Influence of female reproductive hormones on local thermal control of skin blood flow.

Progesterone and estrogen modify thermoregulatory control such that, when both steroids are elevated, body temperature increases and the reflex thermoregulatory control of cutaneous vasodilation is shifted to higher internal temperatures. We hypothesized that the influence of these hormones would also include effects on local thermal control of skin blood flow. Experiments were conducted in women in high-hormone (HH) and low-hormone (LH) phases of oral contraceptive use. Skin blood flow was measured by laser-Doppler flowmetry, and local temperature (T(loc)) was controlled over 12 cm(2) around the sites of blood flow measurement. T(loc) was held at 32 degrees C for 10-15 min and was then decreased at one site from 32 to 20 degrees C in a ramp over 20 min. Next, T(loc) was increased from 32 to 42 degrees C in a ramp over 15 min at a separate site. Finally, T(loc) at both sites was held at 42 degrees C for 30 min to elicit maximum vasodilation; data for cutaneous vascular conductance (CVC) are expressed relative to that maximum. Whole body skin temperature (T(sk)) was held at 34 degrees C throughout each study to minimize reflex effects from differences in T(sk) between experiments. Baseline CVC did not differ between phases [8.18 +/- 1.38 (LH) vs. 8. 41 +/- 1.31% of maximum (HH); P > 0.05]. The vasodilator response to local warming was augmented in HH (P < 0.05, ANOVA). For example, at T(loc) of 40-42 degrees C, CVC averaged 76.41 +/- 3.08% of maximum in HH and 67.71 +/- 4.43% of maximum in LH (P < 0.01 LH vs. HH). The vasoconstrictor response to local cooling was unaffected by phase (P > 0.05). These findings indicate that modifications in cutaneous vascular control by female steroid hormones include enhancement of the vasodilator response to local warming and are consistent with reports of the influence of estrogen to enhance nitric oxide-dependent vasodilator responses.     

Attenuated thermoregulatory sweating and cutaneous vasodilation after 14-day bed rest in humans.

We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental room was air-conditioned (27 degrees C, 30-40% relative humidity). We measured skin blood flow (chest and forearm), skin temperatures (chest, upper arm, forearm, thigh, and calf), and tympanic temperature. We also measured sweat rate by the ventilated capsule method in which the skin area for measurement was drained by dry air conditioned at 27 degrees C under similar skin temperatures in both trials. We calculated cutaneous vascular conductance (CVC) from the ratio of skin blood flow to mean blood pressure. From tympanic temperature-sweat rate and -CVC relationships, we assessed the threshold temperature and sensitivity as the slope response of variables to a given change in tympanic temperature. HDBR increased the threshold temperature for sweating by 0.31 degrees C at the chest and 0.32 degrees C at the forearm, whereas it reduced sensitivity by 40% at the chest and 31% at the forearm. HDBR increased the threshold temperature for cutaneous vasodilation, whereas it decreased sensitivity. HDBR reduced plasma volume by 11%, whereas it did not change plasma osmolarity. The increase in the threshold temperature for sweating correlated with that for cutaneous vasodilation. In conclusion, HDBR attenuated thermoregulatory sweating and cutaneous vasodilation by increasing the threshold temperature and decreasing sensitivity. HDBR increased the threshold temperature for sweating and cutaneous vasodilation by similar magnitudes, whereas it decreased their sensitivity by different magnitudes.     

Effects of food deprivation on daily changes in body temperature and behavioral thermoregulation in rats

Homeothermic animals regulate body temperature (T(b)) by using both autonomic and behavioral mechanisms. In the latter process, animals seek out cooler or warmer places when they are exposed to excessively hot or cold environments. Thermoregulation is affected by the state of energy reserves in the body. In the present study, we examine the effects of 4-day food deprivation on circadian changes in T(b) and on cold-escape and heat-escape behaviors in rats. Continuous measurement of T(b) during food deprivation indicated that the peak T(b) amplitude was not different from baseline values, but the trough amplitude continuously decreased after the onset of food deprivation. Cold-escape behavior was facilitated by food deprivation, whereas heat-escape behavior was unchanged. After the termination of food deprivation, the lowered T(b) returned to normal on the first day. However, cold-escape behavior was still facilitated on the third day after food reintroduction. Autonomic and behavioral thermoregulatory effectors are modulated in the face of food shortage so as to maintain optimal performance during the active period, whereas increasing energy conservation occurs during the quiescent phase.     

