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PubMed1992

The effect of intermittent exposure to cold on the development of hypertension in the rat.

Continuous exposure to a cold (5 degrees C) environment has been shown to induce hypertension in rats. The total time required for the first significant elevation of blood pressure is dependent on a number of factors, including the ambient temperature and the weight of the rat at the time of exposure to cold. The present study was also concerned with the minimal time of daily exposure to cold that would result in a significant elevation of blood pressure. To achieve this, we used four groups of rats. One was exposed to cold for 4 h daily (09:00 to 13:00), a second group was exposed to cold for 8 h daily (09:00 to 17:00), and a third was exposed for 24 h daily. The fourth group remained at 25 degrees C. Systolic blood pressures of the group exposed to continuous cold became elevated significantly above pre-cold exposure level within 2 weeks of cold exposure. Blood pressures of the groups exposed to cold for 4 and 8 h daily became elevated significantly above the level of the warm-adapted control group by day 27 of exposure to cold, but failed to reach the level of the chronically cold-exposed group even after 42 days of exposure to cold. There was a sigmoid-type relationship between the hours per day exposed to cold and systolic blood pressure at the end of the experiment. Thus, graded elevations of systolic blood pressure occur with increasing daily duration of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Topical menthol--a human model for cold pain by activation and sensitization of C nociceptors.

Although cold hyperalgesia is a frequent symptom in patients with neuropathic pain, it is poorly understood. We investigated the mechanisms of cold pain by studying the effect of menthol on pain, temperature perception, touch sensation and skin perfusion. In 10 subjects, 40% l-menthol, and ethanol, serving as control, were topically applied to the forearm in a double-blinded two-way crossover study. Menthol induced significant pain and cold sensations, punctate and cold hyperalgesia and an increase in cutaneous perfusion. Other mechano-sensory and thermal tests were unchanged (touch, cold and warm detection thresholds, heat pain threshold; no dynamic and static hyperalgesia, no wind-up). To investigate the underlying mechanisms, the effects of menthol versus ethanol on the dorsum of the hand were tested during A fibre conduction blockade of the superficial radial nerve in another 10 subjects. The block itself led to hypoaesthesia for mechanical stimuli and anaesthesia for cold perception, but induced an increase in cold-mediated pain. This was due to lack of inhibition of C nociceptors normally exerted by concomitant activation of A fibres. Under these conditions, menthol-induced cold sensation and punctate hyperalgesia were abolished. However, menthol induced spontaneous pain with a trend to higher values than without block. Furthermore, the hyperalgesia to cold stimuli, that was already present during A fibre block, was further increased significantly by menthol. We suggested that menthol acts to sensitize cold-sensitive peripheral vasoactive C nociceptors and activates cold-specific A delta fibres. Punctate hyperalgesia is due to central sensitization based on the ongoing activity in the sensitized cold-sensitive peripheral C nociceptors. In conclusion, topical menthol is a human model for cold pain by exposing for the first time the mechanism of sensitized peripheral cold C nociceptors that may also be involved in neuropathic pain.

Administration, Topical↗
PubMed2005

The Arabidopsis cold-responsive transcriptome and its regulation by ICE1.

To understand the gene network controlling tolerance to cold stress, we performed an Arabidopsis thaliana genome transcript expression profile using Affymetrix GeneChips that contain approximately 24,000 genes. We statistically determined 939 cold-regulated genes with 655 upregulated and 284 downregulated. A large number of early cold-responsive genes encode transcription factors that likely control late-responsive genes, suggesting a multitude of transcriptional cascades. In addition, many genes involved in chromatin level and posttranscriptional regulation were also cold regulated, suggesting their involvement in cold-responsive gene regulation. A number of genes important for the biosynthesis or signaling of plant hormones, such as abscisic acid, gibberellic acid, and auxin, are regulated by cold stress, which is of potential importance in coordinating cold tolerance with growth and development. We compared the cold-responsive transcriptomes of the wild type and inducer of CBF expression 1 (ice1), a mutant defective in an upstream transcription factor required for chilling and freezing tolerance. The transcript levels of many cold-responsive genes were altered in the ice1 mutant not only during cold stress but also before cold treatments. Our study provides a global picture of the Arabidopsis cold-responsive transcriptome and its control by ICE1 and will be valuable for understanding gene regulation under cold stress and the molecular mechanisms of cold tolerance.

