Core Body Temperature In Humans Research Articles

Alpha-2-adrenergic agonists reduce resting energy expenditure in humans during external cooling

ABSTRACT Intravenous alpha-2-adrenergic receptor agonists reduce energy expenditure and lower the temperature when shivering begins in humans, allowing a decrease in core body temperature. Because there are few data about similar effects from oral drugs, we tested whether single oral doses of the sedative dexmedetomidine (1 µg/kg sublingual or 4 µg/kg swallowed) or the muscle relaxant tizanidine (8 mg or 16 mg), combined with surface cooling, reduce energy expenditure and core body temperature in humans. A total of 26 healthy participants completed 41 one-day laboratory studies measuring core body temperature using an ingested telemetry capsule and measuring energy expenditure using indirect calorimetry for up to 6 hours after drug ingestion. Dexmedetomidine induced a median 13% – 19% peak reduction and tizanidine induced a median 15% – 22% peak reduction in energy expenditure relative to baseline. Core body temperature decreased a median of 0.5°C – 0.6°C and 0.5°C – 0.7°C respectively. Decreases in temperature occurred after peak reductions in energy expenditure. Energy expenditure increased with a decrease in core temperature in control participants but did not occur after 4 µg/kg dexmedetomidine or 16 mg tizanidine. Plasma levels of dexmedetomidine but not tizanidine were related to mean temperature change. Decreases in heart rate, blood pressure, respiratory rate, cardiac stroke volume index, and cardiac index were associated with the change in metabolic rate after higher drug doses. We conclude that both oral dexmedetomidine and oral tizanidine reduce energy expenditure and allow decrease in core temperature in humans.

Fuzzy Logic Temperature Control on Blood Warmer Equipped with Patient Temperature and Blood Temperature

Body temperature in humans varies greatly depending on the location where the reading is taken. Normal core body temperature in humans is maintained by the hypothalamus and usually ranges from 36.5°C to 37.5°C. One of the causes of the failure of Too high or too low of a temperature during the blood transfusion procedure may cause blood to freeze or get damaged, both of which can be fatal to humans, therefore the purpose of this tool is to lower blood temperature admission to the patient can be achieved so that there is no temperature drop or temperature drop and so that the blood is not too hot because it can cause damage to red blood cells. This study uses the DS18B20 Sensor to control the heater with PID and Fuzzy controls, the MLX90614 Sensor to adjust the temperature according to the patient's body temperature and the Optocoupler Sensor as an indicator when fluids run out. Previous studies have not used the MLX90614 sensor to detect patient body temperature, have not used TFT Nextion and have not used Fuzzy controls. This Fuzzy control is used as a heater control which then the results are displayed on the Nextion TFT. The results of this study obtained the highest error value of 0.09 with an average error value of 0.04 and obtained the highest overshoot value of 0.8. From the results of the above study it can be concluded that by using the Fuzzy control the response time is slower with a larger overshoot. In the creation of this tool, the benefits that can be derived for the community are facilitating the monitoring of patient temperature and blood temperature during blood transfusions using the Blood Warmer device. The device is also equipped with sensors to detect patient and blood temperatures, and it comes with a Nextion TFT display. Therefore, this device is crucial in assisting the community in performing Blood Transfusions.

PID Temperature Control on Blood Warmer Equipped with Patient Temperature and Blood Temperature

Body temperature in humans varies greatly depending on the location where the reading is taken. Normal core body temperature in humans is maintained by the hypothalamus and usually ranges from 36.5°C to 37.5°C. One of the causes of failure in the blood transfusion process can cause death in humans, one of the factors is the blood temperature that is too high or too low during the blood transfusion process can cause the blood to become frozen or damaged, therefore the purpose of this tool is to lower the blood temperature admission to the patient can be achieved so that there is no reduction in temperature or decrease in temperature and so that the blood is not allowed to get too hot because it can cause damage to red blood cells. This study uses the DS18B20 Sensor to control the heater with PID and Fuzzy controls, the MLX90614 Sensor to set the temperature according to the patient's body temperature and the Optocoupler Sensor as an indicator when fluids run out. When using the PID control with Kp = 4, Ki = 1, and Kd = 4, a faster response time is obtained and there is an overshoot with the highest error value of 0.77 and an average error value of 0.02. The results of the study are displayed on the TFT Nextion. From the results of the research above, it can be concluded that using PID control the response time is faster, but there are drawbacks to high overshoot.

