Control and regulatory mechanisms associated with thermogenesis in flying insects and birds.
(41/200)
Most insects and birds are able to fly. The chitin made exoskeleton of insects poses them several constraints, and this is one the reasons they are in general small sized animals. On the other hand, because birds possess an endoskeleton made of bones they may grow much larger when compared to insects. The two taxa are quite different with regards to their general "design" platform, in particular with respect to their respiratory and circulatory systems. However, because they fly, they may share in common several traits, namely those associated with the control and regulatory mechanisms governing thermogenesis. High core temperatures are essential for animal flight irrespective of the taxa they belong to. Birds and insects have thus evolved mechanisms which allowed them to control and regulate high rates of heat fluxes. This article discusses possible convergent thermogenic control and regulatory mechanisms associated with flight in insects and birds. (+info)
Relationships among the behavioral, noradrenergic, and pituitary-adrenal responses to interleukin-1 and the effects of indomethacin.
(42/200)
Peripheral administration of interleukin-1 (IL-1) is known to activate the hypothalamo-pituitary-adrenal axis (HPA axis) and brain noradrenergic systems. We studied the relationship between these responses using in vivo microdialysis to assess the release of hypothalamic norepinephrine (NE), while simultaneously sampling blood for ACTH and corticosterone, and monitoring body temperature and behavior in freely moving rats. Rats were implanted with microdialysis probes in the medial hypothalamus, with intravenous catheters, and with telethermometers in the abdomen. Each rat was injected with saline and IL-1beta (1 microg ip) in random order, monitoring microdialysate NE, body temperature and plasma ACTH and corticosterone for 2-4 h after injection. Saline injections were followed by transient increases in microdialysate NE and in plasma ACTH and corticosterone. IL-1beta injections resulted in prolonged elevations of microdialysate NE, as well as plasma ACTH and corticosterone, and body temperature. IL-1beta also induced shivering and a prolonged depression of locomotor activity. Pretreatment with indomethacin (10 mg/kg sc) prevented the IL-1beta-induced increases in body temperature and the apparent increase in hypothalamic NE release, but only attenuated the IL-1beta-induced shivering and the increase in plasma ACTH. The results indicate a close temporal relationship between the release of NE and HPA axis activation. Such a relationship is also supported by the similar effects of indomethacin pretreatment on NE and ACTH. The shivering is likely involved in the increase in body temperature, but indomethacin only attenuated the shivering while it blocked the fever. However, the effects of indomethacin clearly indicate that neither the increase in body temperature nor the increase in hypothalamic NE release was essential for HPA axis activation. These results suggest that hypothalamic NE is involved in the IL-1-induced HPA axis activation, but that this is not the only mechanism by which the HPA axis is activated by intraperitoneally injected IL-1. (+info)
Contribution of thermal and nonthermal factors to the regulation of body temperature in humans.
(43/200)
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. (+info)
Reflex activation of rat fusimotor neurons by body surface cooling, and its dependence on the medullary raphe.
(44/200)
The nature of muscle efferent fibre activation during whole body cooling was investigated in urethane-anaesthetized rats. Multiunit efferent activity to the gastrocnemius muscle was detected when the trunk skin was cooled by a water-perfused jacket to below 36.0 +/- 0.7 degrees C. That efferent activity was not blocked by hexamethonium (50 mg kg(-1), i.v.) and was not associated with movement or electromyographic activity. Cold-induced efferent activity enhanced the discharge of afferent filaments from the isotonically stretched gastrocnemius muscle, demonstrating that it was fusimotor. Fusimotor neurons were activated by falls in trunk skin temperature, but that activity ceased when the skin was rewarmed, regardless of how low core temperature had fallen. While low core temperature alone was ineffective, a high core temperature could inhibit the fusimotor response to skin cooling. Fusimotor activation by skin cooling was often accompanied by desynchronization of the frontal electroencephalogram (EEG), but was not a simple consequence of cortical arousal, in that warming the scrotum desynchronized the EEG without activating fusimotor fibres. Inhibition of neurons in the rostral medullary raphe by microinjections of glycine (0.5 m, 120-180 nl) reduced the fusimotor response to skin cooling by 95 +/- 3%, but did not prevent the EEG response. These results are interpreted as showing a novel thermoregulatory reflex that is triggered by cold exposure. It may underlie the increased muscle tone that precedes overt shivering, and could also serve to amplify shivering. Like several other cold-defence responses, this reflex depends upon neurons in the rostral medullary raphe. (+info)
UCP1 is essential for adaptive adrenergic nonshivering thermogenesis.
(45/200)
Participation of brown adipose tissue [through the action of the uncoupling protein-1 (UCP1)] in adaptive adrenergic nonshivering thermogenesis is recognized, but the existence of a response to adrenergic stimulation in UCP1-ablated mice implies that a mechanism for an alternative adaptive adrenergic thermogenesis may exist. Here, we have used UCP1-ablated mice to examine the existence of an alternative adaptive adrenergic nonshivering thermogenesis, examined as the oxygen consumption response to systemically injected norepinephrine into anesthetized or conscious mice acclimated to different temperatures. We confirm that UCP1-dependent adrenergic nonshivering thermogenesis is adaptive, but we demonstrate that the adrenergic UCP1-independent thermogenesis is not recruitable by cold acclimation. Thus, at least in the mouse, no other proteins or enzymatic pathways exist that can participate in or with time take over the UCP1 mediation of adaptive adrenergic nonshivering thermogenesis, even in the total absence of UCP1. UCP1 is thus the only protein capable of mediating cold acclimation-recruited adaptive adrenergic nonshivering thermogenesis. (+info)
Thermal effects of whole head submersion in cold water on nonshivering humans.
