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PubMedDate not supplied

Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a magnesium-dependent disease of the transition from chemical to physical thermoregulation?

The sudden infant death syndrome (SIDS) remains a leading cause of death during the first year. The common epidemiological and pathological data which characterize SIDS include the curve for age at death (with 3 months as modal age), the stigmata of early maternal intrauterine injury, the seasonal predominance in winter, and the absence of an adequate cause of death at autopsy. Some data characterize risk factor subgroups: for example low socioeconomic level, environmental pollution, stress, and mistakes in baby care. Symptoms before death may be lacking, they may be common and non-specific, or rarely they may be acute, corresponding to "apparent life-threatening events" (ALTE). SIDS may be a magnesium-dependent disease of the transition from chemical to physical thermoregulation. This theory originates from a synthesis of our present knowledge of SIDS, maternal magnesium status, and thermoregulation in the baby. It is consistent with all the epidemiological and pathological prerequisites characterizing SIDS. It eliminates the hiatus between relatively minor thermal stress and induced lethal thermal stroke. Logical scepticism about the role of an implausible lethal superacute magnesium deficiency is no longer justified with regard to well established chronic marginal magnesium deficiency. Further experimental and clinical research will be interesting, i.e. ex vivo studies on brown adipose tissue (BAT) and magnesium deficiency under various conditions of thermal exposure. But even now the theory leads to three therapeutic consequences: (1) the need to define the importance of magnesium deficiency in diagnosis and treatment of ALTE; (2) an assessment of the use of new techniques of rewarming (i.e. extracorporeal circulation) in hypothermia cases to distinguish cot death from "apparent death"; (3) investigation of the prevention of SIDS with magnesium through a blinded and randomized multicentre prospective cooperative study of magnesium supplementation in pregnant and lactating women, followed not only in the mother, fetus, and neonate at birth, but also through the first year of life.

Body Temperature Regulation↗
PubMedDate not supplied

Do black-box models of thermoregulation still have any research value? Contribution of system-theoretical models to the analysis of thermoregulation.

The aims and the usefulness of modelling the thermoregulatory system are outlined by demonstrating applications and results of simulation on different levels of complexity. It is shown that both very simple one-loop models and complex models based on spatially distributed parameters have contributed to a better understanding of the system, but that current issues primarily require the latter type. However, mathematical modelling must be performed in conjunction with experimental studies and must be adapted to the amount of basic physiological data. Future fields of modelling are the adaptive mechanisms and the interactions of systems.

Animals↗
PubMed1976

Cost and benefits of lizard thermoregulation.

Lizards thermoregulate by behavioral and physiological adjustments. The resultant control over metabolic processes is generally assumed to be beneficial. However, these thermoregulatory adjustments have associated costs which, if extensive, make thermoregulation impractical. We extend this idea into an abstract mathematical, cost-benefit model of thermoregulation in lizards. Investigation of the model leads to a set of predictions which includes: (1) the physiologically optimal temperature is not always the ecologically optimal temperature; (2) thermoregulation is beneficial only when associated costs are low; (3) thermal specialists will normally thermoregulate more carefully than thermal generalists unless costs are high; and (4) lizards will thermoregulate more carefully if productivity of the habitat is increased or if exploitation competition is reduced. Data on lizards, where available, generally agree with these predicitions.

Animals↗
PubMed1981

Effects of CNS temperature on generation and transmission of temperature signals in homeotherms. A common concept for mammalian and avian thermoregulation.

Neurophysiological studies on avian hypothalamic thermosensitivity have presented evidence for a higher Q10 of cold than of warm signal transmission in the CNS of birds. An identical temperature dependence of central cold and warm signal transmission in mammals is suggested by considerations on the phylogeny of temperature regulation. By taking into account the experimental evidence for the existence of thermosensory afferents in the CNS of mammals and birds, being differently developed in the various sections of the neural axis and exerting quantitatively different influences on the various thermoregulatory effectors, a common concept of homeothermic thermoregulation is proposed resting on the same basic assumptions for mammals and birds. The great diversity of negative as well as positive feedback effects of CNS temperature displacements on homeothermic thermoregulation, which is particularly expressed in avian autonomic and behavioral thermoregulation and, further, certain pathophysiological conditions of disturbed thermoregulation could be accounted for by assuming quantitatively different contributions of the central thermosensory inputs of thermoregulatory effector control, but maintaining the Q10 values of hypothalamic warn and cold signal transmission constant. The proposed model, while basically additive in its mathematical design, meets a number of properties described by multiplicative models of thermoregulation. In additionally generalizes these models of predicting that changes of hypothalamic temperature modify the sensitivities with which any thermoregulatory effector responds to any thermosensory input.