A cross-species translational pharmacokinetic-pharmacodynamic evaluation of core body temperature reduction by the TRPM8 blocker PF-05105679

PF-05105679 is a moderately potent TRPM8 blocker which has been evaluated for the treatment of cold pain sensitivity. The TRPM8 channel is responsible for the sensation of cold environmental temperatures and has been implicated in regulation of core body temperature. Consequently, blockade of TRPM8 has been suggested to result in lowering of core body temperature. As part of the progression to human studies, the effect of PF-05105679 on core body temperature has been investigated in animals. Safety pharmacology studies showed that PF-05105679 reduced core body temperature in a manner that was inversely related to body weight of the species tested (greater exposure to PF-05105679 was required to lower temperature by 1°C in higher species). Based on an allometric (body weight) relationship, it was hypothesized that PF-05105679 would not lower core body temperature in humans at exposures that could exhibit pharmacological effects on cold pain sensation. On administration to humans, PF-05105679 was indeed effective at reversing the cold pain sensation associated with the cold pressor test in the absence of effects on core body temperature.

The circadian rhythm of core body temperature (Part I): The use of modern telemetry systems to monitor core body temperature variability

Abstract The best known daily rhythms in humans include: the sleep-wake rhythm, the circadian core body temperature variability, daily fluctuations in arterial blood pressure and heartbeat frequency, and daily changes in hormone secretion: e.g. melatonin, cortisol, growth hormone, prolactin. The core body temperature in humans has a characteristic sinusoidal course, with the maximum value occurring between 3:00-5:00 pm and the minimum between 3:00-5:00 am. Analysis of literature indicates that the obtained results concerning core body temperature are to a large extent influenced by the type of method applied in the measurement. Depending on test protocols, we may apply various methodologies to measuring core body temperature. One of the newest methods of measuring internal and external body temperature consists in the utilisation of remote temperature sensors transmitting the obtained value via a radio signal. The advantages of this method includes the ability to perform: continuous core temperature measurement, observe dynamic changes in core body temperature occurring in circadian rhythm and the repeatability and credibility of the obtained results, which is presented in numerous scientific reports.

Paracetamol (Acetaminophen) Ingestion and Core Body Temperature within Normothermic and Hot Conditions at Rest

Intravenous paracetamol (acetaminophen; ACT) administration results in dose dependent hypothermia (~4°C) within mice. However, the influence of acute oral ACT ingestion on core body temperature (Tc) in humans has not been clearly elucidated in well controlled normothermic (NORM) conditions nor during dry (DRY) and humid (HUMID) heat stress. PURPOSE: The three aims of this study were to i) identify when the peak plasma concentration occurs after acute oral ACT administration, ii) establish any precooling (PC) effect of ACT in NORM conditions and if they correlate with the peak plasma concentration, and iii) investigate if ACT mediated precooling and/or peak plasma concentration alters Tc in DRY and HUMID conditions. METHODS: Fourteen healthy, Caucasian males were randomly allocated to one of two HOT groups; DRY (120 min at 45°C, 30% r.h.) and HUMID (45 min at 45°C, 70% r.h.). Oral ingestion of ACT (20 mg.kg of LBM) was double blinded, and a standardized breakfast (0700) was consumed prior to ACT consumption to control the gastric emptying rate of ACT. All 14 participants completed a NORM (20°C, 30% r.h.) and a HOT (n = 7 in each group) condition. In the NORM condition, the PC effect of ACT was investigated. In the HOT conditions, participants entered the heat chamber when the peak plasma concentration was reached (100 min). Tc was measured every 5 min in all conditions. RESULTS: ACT significantly (p < 0.001) reduced Tc within NORM by ~0.25°C 100 min post ingestion. This precooling effect translated to a decreased mean Tc in DRY and HUMID (p < 0.05), though Tc rate of rise was unchanged. The peak PC effect was significantly correlated with the peak plasma concentration of ACT. CONCLUSION: Oral ACT ingestion elicited a significant PC effect (~0.25°C) effect in NORM, and when ACT was ingested 100 min prior to DRY and HUMID mean Tc was reduced without a change in rate of rise in Tc. Such ACT mediated increases may prove favorable during exercise heat stress.