Increased heat-escape/cold-seeking behavior following hypertonic saline injection in rats

We examined the effect of hypertonic saline injection on heat-escape/cold-seeking behavior in desalivated rats. Rats were exposed to 40 degrees C heat after normal (154 mM NaCl, control) or hypertonic saline (2,500 mM NaCl) injection (1 ml/100 g body wt). The rats received a 0 degrees C air for 30 s when they entered a specific area in an experimental box. Core temperature (T(c)) surpassed 40 degrees C in both conditions when 0 degrees C air was not available. Hypertonic saline injection produced a lower baseline T(c) than control [36.9 +/- 0.2 and 37.9 +/- 0.2 degrees C (means +/- SE), P < 0.05] and a greater number of 0 degrees C air rewards during the 2-h heat with lower T(c) at the end (48 +/- 1 and 34 +/- 2, 37.6 +/- 0.1, and 37.3 +/- 0.1 degrees C in the control and hypertonic saline injection trial, respectively, P < 0.05, n = 6). However, T(c) was similar (37.7 +/- 0.2 and 37.6 +/- 0.4 degrees C in the control and hypertonic saline injection trial, n = 5) when 0 degrees C air was automatically and intermittently (35 times) given during the heat. Rats augment heat-defense mechanisms in response to osmotic stress by lowering the baseline T(c) and increasing heat-escape/cold-seeking behavior.     

Delayed threshold for active cutaneous vasodilation in patients with Type 2 diabetes mellitus.

Epidemiological evidence suggests decreased heat tolerance in patients with Type 2 diabetes mellitus (T2DM), but it is not known whether the mechanisms involved in thermoregulatory control of skin blood flow are altered in these patients. We tested the hypothesis that individuals with T2DM have a delayed internal temperature threshold for active cutaneous vasodilation during whole body heating compared with healthy control subjects. We measured skin blood flow using laser-Doppler flowmetry (LDF), internal temperature (T or) via sublingual thermocouple, and mean arterial pressure via Finometer at baseline and during whole body heating in 9 T2DM patients and 10 control subjects of similar age, height, and weight. At one LDF site, sympathetic noradrenergic neurotransmission was blocked by local pretreatment with bretylium tosylate (BT) to isolate the cutaneous active vasodilator system. Whole body heating was conducted using a water-perfused suit. There were no differences in preheating T(or) between groups (P > 0.10). Patients with T2DM exhibited an increased internal temperature threshold for the onset of vasodilation at both untreated and BT-treated sites. At BT-treated sites, T or thresholds were 36.28 +/- 0.07 degrees C in controls and 36.55 +/- 0.05 degrees C in T2DM patients (P < 0.05), indicating delayed onset of active vasodilation in patients. Sensitivity of vasodilation was variable in both groups, with no consistent difference between groups (P > 0.05). We conclude that altered control of active cutaneous vasodilation may contribute to impaired thermoregulation in patients with T2DM.     

The median preoptic nucleus is involved in the facilitation of heat-escape/cold-seeking behavior during systemic salt loading in rats

Systemic salt loading has been reported to facilitate operant heat-escape/cold-seeking behavior. In the present study, we hypothesized that the median preoptic nucleus (MnPO) would be involved in this mechanism. Rats were divided into two groups (n = 6 each): one group had the MnPO lesion with ibotenic acid (4.0 mug) and the other was the vehicle control. After subcutaneous injection (10 ml/kg) of either isotonic- (154 mM) or hypertonic-saline (2,500 mM), each rat was placed in a behavior box, where the ambient temperature was changed to 26 degrees C, 35 degrees C, and 40 degrees C every 1 h. The position of a rat in the box and the body core temperature (T(core)) were monitored. A rat could trigger 0 degrees C air for 45 s in the 35 degrees C and 40 degrees C heat when moved in a specific area in the box (operant behavior). In the control group, counts of the operant behavior were greater (P < 0.05) in the hypertonic- than in the isotonic-saline injection (17 +/- 2 and 10 +/- 2 at 35 degrees C, 24 +/- 2 and 18 +/- 1 at 40 degrees C). T(core) remained unchanged throughout the exposure, although the level was lower (P < 0.05) in the hypertonic- than in the isotonic-saline trial (36.6 +/- 0.2 degrees C and 37.4 +/- 0.1 degrees C at 26 degrees C and 36.9 +/- 0.2 degrees C and 37.4 +/- 0.1 degrees C at 40 degrees C, respectively). However, in the MnPO-lesion group, counts of the behavior were similar between the hypertonic- and isotonic-saline injection trials (10 +/- 2 and 8 +/- 1 at 35 degrees C, and 17 +/- 1 and 16 +/- 1 at 40 degrees C, respectively). T(core) increased (P < 0.05) in the heat in both trials (36.8 +/- 0.1 degrees C and 37.4 +/- 0.1 degrees C at 26 degrees C and 37.4 +/- 0.2 degrees C and 37.8 +/- 0.2 degrees C at 40 degrees C in the hypertonic- and isotonic-saline injection trials, respectively). These results may suggest that, at least in part, the MnPO is involved in the facilitation of heat-escape/cold-seeking behavior during osmotic stimulation.     