Animals↗
PubMed1978

[Thermoregulation in prolonged antiorthostatic hypokinesia].

By means of daily thermometry in the axillary area, a study of skin thermotopography in 10 symmetrical points of the body and a study of the Shcherbak thermoregulational reflex the author assessed the function of thermoregulation during a 49 day antiorthostatic (-4 degrees) hypokinesia. The study included 32 male volunteers from 25-39 years of age. It was demonstrated that signs of temperature discomfort appeared shortly after an antiorthostatic position was taken and was due to the initial period of blood redistribution. At the end of the first and beginning of the second month hypokinesia developed and gradual disturbances of thermoregulational dynamics progressed. They were characterized by changes of oral-caudal and proximal-distal correlations of the skin temperature (due to the drop of temperature in the distal parts) and hyporeactivity, areactivity or inversion of thermoregulational processes during the study of the Shcherbak thermoregulational reflex.

Adult↗
PubMed1981

Thermoregulation in adult rats which have been treated with capsaicin as neonates.

1. Subcutaneous or intrahypothalamic injections of capsaicin produce hypothermia in the neonate rat. Repeated injections with increasing doses of capsaicin result in unresponsiveness to this drug (capsaicin-desensitization). 2. Young rats aged 8-10 days which had received serial injections of capsaicin solution (a cumulative dose of 4.63 mg per animal) or of the solvent alone were subsequently tested as adults for their ability to thermoregulate. 3. On exposure to an ambient temperature of 41 degrees C, adult rats which had been capsaicin-desensitized as neonates were unable to thermoregulate against overheating by means of autonomic responses whereas control littermates could maintain normal rectal temperature. However, autonomic thermoregulation against cold was unimpaired in the desensitized rats. 4. Skin-cooling operant behavior in heat stress was impaired in adult rats which had been capsaicin-desensitized as neonates whereas their skin-heated behavior was not different from that of control littermates. 5. These results suggest that the central and peripheral warm-receptors responsible for thermoregulation in the neonate rat are functionally mature at least inasmuch as they form a part of thermoregulatory system involved in lowering body temperature and can be desensitized by capsaicin. Moreover, such receptors, once desensitized 8-10 days after birth, apparently do not regain their function and are not regenerated or replaced during subsequent maturation of the animal.

Animals↗
PubMed1989

Regulatory genes in the thermoregulation of Escherichia coli pili gene transcription.

Expression of several different pilus adhesins by Escherichia coli is subject to thermoregulation. The surface-located fimbrial structures are present during growth at 37 degrees C but are not produced by cells grown at lower temperatures, such as 25 degrees C. As a step toward understanding the molecular mechanism, we have studied the role of different cistrons of a cloned pilus adhesin gene cluster (pap) from a uropathogenic E. coli isolate. By promoter cloning, mRNA analysis, and expression of subcloned genes in trans, we have identified the papI gene as the mediator of thermoregulation at the level of pilus adhesin gene transcription. Expression of the major pilus subunit gene (papA) and several other pilus protein cistrons appeared to be dependent on stimulation by the papB and papI gene products. Constructs carrying different pap DNA regions indicated that none of the known Pap proteins acts directly as thermosensor. The chromosomal rpoH gene and RpoH sigma factor did not appear to be required for pap transcription, and the thermoregulation of pilus gene transcription must be different from that of the heat shock regulon. By overexpressing the papI gene product from an expression plasmid in trans, we could circumvent the temperature regulation and turn on production of pilus adhesin at low temperature. Our results suggest that the level of mRNA encoding the PapI activator is limiting at low growth temperatures and that thermoregulation is due to a determinant in the papI-papB intercistronic region.