The effect of stress on core and peripheral body temperature in humans

Even though there are indications that stress influences body temperature in humans, no study has systematically investigated the effects of stress on core and peripheral body temperature. The present study therefore aimed to investigate the effects of acute psychosocial stress on body temperature using different readout measurements. In two independent studies, male and female participants were exposed to a standardized laboratory stress task (the Trier Social Stress Test, TSST) or a non-stressful control task. Core temperature (intestinal and temporal artery) and peripheral temperature (facial and body skin temperature) were measured. Compared to the control condition, stress exposure decreased intestinal temperature but did not affect temporal artery temperature. Stress exposure resulted in changes in skin temperature that followed a gradient-like pattern, with decreases at distal skin locations such as the fingertip and finger base and unchanged skin temperature at proximal regions such as the infra-clavicular area. Stress-induced effects on facial temperature displayed a sex-specific pattern, with decreased nasal skin temperature in females and increased cheek temperature in males. In conclusion, the amplitude and direction of stress-induced temperature changes depend on the site of temperature measurement in humans. This precludes a direct translation of the preclinical stress-induced hyperthermia paradigm, in which core temperature uniformly rises in response to stress to the human situation. Nevertheless, the effects of stress result in consistent temperature changes. Therefore, the present study supports the inclusion of body temperature as a physiological readout parameter of stress in future studies.

Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans

Reduction of body temperature has been proposed to contribute to the increased lifespan in calorie restricted animals and mice overexpressing the uncoupling protein-2 in hypocretin neurons. However, nothing is known regarding the long-term effects of calorie restriction (CR) with adequate nutrition on body temperature in humans. In this study, 24-hour core body temperature was measured every minute by using ingested telemetric capsules in 24 men and women (mean age 53.7 ± 9.4 yrs) consuming a CR diet for an average of 6 years, 24 age- and sex-matched sedentary (WD) and 24 body fat-matched exercise-trained (EX) volunteers, who were eating Western diets. The CR and EX groups were significantly leaner than the WD group. Energy intake was lower in the CR group (1769 ± 348 kcal/d) than in the WD (2302 ± 668 kcal/d) and EX (2798 ± 760 kcal/d) groups (P < 0.0001). Mean 24-hour, day-time and night-time core body temperatures were all significantly lower in the CR group than in the WD and EX groups (P ≤ 0.01). Long-term CR with adequate nutrition in lean and weight-stable healthy humans is associated with a sustained reduction in core body temperature, similar to that found in CR rodents and monkeys. This adaptation is likely due to CR itself, rather than to leanness, and may be involved in slowing the rate of aging.

Hypoxic cutaneous vasodilation is sustained during brief cold stress and is not affected by changes in CO2

Hypoxia decreases core body temperature in animals and humans during cold exposure. In addition, hypoxia increases skin blood flow in thermoneutral conditions, but the impact of hypoxic vasodilation on vasoconstriction during cold exposure is unknown. In this study, skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to baseline (n = 7). Subjects were exposed to four different conditions in the steady state (normoxia and poikilocapnic, isocapnic, and hypercapnic hypoxia) and were cooled for 10 min using a water-perfused suit in each condition. CVC increased during all three hypoxic exposures (all P < 0.05 vs. baseline), and the magnitude of these steady-state responses was not affected by changes in end-tidal CO(2) levels. During poikilocapnic and hypercapnic hypoxia, cold exposure reduced CVC to the same levels observed during normoxic cooling (P > 0.05 vs. normoxia), whereas CVC remained elevated throughout cold exposure during isocapnic hypoxia (P < 0.05 vs. normoxia). The magnitude of vasoconstriction during cold stress was similar in all conditions (P > 0.05). Thus the magnitude of cutaneous vasodilation during steady-state hypoxia is not affected by CO(2) responses. In addition, the magnitude of reflex vasoconstriction is not altered by hypoxia, such that the upward shift in skin blood flow (hypoxic vasodilation) is maintained during whole body cooling.

