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PubMedDate not supplied

Interactions between body temperature regulation and blood acid-base status in anuran amphibians.

In vertebrate evolution, the transition from aquatic to terrestrial mode of life was associated with considerable changes in the respiratory system and CO2/pH-sensitive receptors became fundamental. The present review focuses on the combined effects of hypercapnia and body temperature in anuran amphibians, that represent a key group for the transition. Recent studies have indicated that temperature affects the hypercapnic drive to breathe. Conversely, hypercapnia modulates the range of preferred body temperature of amphibians and central (CO2/pH) receptors are likely to be involved.

Acid-Base Equilibrium↗
PubMed2004

Body temperature regulation during hemodialysis in long-term patients: is it time to change dialysate temperature prescription?

During hemodialysis procedures, changes in the dialysate temperature can raise or lower body temperature because the blood is returned to the patient in thermal equilibrium with the dialysate. Even a dialysate temperature equal to the patient's body temperature as measured from the tympanic membrane, oral cavity, or axilla can result in an increase in the patient's body temperature, leading to cutaneous vasodilation and the potential for cardiovascular instability and hypotension. This deleterious cycle of events can be prevented by suitably adjusting the dialysate temperature. Lowering the dialysate temperature from 37 degrees C to 34-35.5 degrees C has improved the cardiovascular stability of many hemodialysis patients. Continuous monitoring of blood temperature allows the practitioner to make preemptive changes in dialysate temperature because a small change in body temperature can have enormous cardiovascular implications. For example, only 0.3 degrees C to 0.8 degrees C separates the thresholds for skin vasodilation from that for shivering. A suggested improvement in the hemodialysis procedure is to use devices that allow continuous monitoring of arterial and venous blood temperatures and adjust the dialysate temperature automatically, keeping the patient, not the dialysate, isothermic. Less optimal solutions appear to be (1) to monitor arterial and venous temperatures while manually adjusting the dialysate temperature to maintain arterial (and hence body) temperature stability; (2) to monitor peripheral temperatures (oral, tympanic) at regular intervals and adjust dialysate temperature to maintain the body temperature constant; (3) routinely use a dialysate temperature <37.0 degrees C in all patients unless contraindicated.

Adult↗
PubMed2003

Effects of GABA agonists on body temperature regulation in GABA(B(1))-/- mice.

1. Activation of GABA(B) receptors evokes hypothermia in wildtype (GABA(B(1))+/+) but not in GABA(B) receptor knockout (GABA(B(1))-/-) mice. The aim of the present study was to determine the hypothermic and behavioural effects of the putative GABA(B) receptor agonist gamma-hydroxybutyrate (GHB), and of the GABA(A) receptor agonist muscimol. In addition, basal body temperature was determined in GABA(B(1))+/+, GABA(B(1))+/- and GABA(B(1))-/- mice. 2. GABA(B(1))-/- mice were generated by homologous recombination in embryonic stem cells. Correct gene targeting was assessed by Southern blotting, PCR and Western blotting. GABA(B) receptor-binding sites were quantified with radioligand binding. Measurement of body temperature was done using subcutaneous temperature-sensitive chips, and behavioural changes after drug administration were scored according to a semiquantitative scale. 3. GABA(B(1))-/- mice had a short lifespan, probably caused by generalised seizure activity. No histopathological or blood chemistry changes were seen, but the expression of GABA(B(2)) receptor protein was below the detection limit in brains from GABA(B(1))-/- mice, in the absence of changes in mRNA levels. 4. GABA(B) receptor-binding sites were absent in brain membranes from GABA(B(1))-/- mice. 5. GABA(B(1))-/- mice were hypothermic by approximately 1 degrees C compared to GABA(B(1))+/+ and GABA(B(1))+/- mice. 6. Injection of baclofen (9.6 mg kg-1) produced a large reduction in body temperature and behavioural effects in GABA(B(1))+/+ and in GABA(B(1))+/- mice, but GABA(B(1))-/- mice were unaffected. The same pattern was seen after administration of GHB (400 mg kg-1). The GABA(A) receptor agonist muscimol (2 mg kg-1), on the other hand, produced a more pronounced hypothermia in GABA(B(1))-/-mice. In GABA(B(1))+/+ and GABA(B(1))+/- mice, muscimol induced sedation and reduced locomotor activity. However, when given to GABA(B(1))-/- mice, muscimol triggered periods of intense jumping and wild running. 7. It is concluded that hypothermia should be added to the characteristics of the GABAB(1)-/-phenotype. Using this model, GHB was shown to be a selective GABAB receptor agonist. In addition, GABAB(1)-/- mice are hypersensitive to GABAA receptor stimulation, indicating that GABAB tone normally balances GABAA-mediated effects.

Animals↗
PubMed1996

Control of skin blood flow in the neutral zone of human body temperature regulation.