Adhesins, Escherichia coli↗
PubMed1992

Thermoregulation of the pap operon: evidence for the involvement of RimJ, the N-terminal acetylase of ribosomal protein S5.

Our previous work showed that pap pilin gene transcription is subject to a thermoregulatory control mechanism under which pap pilin is not transcribed at a low temperature (23 degrees C) (L. B. Blyn, B. A. Braaten, C. A. White-Ziegler, D. H. Rolfson, and D. A. Low, EMBO J. 8:613-620, 1989). In order to isolate genes involved in this temperature regulation of gene expression, chromosomal mini-Tn10 (mTn10) mutations that allowed transcription of the pap pilin gene at 23 degrees C were identified, and the locus was designated tcp, for "thermoregulatory control of pap" (C. A. White-Ziegler, L. B. Blyn, B. A. Braaten, and D. A. Low, J. Bacteriol. 172:1775-1782, 1990). In the present study, quantitative analysis showed that the tcp mutations restore pap pilin transcription at 23 degrees C to levels similar to those measured at 37 degrees C. By in vivo recombination, the tcp mutations were mapped to phage E4H10S of the Kohara library of the Escherichia coli chromosome (Y. Kohara, K. Akiyama, and K. Isono, Cell 50:495-508, 1987). The tcp locus was cloned by complementation, in which a 1.3-kb DNA fragment, derived from the Kohara phage, was shown to restore thermoregulation to the mTn10 mutants. DNA sequencing revealed two open reading frames (ORFs) encoding proteins with calculated molecular masses of 22.7 and 20.3 kDa. The sequence of the 22.7-kDa ORF was identical to that of rimJ, the N-terminal acetylase of the ribosomal protein S5. The gene encoding the 20.3-kDa ORF, designated g20.3 here, did not display significant homology to any known DNA or protein sequence. On the basis of Northern (RNA) blot data, rimJ and g20.3 are located within the same operon. Two of the mTn10 transposons in the thermoregulatory mutants were inserted within the coding region of rimJ, indicating that the RimJ protein plays an important role in the temperature regulation of pap pilin gene transcription. However, rimJ itself is not thermoregulated, since rimJ transcripts were detected at both 23 and 37 degrees C. Disruption of the g20.3 gene by insertion and deletion mutagenesis did not affect thermoregulation of the pap operon, suggesting that, although g20.3 lies within the same operon as rimJ, it does not play a role in thermoregulation.

Acetylation↗
PubMed1986

Effects of subanesthetic doses of inert gases on behavioral thermoregulation in mice.

Mice exposed to subanesthetic partial pressures of N2O (0.25 to 0.75 atm) or N2 (5.7 or 11.33 atm) and allowed to choose between a warm and a cool environment showed a marked preference for the cooler environment. This behavior was associated with the onset of hypothermia, with deep body temperature falling by up to about 3 degrees C, usually to a new, steady level. Both the length of time spent in the cooler environment and the degree of the hypothermia produced increased with the partial pressure of N2O or N2 used. The effects of N2O on behavioral thermoregulation and body temperature were reversible. There was a correlation between anesthetic potency and the ability of both gases to alter thermoregulation, suggesting that the effect of these agents on thermoregulation was caused by the same molecular interactions as those which underlie anesthesia. Since both gases elicited changes in behavioral thermoregulation promoting rather than opposing the onset of hypothermia, it is concluded that they may have acted to lower the level at which deep body temperature was being regulated.

Anesthetics↗
PubMed1992

Behavioral thermoregulation by hypoxic rats.

To address whether a shift in hypothalamic thermal setpoint might be a significant factor in induction of hypoxic hypothermia, behavioral thermoregulation was examined in 7 female Sprague-Dawley rats implanted with radiotelethermometers for deep body temperature (Tb) measurement in a thermocline during normoxia (PO2 = 125 torr) and hypoxia (PO2 = 60 torr). Normoxic rats (TNox) selected a mean ambient temperature of 19.7 +/- 1.4 (SE) degrees C and maintained Tb at 37.0 +/- 0.2 degrees C. Hypoxic rats selected a significantly higher ambient temperature (THox = 28.6 +/- 2.2 degrees C) but maintained Tb significantly lower at 35.5 +/- 0.3 degrees C. Without a thermal gradient (ambient temperature = 25 degrees C), Tb during hypoxia was 35.4 +/- 0.4 degrees C. The maintenance of a lower body temperature during hypoxia through behavioral thermoregulation despite having warmer temperatures available supports the hypothesis that the thermoregulatory setpoint of hypoxic rats is shifted to promote thermoregulation at a lower Tb, effectively reducing oxygen demand when oxygen supply is limited.