Pyrogenic Cytokines Did Not Mediate a Stress Interview-Induced Hyperthermic Response in a Patient With Psychogenic Fever: A Case Report

To investigate if pyrogenic cytokines mediated psychological stress-induced hyperthermic response in a patient with psychogenic fever. Despite many case reports on psychogenic fever, the mechanism responsible for how psychological stress increases core body temperature (Tc) in humans is not yet known. A 13-year-old girl with fever (>38 degrees C) of unknown causes was referred to our department because psychogenic fever was suspected. To determine if the fever was actually induced by psychological stress, we conducted a 60-minute stress interview. Her baseline oral temperature was 36.60 degrees C and it began to increase immediately after commencement of the interview, reaching a maximum of 37.42 degrees C 20 minutes after the end of the interview. The plasma level of prostaglandin E(2) and the serum interleukin-6 level were increased 90 minutes after the interview. Serum levels of interleukin-1alpha, interleukin-1beta, and macrophage inflammatory protein-1alpha were all less than their minimum detectable level throughout the observation period. We also measured the patient's thermal preference by immersing her hands in warm (40 degrees C) and cold (20 degrees C) water. Her preference changed from cold to warm only during the increasing phase of oral temperature. This case report shows that a stress interview actually increased Tc in a patient with psychogenic fever. This study suggests that, although pyrogenic cytokines are not involved, the stress interview-induced increase in Tc was an active hyperthermia under the control of the brain, as is infection-induced fever.

Thermoregulatory effects of 3,4-methylenedioxymethamphetamine (MDMA) in humans

Although 3,4-methylenedioxymethamphetamine (MDMA; Ecstasy) has been reported to cause fatal hyperthermia, few studies of the effects of MDMA on core body temperature in humans have been conducted demonstrating increased body temperature. In rats, MDMA causes hyperthermia at warm ambient temperatures but hypothermia at cold ones. In this study, the physiological and subjective effects of MDMA in humans were determined at cold (18 degrees C) and warm (30 degrees C) ambient temperatures in a temperature and humidity-controlled laboratory. Ten healthy volunteers who were recreational users of MDMA were recruited. Four laboratory sessions were conducted in a 2x2 design [i.e., two sessions at 30 degrees C and two at 18 degrees C, two during MDMA (2 mg/kg, p.o.) and two during placebo, in double-blind fashion]. Core body temperature (ingested radiotelemetry pill), skin temperature (four weighted sites), heart rate, blood pressure, metabolic rate (indirect calorimetry), shivering (electromyogram levels), and sweat rate (capacitance hygrometry) were measured as well as subjective effects for several time periods following capsule ingestion. MDMA produced significant elevations in core body temperature and metabolic rate in both warm and cold conditions. MDMA also produced significant elevations in blood pressure and heart rate and significantly increased several ratings of subjective effects similar to those previously reported. There were no differences related to ambient temperature for any of the subjective effects, except that ratings of cold and warm were appropriate to the ambient temperature and were not influenced by MDMA. Unlike findings in rats, MDMA increased core body temperature regardless of ambient temperature in humans. These increases appeared related to increases in metabolic rate, which were substantial. These findings warrant further investigations on the role of MDMA and other stimulants in altering metabolism and thermogenesis.

Homeostatic versus circadian effects of melatonin on core body temperature in humans.