In humans, matching of heat loss and heat production in the "neutral" zone, defined operationally in terms of a range of skin temperatures (Tsk), is accomplished by regulation of skin blood flow (SkBF). Our studies were designed to reveal the characteristics of control of SkBF [from measurements of forearm blood flow (FBF)] in this zone. We controlled the temperature of water sprayed on most of the body of supine men and women at 33 or 35 degrees C in a square-wave pattern (15 min at each temperature) or a step pattern (60 min at 33 degrees C separated by short periods at 35 degrees C). FBF followed Tsk (0.5 ml.min-1.degrees C-1). Esophageal temperature changed approximately 0.11 degrees C with each 2 degrees C change in Tsk, falling with Tsk increase and vice versa. Little influence on FBF, < 0.1 ml.min-1.100 ml-1. degrees C-1, was observed when only the forearm was sprayed with 33 and 35 degrees C water. We conclude that SkBF control in the 33-35 degree C range of Tsk is dominated by the feedforward reflex influence of Tsk on SkBF. The reflex response overcompensates for the effect of Tsk on thermal balance in the neutral zone, so that equilibrium core temperature has an inverse relationship to Tsk.

Adult↗
PubMedDate not supplied

[Disorders of body temperature regulation. 1. Physiopathological study].

In this work, disorders of thermo-regulation are first studied in a synthetic manner from the angle of cellular and haemodynamic disturbances. Then the particular physiopathological aspects concerning hypothermia and hyperthermia are looked at in succession. In his next work, the author will view the clinical and therapeutic study of these phenomena. Extensive bibliography.

Acid-Base Equilibrium↗
PubMed2003

Exercise, hormones, and body temperature. regulation and action of GH during exercise.

UNLABELLED: That physical exercise stimulates pituitary GH secretion has been known for forty years, but the underlying mechanisms as well as the physiological significance remain elusive. We have previously shown that the concomitant increase in core temperature is essential for the exercise-induced GH release, inasmuch as exercise performed at 4 C results in a suppression of GH secretion, whereas passive heating constitutes a potent stimulus for GH release. Moreover, studies in normal subjects show that GH stimulates sweat production and evaporative heat loss during heat exposure with and without exercise, whereas GH-deficiency is associated with reduced sweat secretion and increased heat storage during similar conditions. The neurotransmitters involved in GH secretion during exercise remain uncertain; we therefore investigated the putative role of ghrelin, which is a gut-derived endogenous ligand for the GHS receptor. We measured circulating ghrelin levels before during and after submaximal aerobic exercise in healthy subjects and GH-deficient patients. The circulating ghrelin levels were unchanged during and after exercise in all subjects. Growth hormone stimulates lipolysis and lipid oxidation during basal and fasting conditions and we recently investigated whether GH also regulates substrate metabolism during exercise. The design involved GH-deficient patients studied during exercise with and without GH administration as compared to untreated healthy subjects. Growth hormone predominantly stimulated the turnover of free fatty acids in the recovery phase after exercise. CONCLUSIONS: 1) the increase in GH release during exercise is associated with the concomitant increase in body temperature, 2) GH stimulates sweat secretion and heat evaporation during exercise, which seems to be of distinct physiological significance, 3) ghrelin is not involved in exercise-induced GH release, 4) the impact of GH on substrate metabolism during exercise includes increased FFA turnover.

Body Temperature↗
PubMed2002

[Body temperature regulation as a prognostic criterion for the postoperative period in patients with femoral fractures].

Frequency is studied of adequate, redundant, inert, and reduced types of thermoreactivity in healthy subjects and patients with fractures. Definition of type of thermoreactivity to cooling in patients with fractures of the thighbone permits prognosticating the course of the bone fracture healing process. The symptom of distal hyperthermia/hypothermia is unspecific but is regarded as a supplementary index of the type of thermoreactivity and character of the course of the fracture healing process.

Aged↗
PubMed1994

[Exertion-related disorders in body temperature regulation in 8 participants in the Dam-to-Dam run 1993].

In eight recreational runners (seven men and one woman, aged 16 to 50 years) participating in a 16 kilometer run, disturbances in thermoregulation were diagnosed. Six experienced sudden collapse without any prodromal signs, two were exhausted and had muscle spasms. Heat exhaustion was diagnosed in four runners, exertion-related hyperthermia in three and exertion-related heat stroke in one. As a complication the latter patient developed rhabdomyolysis with low grade intravascular coagulation and acute renal insufficiency. The most important therapy consists of cooling the patient, the most important preventive measures are wearing light clothing and drinking regularly during the run.

Adolescent↗
PubMed1981

Barbiturate physical dependence in mice: effects on body temperature regulation.

