Strategy for evaluation and prevention of risk due to work in thermal environments.
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A strategy in four successive stages is described and justified for the prevention and control of thermal problems in the workplace. This should allow these problems to be approached and solved progressively in small as well as large companies by relying successively, when necessary, on the complementary competencies of the workers themselves, their technical assistance, the occupational health specialists and the experts. The criteria to fulfil at each stage are described and discussed. Appendix 1 describes in detail the methods to be used at stages 2, "Observation" by the workers and their assistance; at stage 3, "Analysis" with the help of specialists; and outlines the stage 4, "Expertise". (+info)
Dobutamine as selective beta(1)-adrenoceptor agonist in in vivo studies on human thermogenesis and lipid utilization.
(58/2331)
The use of dobutamine as selective beta(1)-adrenoceptor agonist in in vivo studies on human thermogenesis and lipid utilization was investigated in 20 men. At 2.5, 5, and 10 microg x kg(-1) x min(-1), dobutamine induced significant increases in energy expenditure, lipid oxidation, and lipolysis. The beta(1)-adrenoceptor antagonist atenolol (bolus: 42.5 microg/kg, infusion: 1.02 microg x kg(-1) x min(-1)) blocked all dobutamine-induced effects on thermogenesis and lipid utilization. All parameters remained at levels comparable to those during saline infusion. The dose of atenolol used did not inhibit beta(2)-adrenoceptor-specific changes in energy expenditure, lipid oxidation, and lipolysis during salbutamol infusion (85 ng x kg(-1) x min(-1)). This indicates that atenolol was specific for beta(1)-adrenoceptors and did not camouflage concomitant beta(2)-adrenoceptor stimulation during dobutamine infusion. Therefore, we conclude that dobutamine can be used as a selective beta(1)-adrenoceptor agonist at dosages +info)
Thermoregulatory thresholds for vasoconstriction in patients anesthetized with various 1-minimum alveolar concentration combinations of xenon, nitrous oxide, and isoflurane.
(59/2331)
BACKGROUND: Nitrous oxide limits intraoperative hypothermia because the vasoconstriction threshold with nitrous oxide is higher than with equi-minimum alveolar concentrations of sevoflurane or isoflurane, presumably because of its stimulating actions on the sympathetic nervous system. Xenon, in contrast, does not cause sympathetic activation. Therefore, the authors tested the hypothesis that the vasoconstriction threshold during xenon-isoflurane anesthesia is less than during nitrous oxide-isoflurane anesthesia or isoflurane alone. METHODS: Fifteen patients each were randomly assigned to one of three 1-minimum alveolar concentration anesthetic regimens: (1) xenon, 43% (0.6 minimum alveolar concentration) and isoflurane, 0.5% (0.4 minimum alveolar concentration); (2) nitrous oxide, 63% (0.6 minimum alveolar concentration) and isoflurane 0.5%; or (3) isoflurane, 1.2%. Ambient temperature was maintained near 23 degrees C and the patients were not actively warmed. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients. A gradient exceeding 0 degrees C indicated significant vasoconstriction. The core-temperature threshold that would have been observed if skin had been maintained at 33 degrees C was calculated from mean skin and distal esophageal temperatures at the time of vasoconstriction. RESULTS: The patients' demographic variables, preinduction core temperatures, ambient operating room temperatures, and fluid balance were comparable among the three groups. Heart rates were significantly less during xenon anesthesia than with nitrous oxide. The calculated vasoconstriction threshold was lowest with xenon (34.6+/-0.8 degrees C, mean +/- SD), intermediate with isoflurane alone (35.1+/-0.6 degrees C), and highest with nitrous oxide (35.7+/-0.6 degrees C). Each of the thresholds differed significantly. CONCLUSIONS: Xenon inhibits thermoregulatory control more than isoflurane, whereas nitrous oxide is the least effective in this respect. (+info)
Thermal energy balance and body temperature: comparison between isolated ultrafiltration and haemodialysis at different dialysate temperatures.
