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PubMed1983

Interactions of cold exposure and starvation on glucose tolerance and insulin response.

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. "Accelerated starvation" induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15-18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.

Acclimatization↗
PubMed2003

Mitochondrial proliferation in the permanent vs. temporary cold: enzyme activities and mRNA levels in Antarctic and temperate zoarcid fish.

Adjustments in mitochondrial properties and capacities are crucial in acclimatization to seasonal cold and in evolutionary cold adaptation of marine ectotherms. Although long-term compensatory increments in aerobic capacity of fish tissues have frequently been described in response to cold, much less is known about transitional phases and gene expression patterns involved. We investigated the time course of adjustment to acute cold in liver of eurythermal eelpout Zoarces viviparus. Whereas citrate synthase (CS) activity rose progressively in liver, cytochrome c oxidase (COX) activity was not altered during cold acclimation. Species-specific RNA probes were used to determine mRNA levels. CS mRNA (nuclear encoded) displayed a delayed, transient increase in response to cold, such that transcript levels did not parallel the change in enzyme activity. The enzyme activities and mRNA levels in the confamilial Antarctic Pachycara brachycephalum indicate cold compensation of CS activity in this cold-adapted species. The ratio of CS and COX activities was elevated in acclimation and adaptation to cold, indicating enhanced citrate synthesis over respiratory chain capacities in cold-adapted liver mitochondria. This may support enhanced lipid synthesis typically found in cold. The ratio of enzyme activity and transcript levels differed largely between Z. viviparus populations from the Baltic and North Seas, indicating the influence of unidentified parameters other than temperature. Transcript levels may not be tightly correlated with enzyme activities during thermal adaptation and thereafter. The time course of the acclimation process indicates that regulation at the translational and posttranslational levels predominates in adjustment to moderate thermal challenges.

Acclimatization↗
PubMed2004

Genetic AT1A receptor deficiency attenuates cold-induced hypertension.

The aim of this study was to test our hypotheses that AT1A receptors play a role in the pathogenesis of cold-induced hypertension (CIH) and in the cold-induced increase in drinking responses to ANG II. Two groups of wild-type (WT) and two groups of AT1A receptor gene knockout (AT1A-KO) mice were used (6/group). Blood pressures (BP) of the four groups were similar during the control period at room temperature (25 degrees C). After the control period, one group of WT and one group of AT1A-KO mice were exposed to cold (5 degrees C), while the remaining groups were kept at 25 degrees C. BP of the cold-exposed WT group elevated significantly within 1 wk of exposure to cold and increased gradually to a maximum level by week 5. However, there was only a slight increase in BP of the cold-exposed AT1A-KO group. The maximal cold-induced increase in BP (DeltaBP) is significantly less in AT1A-KO group (11 +/- 3 mmHg) than in WT group (49 +/- 6 mmHg), indicating that AT1A receptor deficiency attenuates cold-induced elevation of BP. Interestingly, both WT and AT1A-KO mice developed cardiac and renal hypertrophy to the same extent. AT1A-KO caused a significant increase in urine and plasma levels of nitric oxide (NO), indicating that the renin-angiotensin system inhibits NO formation probably via AT1A receptors. Cold exposure inhibited endothelial NO synthase protein expressions and decreased urine and plasma levels of NO, which may be mediated partially by AT1A receptors. AT1A-KO completely abolished the cold-induced increase in drinking responses to ANG II. We conclude that 1) AT1A receptors play an essential role in the pathogenesis of CIH but not cardiac hypertrophy; 2) the role of AT1A receptors in CIH may be mediated partially by its inhibitory effect on the NO system; and 3) cold-induced increase in drinking response to ANG II is mediated by AT1A receptors.

Angiotensin II↗
PubMed1981

Extracerebral deep-body cold sensitivity in the Pekin duck.