Animals↗
PubMed1991

A theoretical model for testis thermoregulation.

Studies going back as far as the early 1920's show that there is a clear relationship between testis temperature and semen quality. The most intriguing question is whether there is a mechanism of thermoregulation which, in the human, maintains testis temperature within certain limits that permit euspermia. Thermoregulation is defined as maintaining some specified (optimum?) temperature plus or minus an error over internal and ambient loss factors. A computer Model has been evolved which contains no regulation or feedback. It appears to predict human testis temperature data gathered in earlier studies. The Model accounts for countercurrent heat exchange in the pampiniform plexus and predicts, with an open loop analysis, that there is no feedback or regulation. As far as thermoregulation is concerned, there appear to be no first-order effects taking place in the human testis. This suggests that ambient temperature changes cause corresponding changes in testis temperature. Also any internal changes in thermal properties such as core temperature variations or variability of the countercurrent heat exchanger will also cause temperature change. Testis temperature as predicted by this Model is the result of the heat energy entering the testis from arterial inflow minus the venous outflow and heat loss from the scrotum. The Model predicts that the heat exchanger will function to provide precooling of arterial blood as external temperatures drop but will fail to precool effectively as temperature rises. This is predicated on the fact that the countercurrent heat exchanger becomes less effective as the temperature gradient across the exchanger becomes smaller and less heat energy is able to be transferred from arterial flow to venous flow. The Model also predicts that any diminution of the heat exchanger mechanism either from reduced venous flow or restricted scrotal heat loss will result in higher testis temperature. Lastly, the Model correctly predicted that febrile patients would experience elevated testis temperature during periods of elevated core temperature. Since more heat energy is available in the arterial blood, more heat energy is delivered to the testis under these conditions. In the human it appears that any internal or external factor causing a temperature change will not trigger or activate a feedback mechanism to control the resulting testis temperature. A major factor in subfertile semen may be the inability to check excessive temperature of the testis which impairs the ability to produce and mature fertile spermatozoa.

Body Temperature↗
PubMed1978

Interactions of behavioral and autonomic thermoregulation in heat stressed pigeons.

The interactions of behavioral and autonomic thermoregulation in pigeons during ambient heat load were studied by simultaneous measurements of instrumental response rate for cold air reinforcement and respiratory rate. When providing sufficient reinforcement-magnitudes, deep body temperatures were stabilized, due to a linear increase of response rate with ambient loads from 40-60 degrees C, without involving an increase in respiratory heat dissipation. This was effected by maintaining the temporal mean of air temperature and consequently of all skin temperatures at a level independent from load temperature (Fig. 3). When the efficiency of instrumental thermoregulation was limited by reducing the reinforcement-magnitude, not only the instrumental response rate increased, but in addition body temperatures and subsequently respiratory rate rose with the thermal load. Thus a positive correlation between body temperatures and response rate and a simultaneous increase of autonomic heat defence activities characterize incomplete behavioral thermoregulation. The instrumental response rate rapidly followed changes of external load temperature without preceding changes of core temperatures or skin temperatures at well feathered areas (Fig. 6). These findings suggest that the input signal controlling instrumental thermoregulatory behavior is related to the rate of change of temperatures at exposed areas of the body shell, whereas the autonomic heat defence response follows the steady displacements of body temperatures. This points to an important difference between the input signals controlling behavioral and autonomic heat defence in the pigeon.

Animals↗
PubMed1995

Ontogeny of thermoregulation in the Djungarian hamster (Phodopus campbelli).