(60/2331)
BACKGROUND: Haemodynamic stability is better maintained during isolated ultrafiltration (i-UF) than during combined ultrafiltration/haemodialysis (UF + HD). This difference might be explained by differences in thermal energy balances. In this study we compared the thermal energy balance of i-UF with UF + HD at different dialysate temperatures (Td) and determined the Td at which the thermal energy balance during UF + HD is similar to the thermal energy balance during i-UF. METHODS: In the first part of the study, 10 chronic haemodialysis patients were compared during three different treatment sessions, i-UF, UF + HD at Td of 35.5 degrees C and UF + HD at Td of 37.5 degrees C. The second part of the study consisted of one session of 1 h of UF + HD (UF + HD ET-set) with a pre-set energy transfer (ET) at the same level of ET found for that particular patient during i-UF in the first part of the study. RESULTS: First part of the study: body temperature (BT) decreased significantly during i-UF (-0.25 +/- 0.25 degrees C, P<0.05) and UF + HD 35.5 degrees C (-0.24 +/- 0.18 degrees C, P<0.05) and increased significantly during UF + HD 37.5 degrees C (+0.18 +/- 0.19 degrees C, P<0.05). The differences between the change in BT during UF + HD 37.5 degrees C compared with the other treatments were significant (P<0.05). ET gave a significantly more negative value during i-UF (-30.8 +/- 3.1 W, P<0.05) than during UF + HD 35.5 degrees C (-23.6 +/- 4.1 W, P<0.05). A slightly positive ET was found during UF + HD 37.5 degrees C (+0.4 +/- 4.7 W, P=not significant). Second part of the study: there was a slight, but not significant, decrease in BT during UF + HD ET-set (-0.17 +/- 0.26 degrees C). The changes in BT did not differ significantly between i-UF and UF + HD ET-set. After 1 h of UF + HD ET-set, the mean Td was 34.75 degrees C (34.0-36.0 degrees C). The correlation between pre-dialysis BT and Td during UF + HD ET-set was significant (r=0.764, P<0.05). CONCLUSION: ET gives a more negative value during i-UF than during UF + HD 35.5 degrees C and than during UF + HD 37.5 degrees C. To obtain the same thermal ET during UF + HD as that achieved during i-UF, a mean Td of 34.75 degrees C is needed, depending on the pre-dialytic BT of the patient. The results of this study may be of relevance in relation to future clinical investigations which can elucidate whether differences in vascular response between i-UF and UF + HD are only related to differences in thermal balance. (+info)
Peripheral and central actions of capsaicin and VR1 receptor.
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Vanilloid receptor subtype 1 (VR1), a capsaicin receptor, is expressed in primary sensory neurons and vagal nerves. Heat and protons as well as capsaicin activate VR1 to induce the influx of cations, particularly Ca2+ and Na+ ions. Characteristic effects of capsaicin are the induction of a burning sensation after acute administration and the desensitization of sensory neurons after large doses and prolonged administration. The latter feature made capsaicin cream applicable for the treatment of chronic pain and pruritus. Capsaicin alters several visceral functions, which may be mediated by action on vagal nerves and central neurons. Capsaicin affects thermoregulation after intra-hypothalamic injection and releases glutamate from the hypothalamus and cerebral cortex slices, while VR1-like immunoreactivity is not apparent in these regions. These findings taken together suggest the existence of other subtypes of vanilloid receptors in the brain. (+info)
The bioenergetics of brown fat mitochondria from UCP1-ablated mice. Ucp1 is not involved in fatty acid-induced de-energization ("uncoupling").