Adaptation, Physiological↗
PubMed1982

Effects of cold exposure on insulin and glucagon secretion in sheep.

The effectiveness of cold exposure on the secretion of insulin and glucagon were examined using five adult sheep. Endocrine responses were studied in a warm environment and after cold exposure (0 C) from 4-19 days. Compared to levels at room temperature, basal plasma glucose levels were elevated during cold exposure, but basal levels of plasma insulin and glucagon were unchanged. Cold exposure significantly decreased the early insulin response to a primed iv infusion of glucose. Plasma glucose and glucagon levels during glucose infusion were unaffected by cold exposure. The decrease in plasma glucose after iv insulin injection (0.2 U/kg BW) was greater during cold exposure than at room temperature. Butyrate injection (0.625 mmol/kg, iv) resulted in a significantly lower secretion of both insulin and glucagon in the cold than in the warm environment. The glucagon response to arginine infusion (0.5 g/kg over 30 min, iv) was elevated by cold exposure, whereas the insulin response to arginine tended to be reduced. Propranolol infusion (20 micrograms/kg . min, iv) caused a slight inhibition of insulin secretion in the cold environment, but did not affect glucagon levels in either the cold or warm environment. Phentolamine infusion (20 micrograms/kg . min, iv) inhibited glucagon secretion, particularly in the cold environment, and caused a markedly greater stimulation of insulin secretion in the cold. It is concluded that cold exposure insufficient to cause hypothermia decreases insulin secretion in response to a variety of stimuli. Effects of cold on glucagon secretion depend upon the stimulating agent used.

Animals↗
PubMed2006

Contribution of TRPM8 channels to cold transduction in primary sensory neurons and peripheral nerve terminals.

Transient receptor potential melastatin 8 (TRPM8) is the best molecular candidate for innocuous cold detection by peripheral thermoreceptor terminals. To dissect out the contribution of this cold- and menthol-gated, nonselective cation channel to cold transduction, we identified BCTC [N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)piperazine-1-carboxamide] as a potent and full blocker of recombinant TRPM8 channels. In cold-sensitive trigeminal ganglion neurons of mice and guinea pig, responses to menthol were abolished by BCTC. In contrast, the effect of BCTC on cold-evoked responses was variable but showed a good correlation with the presence or lack of menthol sensitivity in the same neuron, suggesting a specific blocking action of BCTC on TRPM8 channels. The biophysical properties of native cold-gated currents (I(cold)), and the currents blocked by BCTC were nearly identical, consistent with a role of this channel in cold sensing at the soma. The temperature activation threshold of native TRPM8 channels was significantly warmer than those reported in previous expression studies. The effect of BCTC on native I(cold) was characterized by a dose-dependent shift in the temperature threshold of activation. The role of TRPM8 in transduction was further investigated in the guinea pig cornea, a peripheral territory densely innervated with cold thermoreceptors. All cold-sensitive terminals were activated by menthol, suggesting the functional expression of TRPM8 channels in their membrane. However, the spontaneous activity and firing pattern characteristic of cold thermoreceptors was totally immune to TRPM8 channel blockade with BCTC or SKF96365 (1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride). Cold-evoked responses in corneal terminals were also essentially unaffected by these drugs, whereas responses to menthol were completely abolished. The minor impairment in the ability to transduce cold stimuli by peripheral corneal thermoreceptors during TRPM8 blockade unveils an overlapping functional role for various thermosensitive mechanisms in these nerve terminals.

Animals↗
PubMed2003

Misconceptions about colds and predictors of health service utilization.