Chronic exposure to phenobarbital at a 21-22 degrees C ambient temperature produced marked hypothermia in C57BL/6J male mice, to which functional tolerance gradually developed over a 6.5 day intoxication period. Soon after phenobarbital withdrawal, marked hypothermia again developed, reaching its maximal extent at a time when tremors, convulsions on handling and Straub tail were at their peak frequency. When these mice were placed in a 34 degrees C ambient environment, which prevents the hypothermia, these withdrawal signs were eliminated or greatly reduced in frequency compared to mice at 22 degrees C, whereas the incidence of tonic-clonic seizures was not significantly affected. Core body temperature was found to correlate significantly with the degree of gross intoxication during the intoxication phase and with the withdrawal signs of tremor and Straub tail after withdrawal of the drug. When mice were given a choice between a 23 and a 35 degrees C environment at times of maximal hypothermia, their choice often served to maintain the hypothermic state rather than to reduce it. These results suggest that some of the signs of withdrawal (tremor and Straub tail) may be (in part) secondary responses to a primary dysfunction, which is thermoregulatory in nature.

Animals↗
PubMed1977

Body temperature regulation and thermoneutrality in rats.

Various concepts of thermoneutrality were considered for a proposed study of the role of hypothalamic amines in temperature regulation of rats. The classic definition, the ambient temperature over which metabolic rate is minimum and constant, gave a range of approximately 28 to 32 degrees C. However, within this temperature range rats were inactive, the inactivity apparently representing a behavioural response to heat stress and itself responsible for the reduced metabolic rate; certain thermoregulatory effectors were also activated to increase heat loss. Therefore an alternative range, 18.0 +/- 1.9 (mean +/- S.D.) to 28.1 +/- 1.0 degrees C, was defined in which rats displayed normal activity, behavioural thermoregulations being absent.

Animals↗
PubMed1996

Body temperature regulation in the newborn infant: interaction with sleep and clinical implications.

Thermoregulation in newborn infant differs from that of adult. Comparisons between sleep stages show that, during rapid eye movements (REM) sleep, the impairment of thermoregulatory responses in adult is not observed in newborn. Both behavioral and autonomic temperature regulations are always operative in the range of air temperatures usually imposed. The interaction between sleep and thermoregulation seems to be less important in newborns than in adults, suggesting that sleep processes are well protected, reducing the probability of occurrence of central dysfunction. According to the model describing thermoregulation during sleep on the basis of changes in the hierarchical dominance of brain structures, either the influence of diencephalic structures is never depressed in REM sleep or the functional autonomy of the rhombencephalon is still relevant in the immature encephalon of the newborn. The thermoregulatory model also allows understanding of inter-individual differences in thermoregulation and levels of thermoneutrality. An attempt has also been made to learn the role of heat stroke in the production of sudden infant death syndrome when body heat loss is hampered.

Adaptation, Physiological↗
PubMed2000

Effects of color temperature of fluorescent lamps on body temperature regulation in a moderately cold environment.

A study on the effects of different color temperatures of fluorescent lamps on skin and rectal temperatures in a moderately cold environment involving (i) changes in skin temperature of 7 male subjects exposed to an ambient temperature ranging from 28 degrees C to 18 degrees C (experiment I) and (ii) changes in skin and rectal temperatures and metabolic heat production of 11 male subjects exposed to ambient temperature of 15 degrees C for 90 min (Experiment II) was conducted. In Experiment I, the reduction of mean skin temperature from the control value was significantly greater under 3000 K than under 5000 K or 7500 K lighting. In Experiment II, the reductions in mean skin temperature and rectal temperature were respectively greater and smaller under 3000 K than those under 5000 K or 7500 K lighting. However, metabolic heat production was not affected by color temperature conditions. The relationships between morphological and physiological parameters revealed that no significant relation of rectal temperature to body surface area per unit body weight was found only under 3000 K. Furthermore, while the mean skin temperature was independent on the mean skinfold thickness under 3000 K, a significant negative correlation between the rectal and mean skin temperatures was observed. Therefore, body heat loss might be suppressed effectively by increasing the vasoconstrictor tone under a color temperature of 3000 K, and the body shell was dependent only on morphological factors under 5000 K and 7500 K lighting.

Adult↗
PubMed1984

Effects of hypothalamic noradrenaline depletion with 6-hydroxydopamine on the body temperature regulation of the rat.

Rats which had been pretreated with 3 intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine (6-OHDA) to cause a selective depletion of hypothalamic noradrenaline to 26.7% of control hypothalamic noradrenaline maintained rectal temperature within the normal limits displayed by the control group. However, noradrenaline-depleted rats displayed a decrease in both cutaneous temperature and metabolic heat production in the cold (8 degrees C). Intrahypothalamic injections of 6-OHDA in normal rats at room temperature (22 degrees C) caused an acute hyperthermia of up to 1.1 degree C which lasted for about 6 h. The acute hyperthermia in response to 6-OHDA was due to both cutaneous vasoconstriction and increased metabolism in the rat. Selective depletion of hypothalamic noradrenaline without affecting hypothalamic dopamine by prior treatment with 6-OHDA markedly reduced the hyperthermic responses to a subsequent dose of 6-OHDA. Therefore, the acute hyperthermic responses to 6-OHDA may be related to a release of noradrenaline in the hypothalamus. The data indicate that activation of noradrenergic pathways in the hypothalamus facilities heat production and inhibits heat loss mechanisms in the rat.

Animals↗