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The bioenergetics of brown fat mitochondria isolated from UCP1-ablated mice were investigated. The mitochondria had lost the high GDP-binding capacity normally found in brown fat mitochondria, and they were innately in an energized state, in contrast to wild-type mitochondria. GDP, which led to energization of wild-type mitochondria, was without effect on the brown fat mitochondria from UCP1-ablated mice. The absence of thermogenic function did not result in reintroduction of high ATP synthase activity. Remarkably and unexpectedly, the mitochondria from UCP1-ablated mice were as sensitive to the de-energizing ("uncoupling") effect of free fatty acids as were UCP1-containing mitochondria. Therefore, the de-energizing effect of free fatty acids does not appear to be mediated via UCP1, and free fatty acids would not seem to be the intracellular physiological activator involved in mediation of the thermogenic signal from the adrenergic receptor to UCP1. In the UCP1-ablated mice, Ucp2 mRNA levels in brown adipose tissue were 14-fold higher and Ucp3 mRNA levels were marginally lower than in wild-type. The Ucp2 and Ucp3 mRNA levels were therefore among the highest found in any tissue. These high mRNA levels did not confer on the isolated mitochondria any properties associated with de-energization. Thus, the mere observation of a high level of Ucp2 or Ucp3 mRNA in a tissue cannot be taken as an indication that mitochondria isolated from that tissue will display innate de-energization or thermogenesis. (+info)
Influence of thyrotrophin-releasing hormone on thermoregulatory adaptation after birth in near-term lambs delivered by caesarean section.
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We investigated the hypothesis that exogenous stimulation with thyrotrophin-releasing hormone (TRH) immediately prior to umbilical cord clamping can improve thermoregulatory adaptation after birth in near-term lambs delivered by Caesarean section. Lambs received an umbilical vein injection of saline +/- TRH (8 microg) prior to cord clamping. The rate of change in colonic temperature and oxygen consumption after birth were not influenced by TRH, but TRH-treated lambs exhibited a greater incidence of shivering compared with controls over the first hour of neonatal life. Two and a half hours after birth, TRH-treated lambs possessed brown adipose tissue (BAT) with a higher thermogenic activity (i.e. GDP binding to mitochondrial protein), but their BAT had a reduced DNA content and they had less hepatic glycogen than control lambs. TRH administration had no effect on iodothyronine 5' deiodinase activity in BAT and liver, or on plasma concentrations of total triiodothyronine, thyroxine, cortisol or free fatty acids. Three TRH-treated but no control lambs, failed to establish continuous breathing, so tissues from these treated lambs together with time-matched controls were sampled 25 min after birth. These 'non-surviving' TRH-treated lambs had very high plasma catecholamine concentrations, but their lung weights were similar to controls. 'Surviving' TRH-treated lambs possessed lungs with less DNA than non-surviving TRH-treated lambs. It is concluded that umbilical vein injection of TRH prior to umbilical cord clamping increases the recruitment of both shivering and non-shivering thermogenesis after birth. (+info)
The diving physiology of bottlenose dolphins (Tursiops truncatus). III. Thermoregulation at depth.
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During diving, marine mammals initiate a series of cardiovascular changes that include bradycardia and decreased peripheral circulation. Because heat transfer from thermal windows located in peripheral sites of these mammals depends on blood flow, such adjustments may limit their thermoregulatory capabilities during submergence. Here, we demonstrate how the thermoregulatory responses of bottlenose dolphins (Tursiops truncatus) are coordinated with the diving response. Heart rate, skin temperature and heat transfer from the dorsal fin and flank were measured while dolphins rested on the water surface, stationed 5-50 m under water and floated at the surface immediately following a dive. The results showed that heat flow ranged from 42.9+/-7.3 to 126.2+/-23.1 W m(-)(2) and varied with anatomical site and diving activity. Upon submergence, heat flow declined by 35 % from the dorsal fin and by 24 % from the flank. An immediate increase in heat flow to levels exceeding pre-dive values occurred at both sites upon resurfacing. Changes in heart rate during diving paralleled the thermoregulatory responses. Mean pre-dive heart rate (102.0+/-2.6 beats min(-)(1), N=26) decreased by 63.4 % during dives to 50 m and immediately returned to near resting levels upon resurfacing. These studies indicate that heat dissipation by dolphins is attenuated during diving. Rather than challenge the diving response, heat transfer is delayed until post-dive periods when the need for oxygen conservation is reduced. (+info)