At birth, altricial Djungarian hamster pups require exogenous heat to grow and gain little benefit from huddling with their littermates. By day 6 huddled pups begin effective thermogenesis although isolated pups do not show spontaneous increases in temperature until day 9. On day 12, isolated pups can resist cooling for short periods of time and huddles do not cool within a 15 min test. By day 15, isolated pups can thermoregulate, although at a lower core body temperature than is typical of adults, and both huddling contact with littermates and direct contact with the dam are reduced. At weaning, pups are effectively thermally independent. This ontogeny is correlated with behavioral, morphological and physiological changes during pup development including brown adipose tissue (BAT) thermogenesis, pelage development and body size. The onset of thermogenesis, and then thermoregulation, causes temporary reductions in pup growth rate on days 6 and 7 and again on days 12 and 13. Body weight, rather than pup age, appears critical for independent thermoregulation. These results are discussed relative to the extent of maternal hyperthermia and the physiological demands of the concurrent gestation characteristic of reproduction in Djungarian hamsters.

Adipose Tissue, Brown↗
PubMed1983

Evidence against involvement of beta-endorphin in thermoregulation in the cat.

In the cat naloxone has little, if any, effect on temperature under usual laboratory conditions and does not reduce febrile responses to leukocytic pyrogen. Hence, endogenous opioid peptides that are antagonized by naloxone are not essential for induction of fever or for maintenance of normal temperature in the absence of appreciable thermal stress. The purpose of this study was to assess the contribution of such endogenous opioids to thermoregulation in cats exposed to more severe thermal and non-thermal stresses. Changes in temperature of unanesthetized cats were determined after third cerebral ventricular injections of large doses (100, 250 micrograms) of naloxone or saline vehicle. Naloxone had no appreciable effect on the temperature of cats acutely exposed to hot (34 degrees C) or cold (4 degrees C) environments, either before or after tolerance to morphine had been induced by progressively greater daily or twice-daily intraventricular doses of 10-70 micrograms morphine sulfate. Naloxone also did not significantly affect the temperature of cats subjected to neck-restraint or forced to stand on a small platform if they were to avoid contact with ice water. These results provide no indication that an endogenous opioid peptide, such as beta-endorphin, that is antagonized by naloxone contributes appreciably to thermoregulation in cats. They do not rule out the possibility that endogenous opioids, such as Met-enkephalin, that are not readily antagonized by naloxone are important for normal thermoregulation.

Animals↗
PubMedDate not supplied

The effects of MIF-I, beta-endorphin and alpha-MSH on d-amphetamine induced paradoxical behavioral thermoregulation: possible involvement of the dopaminergic system.

The neuropharmacological basis for d-amphetamine induced paradoxical behavioral thermoregulation remains unclear. This study examined thermoregulatory behavior of rats in a runway device that housed a heat source at one end and in which locomotion along the length of the runway could be observed. Sprague Dawley rats were pretreated with IP injections of saline, beta-endorphin, MIF-1, or alpha-MSH, with a repeat injection after 30 min. In a second experiment, d-amphetamine was administered as the repeat drug for all Ss. The results showed clear differences for heat-source-on vs. heat-source off. All peptides induced hypermotility, although no differentiated effects for the peptides on d-amphetamine induced paradoxical behavioral thermoregulation were found. These findings are discussed in light of the theoretical possibilities that: (a) a ceiling effect exists; (b) there are separate control systems for maintaining body temperature and another for behavioral thermoregulatory responses, and (c) other neurotransmitters may be involved in such induced paradoxical behavioral thermoregulation.

Animals↗
PubMed1992

Thermoregulation and fever in normal persons and in those with spinal cord injuries.

Thermoregulation and fever are primarily mediated through the hypothalamus and its effector mechanisms. In persons with complete spinal cord injuries above T-6, thermoregulation is substantially impaired because of the interruption of neuronal pathways to and from the hypothalamus. These same pathways are important in the production of fever in response to infections, and injury to these pathways in patients with high-level spinal cord injuries should diminish their ability to mount a febrile response. In clinical practice, however, measurements of body temperature are used to make decisions in patients with spinal cord injuries in a manner similar to that in patients without spinal cord injuries. In this article, we review the literature on thermoregulation and fever in normal persons and in those with complete spinal cord injuries and propose possible mechanisms for fever in persons with high-level spinal cord injuries.

Body Temperature↗