OBJECTIVE: Colds accounted for 1.6 million emergency department (ED) visits and 25 million ambulatory visits by children and adults in 1998. Although most colds are caused by viruses and do not require medical intervention, many families seek health care for the treatment of colds. Parental misconceptions about the cause and appropriate treatment of colds may contribute to unnecessary health service utilization. The objective of this study was to determine predictors of reported ED use and ambulatory care use for colds among families with young children. METHODS: This study was an observational, prospective cohort study to determine attack rates for respiratory illnesses within families that have at least 1 child who is 6 months to 5 years of age and enrolled in out-of-home child care. Families were randomly selected from 5 pediatric practices in Massachusetts and were considered eligible when the child was enrolled in child care with at least 5 other children for >or=10 hours per week. Enrolled families were asked to complete a survey that assessed knowledge about colds, antibiotic indications, and frequency of health service utilization. Predictors of self-reported use of health care services were assessed in multivariate logistic regression models. RESULTS: Of the 261 families enrolled in the study, 197 families (75%) returned completed surveys. Although 93% of parents understood that viruses caused colds, 66% of parents also believed that colds were caused by bacteria. Fifty-three percent believed that antibiotics were needed to treat colds. Parents reported that they would visit the ED (23%) or their doctor's office (60%) when their child had a cold. Predictors of ED use on multivariate analysis included Medicaid insurance (odds ratio [OR]: 17.6 [2.2-139.3]), history of wheezing (OR: 18.3 [4.4-75.8]), and belief that antibiotics treat colds (OR: 4.2 [1.4-12.9]). Predictors of ambulatory care use included parent younger than 30 years (OR: 10.0 [1.6-64.3]), history of wheezing (OR: 5.6 [1.1-29.7]), and belief that antibiotics treat colds (OR: 3.8 [1.7-8.5]). CONCLUSIONS: Misconceptions about the appropriate treatment of colds are predictive of increased health service utilization. Targeted educational interventions for families may reduce inappropriate antibiotic-seeking behavior and unnecessary health service utilization for colds.

Adult↗
PubMed1995

Increased dipsogenic responsiveness to angiotensin II in rats exposed to cold: rate of loss after return to thermoneutral ambient temperature.

Subcutaneous administration of angiotensin II (Ang II) to rats exposed chronically to 5 degrees C induced an increased drinking response compared with that of warm-acclimated controls. The exaggerated drinking response was also observed when graded doses of Ang II were administered into the lateral cerebroventricle (icv) of chronically cold-exposed rats. A maximal drinking response occurred in cold-treated, but not in control, rats when the lowest dose of Ang II (1.6 ng/rat) was administered icv. Thus, it is clear that the dipsogenic responsiveness to either centrally or peripherally administered Ang II is increased by chronic exposure to cold. To assess whether the increased responsiveness was retained after removal from cold, graded doses of Ang II were administered to rats removed from cold to a thermoneutral environment. The results again showed a maximal responsiveness to the lowest dose of Ang II administered (25 micrograms/kg, sc) to cold-treated rats that had either just been removed from cold or removed from cold 2 hr prior to treatment. Cold-exposed rats had an ED50 for Ang II-induced drinking that was about half that of their warm-acclimated controls. To assess how long the cold-induced increase in dipsogenic responsiveness to Ang II lasted after return to a thermoneutral temperature, rats were removed from cold for 24, 48, or 60 hr and then administered graded doses of Ang II (25, 50, or 100 micrograms/kg, sc). The results suggest that between 46 and 52 hr after removal from cold, the cold-induced increase in dipsogenic responsiveness to Ang II returned to the level of the controls. Hence, the physiological changes in the dipsogenic mechanism induced by exposure to cold are not immediately reversible when the rats are returned to a thermoneutral ambient temperature.

Angiotensin II↗
PubMed1987

[Cold constitution: analysis of the questionnaire].

"Hie-sho" means having a cold constitution. The authors studied basic data for cold constitution with a questionnaire and with the Cornell Medical Index. The subjects were 318 females, and the average age was 26.4 +/- 6.1 (Mean +/- SD) and the range was 20 approximately 51 years of age. The results were as follows: (1) 38.7% of the subjects had been conscious of having a cold constitution, and it was recognized that the subjects with a cold constitution are found not only in the climacterium but also in the young. (2) The average age of onset of cold constitution was 19.3 +/- 5.1 years old. (3) The parts of the body that usually felt cold were first the feet and then the hands. (4) In winter or at bedtime the cold sensation was increased. And it is characteristic that the sensation was changed by weather or by body condition, especially by the stimulation of coldness. (5) Most subjects with a cold constitution took care in their daily life, but very few of them were treated. (6) Many other physical symptoms were recognized in subjects with a cold constitution, and their CMI scores were high. Therefore these data may be regarded as indicating that most cases of cold constitution are a partial symptom of vegetative disturbance (autonomic nerve dysfunction). (7) Most of the mothers of subjects with a cold constitution also had a cold constitution, which suggests the involvement of a hereditary factor concerning in the development of a cold constitution.

