesting the opioid receptor mediation. Intracerebral injection of IFN alpha and beta-endorphin in the rat and mouse resulted in the suppression of cytotoxic activity of natural killer cells in the spleen by activation of brain opioid receptor, which was shown to be mediated predominantly by splenic sympathetic nerves. The results suggest a view that immune cytokines may provide afferent links for the regulatory circuits between the brain and the immune system.

Animals↗
PubMed2006

Heat illness during working and preventive considerations from body fluid homeostasis.

The purposes of this review are to show pathophysiological mechanisms for heat illness during working in a hot environment and accordingly provide some preventive considerations from a viewpoint of body fluid homeostasis. The incidence of the heat illness is closely associated with body temperature regulation, which is much affected by body fluid state in humans. Heat generated by contracting muscles during working increases body temperature, which, in a feedback manner, drives heat-dissipation mechanisms of skin blood flow and sweating to prevent a rise in body temperature. However, the impairment of heat-dissipation mechanisms caused by hard work in hot, humid, and dehydrated conditions accelerates the increase in body temperature, and, if not properly treated, leads to heat illness. First, we overviewed thermoregulation during working (exercising) in a hot environment, describe the effects of dehydration on skin blood flow and sweating, and then explained how they contributes to the progression toward heat illness. Second, we described the advantageous effects of blood volume expansion after heat acclimatization on temperature regulation during exercise as well as those of restitution from dehydration by supplementation of carbohydrate-electrolyte solution. Finally, we described that the deteriorated thermoregulation in the elderly is closely associated with the impaired body fluid regulation and that blood volume expansion by exercise training with protein supplementation improves thermoregulation.

Body Fluids↗
PubMed1980

Temperature regulation and prostaglandin E1 fever in scorpions.

1. Scorpions Buthus occitanus and Androctonus australis were placed in a temperature gradient where they could select their thermopreferendum. Intrathoracic temperature was recorded continuously. 2. Both species selected 24.8 +/- 1.0 degrees C as their preferred body temperature. No nycthemeral cycle of preference was observed in the experimental conditions. Saline injection did not modify this thermopreferendum. 3. Prostaglandin E1 (PGE1) produced a fever. Duration and magnitude of fevers were related to PGE1 doses in a bell-shaped curve. The longest and highest fevers were obtained with 4 microgram . g-1 PGE1. 4. These results show that there is an ability to produce fever and, thus, indirectly, that there is a set point in body temperature regulation in arthropods, among the oldest known terrestrial animals.

Animals↗
PubMed1975

[Body shape and temperature regulation. Studies on Indian students].

On a sample of n = 23 Indian students associations between the heat loss ability after thermic stress and anthropometric variables (body height, body weight, body surface, weight/surface ratio) could be seen. The biological meaning of these findings is discussed with special reference to the climatic associated geographical variability of the human physique.

Adult↗
PubMed1975

[Hyperthermia in the rabbit. I. Studies on influencing circulation with exogenic hyperthermia].

Increasing the environmental temperature to 35 degrees C produced hyperthermia in 11 female rabbits, 80-90 days old. At the onset of hyperthermia the heart rate increased, but there was no further change after about two hours (range 1-3 hours); it remained constant at an increased rate until the end of the experiment. Blood pressure fell at first, but it had increased again after 90 minutes, and underwent no further change during the experiment. The mechanism of these circulatory changes were discussed in relation to the neutral control of body temperature regulation.

Animals↗
PubMed1970

Regulation of oxygen consumption and body temperature during torpor in a hummingbird, Eulampis jugularis.

The West Indian hummingbird, Eulampis jugularis, maintained its body temperature in torpor at 18 degrees to 20 degrees C over an ambient temperature range of 2.5 degrees to 18 degrees C. At ambient below 18 degrees C oxygen consumption during torpor increased linearly with decreasing temperature. Thermal conductances were the same for resting and torpid Eulampis regulating their body temperatures at 40 degrees and 18 degrees C, respectively.

Animals↗