(46/200)
This study isolated the effect of whole head submersion in cold water, on surface heat loss and body core cooling, when the confounding effect of shivering heat production was pharmacologically eliminated. Eight healthy male subjects were studied in 17 degrees C water under four conditions: the body was either insulated or uninsulated, with the head either above the water or completely submersed in each body-insulation subcondition. Shivering was abolished with buspirone (30 mg) and meperidine (2.5 mg/kg), and subjects breathed compressed air throughout all trials. Over the first 30 min of immersion, exposure of the head increased core cooling both in the body-insulated conditions (head out: 0.47 +/- 0.2 degrees C, head in: 0.77 +/- 0.2 degrees C; P < 0.05) and the body-exposed conditions (head out: 0.84 +/- 0.2 degrees C and head in: 1.17 +/- 0.5 degrees C; P < 0.02). Submersion of the head (7% of the body surface area) in the body-exposed conditions increased total heat loss by only 10%. In both body-exposed and body-insulated conditions, head submersion increased core cooling rate much more (average of 42%) than it increased total heat loss. This may be explained by a redistribution of blood flow in response to stimulation of thermosensitive and/or trigeminal receptors in the scalp, neck and face, where a given amount of heat loss would have a greater cooling effect on a smaller perfused body mass. In 17 degrees C water, the head does not contribute relatively more than the rest of the body to surface heat loss; however, a cold-induced reduction of perfused body mass may allow this small increase in heat loss to cause a relatively larger cooling of the body core. (+info)
Shivering in the cold: from mechanisms of fuel selection to survival.
(47/200)
In cold-exposed adult humans, significant or lethal decreases in body temperature are delayed by reducing heat loss via peripheral vasoconstriction and by increasing rates of heat production via shivering thermogenesis. This brief review focuses on the mechanisms of fuel selection responsible for sustaining long-term shivering thermogenesis. It provides evidence to explain large discrepancies in fuel selection measurements among shivering studies, and it proposes links between choices in fuel selection mechanism and human survival in the cold. Over the last decades, a number of studies have quantified the contributions of carbohydrate (CHO) and lipid to total heat generation. However, the exact contributions of these fuels still remain unclear because of large differences in fuel selection measurements even at the same metabolic rate. Recent advances on the mechanisms of fuel selection during shivering provide some plausible explanations for these discrepancies between shivering studies. This new evidence indicates that muscles can sustain shivering over several hours using a variety of fuel mixtures achieved by modifying diet (changing the size of CHO reserves) or by changing muscle fiber recruitment (increasing or decreasing the recruitment of type II fibers). From a practical perspective, how does the choice of fuel selection mechanism affect human survival in the cold? Based on a glycogen-depletion model, estimates of shivering endurance show that, whereas the oxidation of widely different fuel mixtures does not improve survival time, the selective recruitment of fuel-specific muscle fibers provides a substantial advantage for cold survival. By combining fundamental research on fuel metabolism and applied strategies to improve shivering endurance, future research in this area promises to yield important new information on what limits human survival in the cold. (+info)
Ondansetron does not reduce the shivering threshold in healthy volunteers.
(48/200)
BACKGROUND: Ondansetron, a serotonin-3 receptor antagonist, reduces postoperative shivering. Drugs that reduce shivering usually impair central thermoregulatory control, and may thus be useful for preventing shivering during induction of therapeutic hypothermia. We determined, therefore, whether ondansetron reduces the major autonomic thermoregulatory response thresholds (triggering core temperatures) in humans. METHODS: Control (placebo) and ondansetron infusions at the target plasma concentration of 250 ng ml(-1) were studied in healthy volunteers on two different days. Each day, skin and core temperatures were increased to provoke sweating; then reduced to elicit peripheral vasoconstriction and shivering. We determined the core-temperature sweating, vasoconstriction and shivering thresholds after compensating for changes in mean-skin temperature. Data were analysed using t-tests and presented as means (sds); P<0.05 was taken as significant. RESULTS: Ondensetron plasma concentrations were 278 (57), 234 (55) and 243 (58) ng ml(-1) at the sweating, vasoconstriction and shivering thresholds, respectively; these corresponded to approximately 50 mg of ondansetron which is approximately 10 times the dose used for postoperative nausea and vomiting. Ondansetron did not change the sweating (control 37.4 (0.4) degrees C, ondansetron 37.6 (0.3) degrees C, P=0.16), vasoconstriction (37.0 (0.5) degrees C vs 37.1 (0.3) degrees C; P=0.70), or shivering threshold (36.3 (0.5) degrees C vs 36.3 (0.6) degrees C; P=0.76). No sedation was observed on either study day. CONCLUSIONS: /b>. Ondansetron appears to have little potential for facilitating induction of therapeutic hypothermia. (+info)