Adult↗
PubMed1992

Effects of cold stress on some 5-HT1A, 5-HT1C and 5-HT2 receptor-mediated responses.

The purpose of the present study was to analyze the influence of stress (24-h cold exposure) on presynaptic 5-HT1A receptors, and on postsynaptic 5-HT1A, 5-HT1C and 5-HT2 receptors. Cold exposure for 24 h affected neither pargyline-induced decreases in 5-hydroxyindoleacetic acid (5-HIAA) levels in midbrain and rest of brain, nor plasma glucose and corticosterone levels. Treatment with the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.5-1 mg/kg), 3-5 h after the end of cold exposure triggered less intense flat body posture and forepaw treading in cold-exposed rats than in controls. On the other hand, 15- and 30-min plasma glucose responses to 8-OH-DPAT (0.25-0.5 mg/kg, 3-5 h after cold) or to the alpha 2-adrenoceptor agonist, clonidine (0.025 mg/kg), were not affected by cold, while the 15-min, but not the 30 min, plasma corticosterone response to 8-OH-DPAT was slightly amplified in cold-exposed rats. Cold exposure affected neither the inhibitory effect of 8-OH-DPAT (0.25-0.5 mg/kg, 3-5 h after cold) on midbrain 5-HIAA levels, nor the hypothermic effect of 8-OH-DPAT (0.5-1 mg/kg, 3-5 h after cold). Lastly, the hypoactivity elicited by the 5-HT1C receptor agonist, m-chlorophenyl-piperazine (1.5-3 mg/kg, 3-5 h after cold), or head shakes elicited by the 5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (1-2 mg/kg, 3-5 h after cold), were of similar intensities in control and in cold-exposed rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

A spontaneous increase of salt intake and changes of colonic temperature in mice exposed to cold.

The effect of repeated short-term exposure to cold on spontaneous salt (NaCl) intake and colonic temperature was investigated in two experiments on mice. In Experiment 1, half of a group of test animals were exposed to cold (7-9 degrees C; 6h/day; 4 days), and half of both the exposed and non-exposed animals were allowed to choose between drinking water with (0.9%) and without (0%) NaCl. Food and fluids were provided all day long during the experiment. Mice provided with NaCl solution showed increased salt intake with cold exposure. Colonic temperature of mice was measured twice a day at the beginning and the end of cold exposure. Different changes in colonic temperature among the groups were observed at the end of cold exposure. In mice exposed to cold and provided with NaCl solution, colonic temperatures stayed unchanged, whereas in those without NaCl solution colonic temperatures decreased significantly after cold exposure. In Experiment 2, all the mice were exposed to cold as in Experiment 1. Four patterns of feeding of food and fluids were applied to groups of eight mice each: removal of food and fluids during cold; removal during 9 h before cold and during cold; removal during cold and during 9 h after cold, and feeding all day long. Half the mice in each feeding pattern were allowed to choose NaCl fluids (0% & 0.9%). Colonic temperature was measured as in Experiment 1. In all the feeding patterns, colonic temperature was significantly lower in the mice without NaCl solution than those with NaCl solution. Among four feeding patterns in mice with NaCl solution, colonic temperature was significantly higher in the case of feeding all day long than in the other three patterns.

Analysis of Variance↗
PubMedDate not supplied

Body fluid distribution in rats with cold-induced hypertension.