Minimal changes in hypothalamic temperature accompany microwave-induced alteration of thermoregulatory behavior

This study probed the mechanisms underlying microwave-induced alterations of thermoregulatory behavior. Adult male squirrel monkeys (Saimiri sciureus), trained to regulate the temperature of their immediate environment (Ta) behaviorally, were chronically implanted with Teflon reentrant tubes in the medical preoptic/anterior hypothalamic area (PO/AH), the brainstem region considered to control normal thermoregulatory processes. A Vitek temperature probe inserted into the tube measured PO/AH temperature continuously while changes in thermoregulatory behavior were induced by either brief (10-min) or prolonged (2.5-h) unilateral exposures to planewave 2,450-MHz continuous wave (CW) microwaves (E polarization). Power densities explored ranged from 4 to 20 mW/cm2 (rate of energy absorption [SAR] = 0.05 [W/kg]/cm2]). Rectal temperature and four representative skin temperatures were also monitored, as was the Ta selected by the animal. When the power density was high enough to induce a monkey to select a cooler Ta (8 mW/cm2 and above), PO/AH temperature rose approximately 0.3 degrees C but seldom more. Lower power densities usually produced smaller increases in PO/AH temperature and no reliable change in thermoregulatory behavior. Rectal temperature remained constant while PO/AH temperature rose only 0.2-0.3 degrees C during 2.5-h exposures at 20 mW/cm2 because the Ta selected was 2-3 degrees C cooler than normally preferred. Sometimes PO/AH temperature increments greater than 0.3 degrees C were recorded, but they always accompanied inadequate thermoregulatory behavior. Thus, a PO/AH temperature rise of 0.2-0.3 degrees C, accompanying microwave exposure, appears to be necessary and sufficient to alter thermoregulatory behavior, which ensures in turn that no greater temperature excursions occur in this hypothalamic thermoregulatory center.     

Reflex control of cutaneous vasoconstrictor system is reset by exogenous female reproductive hormones.

To determine whether cardiovascular influences of exogenous female steroid hormones include effects on reflex thermoregulatory control of the adrenergic cutaneous vasoconstrictor system, we conducted ramp decreases in skin temperature (T(sk)) in eight women in both high- and low (placebo)-progesterone/estrogen phases of oral contraceptive use. With the use of water-perfused suits, T(sk) was held at 36 degrees C for 10 min (to minimize initial vasoconstrictor activity) and was then decreased in a ramp, approximately 0.2 degrees C/min for 12-15 min. Subjects rested supine for 30-40 min before each experiment, and the protocol was terminated before the onset of shivering. Skin blood flow was monitored by laser-Doppler flowmetry and arterial pressure by finger photoplethysmography. In all experiments, cutaneous vasoconstriction began immediately with the onset of cooling, and cutaneous vascular conductance (CVC) decreased progressively with decreasing T(sk). Regression analysis of the relationship of CVC to T(sk) showed no difference in slope between phases (low-hormone phase: 17.67 +/- 5.57; high-hormone phase: 17.40 +/- 8.00 %baseline/ degrees C; P > 0.05). Additional studies involving local blockade confirmed this response as being solely due to the adrenergic vasoconstrictor system. Waking oral temperature (T(or)) was significantly higher on high-hormone vs. low-hormone days (36.60 +/- 0.11 vs. 36.37 +/- 0.09 degrees C, respectively; P < 0.02). Integrative analysis of CVC in terms of simultaneous values for T(sk) and T(or) showed that the cutaneous vasoconstrictor response was shifted in the high-hormone phase such that a higher T(or) was maintained throughout cooling (P < 0.05). Thus reflex thermoregulatory control of the cutaneous vasoconstrictor system is shifted to higher internal temperatures by exogenous female reproductive hormones.     