Evidence obtained in animals has suggested a link of the pineal gland and its hormone melatonin with the regulation of core body temperature (CBT). Depending on the species considered, melatonin intervenes in generating seasonal rhythms of daily torpor and hibernation, in heat stress tolerance, and in setting the CBT set point. In humans, the circadian rhythms of melatonin is strictly associated with that of CBT, the nocturnal decline of CBT being inversely related to the rise of melatonin. Whereas there is inconsistent evidence for the suggestion that the decline of CBT may prompt the release of melatonin, conversely, stringent data indicate that melatonin decreases CBT. Administration of melatonin during the day, when it is not normally secreted, decreases CBT by about 0.3 to 0.4 degree C, and suppression of melatonin at night enhances CBT by about the same magnitude. Accordingly, the nocturnal rise of melatonin contributes to the circadian amplitude of CBT. The mechanisms through which melatonin decreases CBT are unclear. It is known that melatonin enhances heat loss, but a reduction of heat production cannot be excluded. Besides actions on peripheral vessels aimed to favor heat loss, it is likely that the effect of melatonin to reduce CBT is exerted mainly in the hypothalamus, where thermoregulatory centers are located. Recent observations have shown that the acute thermoregulatory effects induced by melatonin and bright light are independent of their circadian phase-shifting effects. The effect of melatonin ultimately brings a saving of energy and is reduced in at least two physiological situations: aging and the luteal menstrual phase. In both conditions, melatonin does not exert its CBT-lowering effects. Whereas in older women this effect may represent an age-related alteration, in the luteal phase this modification may represent a mechanism of keeping CBT higher at night to promote a better embryo implantation and survival.

Acute phase-shifting effects of melatonin associated with suppression of core body temperature in humans

Appropriately administered melatonin is able to phase shift circadian rhythms, to induce transient sleepiness and to suppress core body temperature. The relationships between these phenomena have not been fully explored. In a double-blind, placebo-controlled crossover study, 8 healthy males maintained a regular sleep-wake cycle in a natural environment throughout. From dusk until 2400 h on days (D) 1–4 subjects were in dim artificial lighting (<100 lux) with darkness (<1 lux) from 2400-0800 h. Sunglasses were worn during the day when outside. At 1700h on D3 either melatonin (5 mg) or placebo was administered. Saliva samples were collected at 30 min intervals, 1600–2400 h on D3 and D4, and subjective alertness rated at 30 min intervals from 1600–2400 h on D3 and hourly from 0800–2400 h D4. Sleep quality was rated on nights 2, 3 and 4 and core temperature was recorded throughout. Melatonin induced a significant suppression of temperature and alertness peaking 2.5 h after the dose, together with improved sleep quality on the night of D3 and a phase advance of the endogenous melatonin rhythm on D4. The degree of phase shift was related to the amount of temperature suppression in 6 of 7 subjects with detectable melatonin, suggesting that temperature suppression is an integral part of the phase-shifting mechanism.

Selective SWS suppression does not affect the time course of core body temperature in men.

In eight healthy middle-aged men, sleep and core body temperature were recorded under baseline conditions, during all-night SWS suppression by acoustic stimulation, and during undisturbed recovery sleep. SWS suppression resulted in a marked reduction of sleep stages 3 and 4 but did not affect the time course of core body temperature. These data suggest that sleep stages 3 and 4 of nonREM sleep (i.e. SWS) do not play a major role in the regulation of core body temperature in humans.

Effect of a single 3-hour exposure to bright light on core body temperature and sleep in humans

Seven human subjects were exposed to bright light (BL, approx, 2500 lux) and dim light (DL, approx, 6 lux) during 3 h prior to nocturnal sleep, in a cross-over design. At the end of the BL exposure period core body temperature was significantly higher than at the end of the DL exposure period. The difference in core body temperature persisted during the first 4 h of sleep. The latency to sleep onset was increased after BL exposure. Rapid-eye movement sleep (REMS) and slow-wave sleep (SWS; stage 3 + 4 of non-REMS) were not significantly changed. Eight subjects were exposed to BL from 20.30 to 23.30 h while their eyes were covered or uncovered. During BL exposure with uncovered eyes, core body temperature decreased significantly less than during exposure with covered eyes. We conclude that bright light immediately affects core body temperature and that this effect is mediated via the eyes.