The purpose of this experiment was to determine body fluid distribution during chronic cold exposure and to further understand the mechanism of cold-induced hypertension. Blood pressures, hematocrit, and the plasma, blood, and extracellular fluid volumes were measured in rats at intervals of 1, 3, and 5 weeks after exposure to cold (5 degrees C). Resting systolic, diastolic, and mean blood pressures measured by direct arterial cannula were significantly elevated in a time-dependent manner over the duration of cold exposure. The increase in diastolic blood pressure, which reflects the peripheral vascular resistance, exceeded that of systolic blood pressure after both 3 and 5 weeks of exposure to cold. Pulse pressure was significantly decreased by 3 and 5 weeks of cold exposure. The plasma, blood, and extracellular fluid volumes were significantly increased after both 1 and 3 weeks of exposure to cold, but had returned to control levels by 5 weeks of cold exposure. Cold exposure, however, did not affect the hematocrit. The 2-h water intake after the cold-exposed rats were returned to warm (25 degrees C) (thermogenic drinking) was significantly increased compared to that of warm-acclimated rats during the first, third, and fifth week of exposure to cold. The present results suggest that the development of cold-induced hypertension is associated with blood volume expansion, and that the elevated blood pressure is maintained by increased peripheral vascular resistance without blood volume expansion. The results also imply that exposure to cold induces a dehydration in rats.

Acclimatization↗
PubMed1995

A canine study of cold water drowning in fresh versus salt water.

OBJECTIVE: To compare the pathophysiologic changes occurring during drowning in cold fresh water and cold salt water with reference to viability. DESIGN: Randomized, prospective, controlled submersion experiments in two contrasting cold liquids. SETTING: A laboratory at a large university-affiliated medical institution. SUBJECTS: Thirteen healthy, anesthetized mongrel dogs. Three dogs served as controls and were immersed but not submerged. The remainder were submerged in cold fresh water or cold salt water (4 degrees C). INTERVENTIONS: Catheters were placed in the femoral artery, right carotid artery and right internal jugular vein. Electrocardiogram, pneumogram, and rectal temperatures were measured continuously during submersion/immersion. MEASUREMENTS AND MAIN RESULTS: Cold water submersion with drowning produced a large initial decrease in carotid artery temperature (approximately 7.5 degrees C in the first 2 mins) compared with a minor decrease (approximately 0.8 degrees C with immersion). No significant differences were noted in the rate of decrease of temperature between drowning in fresh water and salt water. During cold fresh water drowning, aspiration produced gross hemodilution with an average increase in body weight of 16.5%. Hematocrit values, serum sodium concentrations, and osmolality decreased while serum potassium concentrations, catecholamines, and free hemoglobin increased. All measured biochemical data (except PaO2) remained at viable levels. By contrast, during cold salt water drowning, average body weight increased by only 6%, with hemoconcentration and a shrinkage of vascular volume. Hematocrit and hemoglobin values increased by 30%, but initial plasma free hemoglobin values remained unchanged. Serum sodium concentrations, osmolality, and potassium concentrations increased rapidly to critical levels. CONCLUSIONS: On submersion in cold water, all of the experimental animals developed tachypnea immediately, followed by aspiration with predictable effects. The biochemical and pathophysiologic changes in cold water drowning approximated those changes reported for warm water drowning for both fresh and salt water with one exception and continued aspiration of cold water produced extremely rapid core cooling as long as the circulation remained intact. This process of acute submersion hypothermia may protect the brain temporarily from lethal damage, as reported in cases of cold fresh water drowning. Concentrations of circulating catecholamines increased exponentially in both groups of test animals. Clinically, their acute effects on the circulation, compounded by significant hypothermia and extreme anoxia, must hamper the detection of residual circulation at rescue and may play a role in sudden death from cold water in the absence of drowning.

Animals↗
PubMed2006

Transcriptome analysis of cold acclimation in barley albina and xantha mutants.

Previously, we have shown that barley (Hordeum vulgare) plants carrying a mutation preventing chloroplast development are completely frost susceptible as well as impaired in the expression of several cold-regulated genes. Here we investigated the transcriptome of barley albina and xantha mutants and the corresponding wild type to assess the effect of the chloroplast on expression of cold-regulated genes. First, by comparing control wild type against cold-hardened wild-type plants 2,735 probe sets with statistically significant changes (P = 0.05; > or = 2-fold change) were identified. Expression of these wild-type cold-regulated genes was then analyzed in control and cold-hardened mutants. Only about 11% of the genes cold regulated in wild type were regulated to a similar extent in all genotypes (chloroplast-independent cold-regulated genes); this class includes many genes known to be under C-repeat binding factor control. C-repeat binding factor genes were also equally induced in mutants and wild-type plants. About 67% of wild-type cold-regulated genes were not regulated by cold in any mutant (chloroplast-dependent cold-regulated genes). We found that the lack of cold regulation in the mutants is due to the presence of signaling pathway(s) normally cold activated in wild type but constitutively active in the mutants, as well as to the disruption of low-temperature signaling pathway(s) due to the absence of active chloroplasts. We also found that photooxidative stress signaling pathway is constitutively active in the mutants. These results demonstrate the major role of the chloroplast in the control of the molecular adaptation to cold.