Heat loss responses in rats acclimated to heat loaded intermittently

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Delayed distribution of active vasodilation and altered vascular conductance in aged skin.

Reflex vasodilation is attenuated in aged skin during hyperthermia. We used laser-Doppler imaging (LDI) to test the hypothesis that the magnitude of conductance and the spatial distribution of vasodilation are altered with aging. LDI of forearm skin was compared in 12 young (19- to 29-yr-old) and 12 older (64- to 75-yr-old) men during supine passive heating. Additionally, iontophoresis of bretylium tosylate was performed in a subset of subjects to explore the involvement of sympathetic vasoconstriction in limiting skin blood flow. Passive heating with water-perfused suits clamped mean skin temperature at 41.0 +/- 0.5 degrees C, causing a ramp increase in esophageal temperature (T(es)) to 相似文献   

Temperature regulation during acute heat loads in rats after short-term heat exposure.

Eleven rats were kept at an ambient temperature of 33.5 degrees C (HC) for 4-5 consecutive days, 9 additional rats were subjected to 33.5 degrees C for approximately 5 h daily (HI) for the same period, and 12 controls (Cn) were kept at 24 degrees C. After the exposure, the rats were placed in a direct calorimeter, where the wall temperature was set at 24 degrees C, and subjected to direct internal heating (6.2 W.kg-1, 30 min) through an intraperitoneal electric heater. After the first heat load and when thermal equilibrium had been attained again, the rats were subjected to indirect external warming by raising the jacket water temperature surrounding the calorimeter from 24.0 to 38.8 degrees C in 90 min. Hypothalamic (Thy) and colonic temperatures (Tco), evaporative and nonevaporative heat loss, and metabolic heat production (M) before the acute heat loads did not differ among the groups. During heat loads, the latent times for the onsets of the rises in tail skin temperature and evaporation were significantly longer, and Thy and Tco at the start of increases in heat losses tended to be higher, in the HC than in the Cn. M significantly decreased in all groups, but the magnitude and duration of reduction in M were significantly greater in the HC than in the Cn. There were no differences between the thermoregulatory responses to heat loads of the HI and Cn. These results suggest that in HC the threshold core temperature for heat loss response and the upper critical temperature have already shifted to a higher level and that HC respond to heat stress more strongly with the reduction of M than Cn. Short-term intermittent heat exposure had little effect on the thermoregulatory mechanisms in rats.     

Antipyresis due to centrally administered vasopressin differentially alters thermoregulatory effectors depending on the ambient temperature

The intracerebroventricular (i.c.v.) administration of arginine vasopressin (AVP), in the febrile rat elicits an antipyresis at cold, warm and neutral ambient temperatures. These experiments were conducted, therefore, to elucidate the thermoregulatory effector mechanisms responsible for this antipyretic effect. At 25 degrees C, AVP-induced antipyresis was mediated by tail skin vasodilation while metabolic rate was unaffected. At 4 degrees C, the antipyresis produced by AVP was approximately double that seen at 25 degrees C. This effect appeared to be mediated exclusively by inhibition of heat production since the metabolic rate decreased markedly following AVP. This antipyresis at 4 degrees C was accompanied by cutaneous vasoconstriction. At 32 degrees C, neither vasomotor tone, metabolic rate nor evaporative heat loss could be shown to contribute to the small antipyretic effect elicited by AVP. We conclude from these data that i.c.v. AVP is producing antipyresis by affecting the febrile body temperature set-point mechanism since the thermoregulatory strategy to lose heat varies at different ambient temperatures and the decrease in body temperature cannot be shown to be due to changes in a single effector mechanism.     