Acclimatization↗
PubMed1972

Habituation and acclimatization of sheep to cold following exposures of varying length and severity.

1. Male and female Scottish Blackface sheep were shorn and exposed for 2 weeks either to a thermoneutral temperature (+30 degrees C), to chronic cold (+8 degrees C) or to +30 degrees C interrupted by daily short cold shocks (-10 degrees C). During and at the end of these conditioning treatments, the sheep also received two acute cold exposures (-20 degrees C, 4 m.p.h. wind for 2-8 hr) 1 week apart. Some of these sheep and a fourth (control) group, were subsequently re-shorn and slowly cooled to +8 degrees C.2. Resting metabolism and the metabolic response to cooling (both inferred from heart rates) were increased by previous chronic cold treatment. Resistance to body cooling (measured during acute cold exposure) was generally increased by both chronic and acute cold, and non-shivering thermogenesis was probably induced in the female sheep. These effects were defined as acclimatization.3. In contrast, cold shocks reduced the subsequent metabolic response to cold and encouraged facultative body cooling. This pattern of response (defined as habituation) therefore caused greater thermolability.4. Habituation and acclimatization were antagonistic. Habituation was removed by acute cold exposure and, conversely, acclimatization was inhibited by short cold shocks.5. There were sex differences in response but these were confounded by probable differences in insulation and in body condition (males thinner).6. It was concluded that the induction of different forms of adaptation depended on the length, severity and frequency of cold exposures. Habituation to whole body cold exposure apparently involved central nervous system centres normally receiving peripheral cold stimuli.

Acclimatization↗
PubMed2005

Effects of chronic cold exposure on the endothelin system.

Cold temperatures have adverse effects on the human cardiovascular system. Endothelin (ET)-1 is a potent vasoconstrictor. We hypothesized that cold exposure increases ET-1 production and upregulates ET type A (ETA) receptors. The aim of this study was to determine the effect of cold exposure on regulation of the ET system. Four groups of rats (6-7 rats/group) were used: three groups were exposed to moderate cold (6.7 +/- 2 degrees C) for 1, 3, and 5 wk, respectively, and the remaining group was maintained at room temperature (25 degrees C) and served as control. Cold exposure significantly increased ET-1 levels in the heart, mesenteric arteries, renal cortex, and renal medulla. Cold exposure increased ETA receptor protein expression in the heart and renal cortex. ET type B (ETB) receptor expression, however, was decreased significantly in the heart and renal medulla of cold-exposed rats. Cold exposure significantly increased the ratio of ETA to ETB receptors in the heart. An additional four groups of rats (3 rats/group) were used to localize changes in ETA and ETB receptors at 1, 3, and 5 wk of cold exposure. Immunohistochemical analysis showed an increase in ETA, but a decrease in ETB, receptor immunoreactivity in cardiomyocytes of cold-exposed rats. Increased ETA receptor immunoreactivity was also found in vascular smooth muscle cells of cold-exposed rats. Cold exposure increased ETA receptor immunoreactivity in tubule epithelial cells in the renal cortex but decreased ETB receptor immunoreactivity in tubule epithelial cells in the renal medulla. Therefore, cold exposure increased ET-1 production, upregulated ETA receptors, and downregulated ETB receptors.

Animals↗
PubMed1998

Thermal responses from repeated exposures to severe cold with intermittent warmer temperatures.