Physical fitness and thermoregulatory reactions in a cold environment in men

The relationship between the physical fitness level (maximal O2 consumption, VO2max) and thermoregulatory reactions was studied in 17 adult males submitted to an acute cold exposure. Standard cold tests were performed in nude subjects, lying for 2 h in a climatic chamber at three ambient air temperatures (10, 5, and 1 degrees C). The level of physical fitness conditioned the intensity of thermoregulatory reactions to cold. For all subjects, there was a direct relationship between physical fitness and 1) metabolic heat production, 2) level of mean skin temperature (Tsk), 3) level of skin conductance, and 4) level of Tsk at the onset of shivering. The predominance of thermogenic or insulative reactions depended on the intensity of the cold stress: insulative reactions were preferential at 10 degrees C, or even at 5 degrees C, whereas colder ambient temperature (1 degree C) triggered metabolic heat production abilities, which were closely related to the subject's physical fitness level. Fit subjects have more efficient thermoregulatory abilities against cold stress than unfit subjects, certainly because of an improved sensitivity of the thermoregulatory system.     

Estrogen modifies the temperature effects of progesterone.

To test the hypothesis that progestin-mediated increases in resting core temperature and the core temperature threshold for sweating onset are counteracted by estrogen, we studied eight women (24 +/- 2 yr) at 27 degrees C rest, during 20 min of passive heating (35 degrees C), and during 40 min of exercise at 35 degrees C. Subjects were tested four times, during the early follicular and midluteal menstrual phases, after 4 wk of combined estradiol-norethindrone (progestin) oral contraceptive administration (OC E+P), and after 4 wk of progestin-only oral contraceptive administration (OC P). The order of the OC P and OC E+P were randomized. Baseline esophageal temperature (T(es)) at 27 degrees C was higher (P < 0.05) in the luteal phase (37.08 +/- 0.21 degrees C) and in OC P (37.60 +/- 0.31 degrees C) but not during OC E+P (37.04 +/- 0.23 degrees C) compared with the follicular phase (36.66 +/- 0.21 degrees C). T(es) remained above follicular phase levels throughout passive heating and exercise during OC P, whereas T(es) in the luteal phase was greater than in the follicular phase throughout exercise (P < 0.05). The T(es) threshold for sweating was also greater in the luteal phase (38.02 +/- 0.28 degrees C) and OC P (38.07 +/- 0.17 degrees C) compared with the follicular phase (37.32 +/- 0.11 degrees C) and OC E+P (37.46 +/- 0.18 degrees C). Progestin administration raised the T(es) threshold for sweating during OC P, but this effect was not present when estrogen was administered with progestin, suggesting that estrogen modifies progestin-related changes in temperature regulation. These data are also consistent with previous findings that estrogen lowers the thermoregulatory operating point.     

Skin blood flow during incremental exercise in a thermoneutral and a hot dry environment

Eight physically fit men performed two incremental bicycle ergometer tests, one in an ambient temperature of 25 degrees C and the other at 40 degrees C. Oesophageal temperature (Tes) increased continuously throughout the tests up to 38.0 and 38.3 degrees C, respectively. In both environments, forearm blood flow (plethysmography) was linearly related to Tes above the Tes threshold for vasodilation, but at the heaviest work loads this relationship was clearly attenuated and therefore indicated skin vasoconstriction, which tended to be more pronounced at 25 degrees C. During recovery at 25 degrees C, in some subjects the forearm blood flow increased above the levels observed at the end of the graded exercise in spite of a decreasing Tes. Skin blood flow, measured by laser Doppler flow meter at the shoulder, was quantitatively different but, on average, seemed to reveal the same response pattern as the forearm blood flow. In spite of the higher level of skin blood flow in the heat, blood lactate accumulation did not differ between the two environments. The present results suggest that there is competition between skin vasoconstriction and vasodilation at heavy work rates, the former having precedence in a thermoneutral environment to increase muscle perfusion. During short-term graded exercise in a hot environment, skin vasoconstriction with other circulatory adjustments seems to be able to maintain adequate muscle perfusion at heavy work levels, but probably not during maximum exercise.     

Thermoregulation in the cold after physical training at different ambient air temperatures

Since human thermoregulation at rest is altered by cold exposure, it was hypothesized that physical training under cold conditions would alter thermoregulation. Three groups (n = 8) of male subjects (mean age 24.3 +/- 0.9 years) were evaluated: group T (interval training at 21 degrees C), group CT (interval training at 1 degrees C), and group C (no training, equivalent exposure to 1 degrees C). Each group was submitted, before and after 4 weeks of interval training (5 d/week), to a cold air test at rest (SCAT) (dry bulb temperature (Tdb) = 1 degrees C) for a 2-h period for evaluation of the thermoregulatory responses. During SCAT, after the training/acclimation period, group T exhibited a higher rectal temperature (Tre) (P < 0.05) without significant change in mean skin temperature (Tsk) whereas metabolic heat production (M) was higher at the beginning of the SCAT (P < 0.05). For group CT, no thermoregulatory change was observed. Group C showed a lower Tre (P < 0.05) without significant change in either Tsk or in M, suggesting the development of a hypothermic general cold adaptation. This study showed, first, that the cold thermoregulatory responses induced by an interval training differed following the climatic conditions of the training and, second, that this training performed in the cold prevented the development of a general cold adaptation.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