This study was conducted to evaluate physiological reaction and manual performance during exposure to warm (30 degrees C) and cool (10 degrees C) environments after exposure to very low temperatures (-25 degrees C). Furthermore, this experiment was conducted to study whether it is desirable to remove cold-protective jackets in warmer rooms after severe cold exposure. Eight male students remained in an extremely cold room for 20 min, after which they transferred into either the warm room or the cool room for 20 min. This pattern was repeated three times, and the total cold exposure time was 60 min. In the warm and cool rooms, the subjects either removed their cold-protective jackets (Condition A), or wore them continuously (Condition B). Rectal temperature, skin temperatures, manual performance, blood pressure, thermal, comfort and pain sensations were measured during the experiment. The effects of severe cold on almost all measurements in the cool (10 degrees C) environment were greater than those in the warm (30 degrees C) environment under both clothing conditions. The effects of severe cold on all measurements under Condition A except rectal temperature and toe skin temperature were significantly greater than those under Condition B in the cool environment but, not at all differences between Condition A and Condition B in the warm environments were significant. It was recognized that to remove cold-protective jackets in the cool room (10 degrees C) after severe cold exposure promoted the effects of severe cold. When rewarming in the warm resting room (30 degrees C), the physiological and psychological responses and manual performance were not influenced by the presence or absence of cold-protective clothing. These results suggest that it is necessary for workers to make sure to rewarm in the warm room outside of the cold storage and continue to wear cold-protective clothing in the cool room.

Adult↗
PubMed1988

[Effects of cold acclimation and repetitive stress on stress-induced neuroendocrine response].

In order to elucidate the mechanism (S) involved in improved cold tolerance by means of enhanced non-shivering thermogenesis of the repetitively stressed rats, noradrenaline (NA) turnover of brown adipose tissue (BAT) and adrenocortical responses were investigated. (1) NA turnover of BAT in the cold-acclimated rats was greater than that in the resting controls. NA level of BAT in the cold-acclimated rats decreased to about 40% of the control level. It was thus inferred that this lower NA levels was induced by accelerated NA turnover. (2) NA turnover of BAT in the stressed rats after repetitive immobilization stress was higher than that of the non-stressed controls. Therefore, increased sympathetic activity of BAT would be one of the mechanisms of cross adaptation between cold and stress. (3) NA turnovers of BAT in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C). NA turnovers of BAT in the controls and the stressed rats were increased by acute immobilization stress. (4) Plasma corticoids (corticosterone and deoxycorticosterone) in the cold-acclimated rats were higher than that of controls. Plasma corticoids in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C, 15 min) and acute immobilization stress (30 min). The extents of increases in plasma corticoids in the stressed rats, but not in the cold-acclimated ones, were greater than those in the controls. It was suggested that repetitive immobilization stress could enhance nonshivering thermogenesis via an enhanced responsiveness of adrenocortical secretion to acute stress and cold. It would be concluded from these results that enhanced responses of corticoid secretion and accelerated sympathetic activity were associated with the establishment of cross adaptation between cold and stress. It was suggested that the extent of participation of these factors was not necessarily the same between the cold-acclimated and the stressed organisms.

Acclimatization↗
PubMed1987

Effect of hydrostatic pressure on plasma concentrations of norepinephrine during cold water immersion.

Head-out immersion of humans in cold water concurrently stimulates low-pressure receptors and cutaneous cold receptors. In theory, the low-pressure receptors inhibit sympathetic nerve activity to the extent of modifying plasma norepinephrine responses to chilling of the skin. Human plasma norepinephrine concentrations ([NE]p's) were measured when low-pressure receptors were stimulated by 6 h of head-out immersion in thermoneutral water (35 degrees C). The experimental protocol was repeated when cold receptors were activated by a separate exposure to 14.8 degrees C air. Furthermore, both types of receptors were activated by 6 h of immersion in cold water (29.8 degrees C). The control exposure maintained [NE]p close to a constant value of 0.34 ng/ml. Thermoneutral water reduced [NE]p to 0.18 ng/ml after 30 min of immersion, but the change was not statistically significant (two-way ANOVA). [NE]p increased to peak values of 1.5 ng/ml in cold air (P less than 0.05) and 1.1 ng/ml in cold water (P less than 0.5), with no significant differences observed between [NE]p's in cold air and cold water. Equal rates of body heat loss occurred during the exposures to cold air and cold water. Since [NE]p's were comparably raised by separate exposures to cold water and cold air, stimulation of low-pressure receptors by immersion did not significantly depress peripheral vasomotor nerve activity during head-out immersion in cold water.

Adult↗