Effects of thermal underwear on thermal and subjective responses in winter

This study was conducted to obtain basic data in improving the health of Koreans, saving energy and protecting environments. This study investigated the effects of wearing thermal underwear for keeping warm in the office in winter where temperature is not as low as affecting work efficiency, on thermoregulatory responses and subjective sensations. In order to create an environment where every subject feels the same thermal sensation, two experimental conditions were selected through preliminary experiments: wearing thermal underwear in 18 degrees C air (18-condition) and not wearing thermal underwear in 23 degrees C air (23-condition). Six healthy male students participated in this study as experiment subjects. Measurement items included rectal temperature (T(re)), skin temperature (T(sk)), clothing microclimate temperature (T(cm)), thermal sensation and thermal comfort. The results are as follows: (1) T(re) of all subjects was maintained constant at 37.1 degrees C under both conditions, indicating no significant differences. (2) (T)(sk) under the 18-condition and the 23-condition were 32.9 degrees C and 33.7 degrees C, respectively, indicating a significant level of difference (p<0.05). (3) Among local skin temperature, trunk part (forehead and abdomen) did not show significant differences. After 90-min exposure, the skin temperature of hands and feet under the 18-condition was significantly lower than that under the 23-condition (p<0.001). (4) More than 80% of all the respondents felt comfortable under both conditions. It was found (T)(sk) decreased due to a drop in the skin temperature of hands and feet, and the subjects felt cooler wearing only one layer of normal thermal underwear at 18 degrees C. Yet, the thermal comfort level, T(re) and T(cm) of chest part under the 18-condition were the same as those under the 23-condition. These results show that the same level of comfort, T(re) and T(cm) can be maintained as that of an environment about 5 degrees C higher in the office in winter, by wearing one layer of thermal underwear. In this regard, this study suggests that lowering indoor temperature by wearing thermal underwear in winter can contribute to saving energy and improving health.     

Influence of hormone replacement therapy and aspirin on temperature regulation in postmenopausal women

Postmenopausal women receiving estrogen-replacement therapy (ERT) regulate body temperature (T(b)) at a lower level than women not receiving hormone replacement therapy (untreated) and women using estrogen plus progesterone therapy (E + P), but it is not clear if reproductive hormones alter T(b) by directly acting on central thermoregulatory centers or indirectly via a secondary mediator(s). The purpose of the present investigation was to examine the possible involvement of pyrogenic cytokines and cyclooxygenase (COX) products (e.g., prostaglandins) in the regulation of T(b) in three groups of postmenopausal women (8 ERT, 7 E + P, and 8 untreated). We measured ex vivo secretion of cytokine agonists [tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta and -6] and modifiers (IL-2 soluble receptor, IL-1 receptor antagonist, soluble TNF receptor type I, soluble TNF receptor type II, soluble IL-6 receptor, and soluble glycoprotein 130) from peripheral blood mononuclear cells and thermoregulatory responses at rest and during 1 h of passive whole body heating in the postmenopausal women before and after 3 days of placebo or aspirin (50 mg. day(-1). kg(-1)). With and without aspirin, the ERT group had a lower baseline rectal temperature (T(re); 0.44 degrees C, P < 0.004) and a reduced T(b) threshold for cutaneous vasodilation (0.29 degrees C and 0.38 degrees C, P < 0.01) compared with the untreated and E + P groups, respectively. In the placebo condition, waking morning oral temperature (T(or)) correlated with ex vivo secretion of the proteins associated with IL-6 bioactivity. Aspirin caused significant reductions in waking T(or) in the E + P group and in baseline T(re) in the untreated group. However, the difference in thermoregulation brought about by steroid hormone treatment could not be explained by these relatively modest apparent influences by cytokines and COX products. Therefore, the altered thermoregulation induced by reproductive steroid therapy appears to occur via a mechanism distinct from a classic infection-induced fever.     

Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats

Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.