Pekin ducks, in which cerebral cold sensitivity is negligible, were submitted to general body cooling at warm, thermoneutral, and cold ambient temperature (Ta) with an intestinal thermode. In some animals, hypothermia was enhanced by additional hypothalamic cooling that suppressed cold defense. In other animals, the spinal cord was cooled, either selectively or during intestinal cooling. From core temperature (Tc) and metabolic heat production (M) an overall cold sensitivity of about -5 to -6 W . kg-1 . degrees C-1 was determined at thermoneutrality. Maximum M amounted to four to five times the resting M of 3.8 W . kg-1 and was attained when Tc fell by 2.5 degrees C or more. In the cold, threshold Tc for the activation of M was elevated; overall cold sensitivity remained constant. In the warmth, threshold Tc was lowered; overall cold sensitivity was reduced, if mean skin temperature (Tsk) remained at aout 39 degrees C or higher. Spinal cold sensitivity amounted to about -0.25 W . kg-1 . degrees C-1 at normal Tc and thermoneutral and warm Ta; it increased to aout -0.50 W . kg-1 . degrees C-1 in the cold and during hypothermia. Peripheral cold sensitivity was estimated from Tsk and M as -0.4 to -0.8 W . kg-1 . degrees C-1. It is concluded that overall cold sensitivity in ducks mainly depends on deep-body temperature sensors outside of the central nervous system.

Animals↗
PubMed1985

Urinary responses to cold temperature during water immersion.

If cold temperature combines with ambient water pressure to stimulate the Henry-Gauer reflex in humans, then free water clearance (CH2O) should be greater during immersion in cold water (29.8 degrees C) than during exposure to cold air (14.8 degrees C) or immersion in thermoneutral water (35 degrees C). Urinary responses to these environments were compared with control measurements made during 6 h of sitting in thermoneutral air (27.6 degrees C). CH2O was not significantly greater in cold water than in the other environments. Rather, the diuretic response was characterized by an increased osmolar clearance (P less than 0.05). Cold temperature and water pressure additively raised urinary output during cold water immersion, with ambient water pressure accounting for two-thirds of the urinary water loss. An elevated rate of sodium excretion (P less than 0.05) began significantly earlier in cold water than in thermoneutral water. This effect of low temperature might have resulted from cold-induced vasoconstriction, since cold temperatures was observed to reduce the foot volume. Sodium excretion was inversely proportional to vital capacity, indicating a responsiveness of the kidney to expansion of the central blood volume. In addition to the effects of water pressure and cold temperature, urinary function was also sensitive to time. The rate of potassium excretion was significantly elevated at min 199 of exposure to all environments. Failure of CH2O to increase above control values indicated that the human diuretic response to cold water immersion is atypical for the Henry-Gauer reflex.

Body Temperature Regulation↗
PubMed2000

Skeletal and cardiac muscle protein turnover during cold acclimation in young rats.

The effect of long-term cold exposure on skeletal and cardiac muscle protein turnover was investigated in young growing animals. Two groups of 36 male 28-day-old rats were maintained at either 5 degrees C (cold) or 25 degrees C (control). Rates of protein synthesis and degradation were measured in vivo on days 5, 10, 15, and 20. Protein mass by day 20 was approximately 28% lower in skeletal muscle (gastrocnemius and soleus) and approximately 24% higher in heart in cold compared with control rats (P < 0.05). In skeletal muscle, the fractional rates of protein synthesis (k(syn)) and degradation (k(deg)) were not significantly different between cold and control rats, although k(syn) was lower (approximately -26%) in cold rats on day 5; consequent to the lower protein mass, the absolute rates of protein synthesis (approximately -21%; P < 0. 05) and degradation (approximately -13%; P < 0.1) were lower in cold compared with control rats. In heart, overall, k(syn) (approximately +12%; P < 0.1) and k(deg) (approximately +22%; P < 0.05) were higher in cold compared with control rats; consequently, the absolute rates of synthesis (approximately +44%) and degradation (approximately +54%) were higher in cold compared with control rats (P < 0.05). Plasma triiodothyronine concentration was higher (P < 0.05) in cold compared with control rats. These data indicate that long-term cold acclimation in skeletal muscle is associated with the establishment of a new homeostasis in protein turnover with decreased protein mass and normal fractional rates of protein turnover. In heart, unlike skeletal muscle, rates of protein turnover did not appear to immediately return to normal as increased rates of protein turnover were observed beyond day 5. These data also indicate that increased rates of protein turnover in skeletal muscle are unlikely to contribute to increased metabolic heat production during cold acclimation.

Acclimatization↗
PubMed1991

Prevention of cold-induced increase in blood pressure of rats by captopril.

To assess the possibility that the renin-angiotensin system may play a role in the development of cold-induced hypertension, three groups of rats were used. Two groups were exposed to cold (5 +/- 2 degrees C) while the remaining group was kept at 26 +/- 2 degrees C. One group of cold-treated rats received food into which captopril (0.06% by weight) had been thoroughly mixed. The remaining two groups received the same food but without captopril. Systolic blood pressure of the untreated, cold-exposed group increased significantly above that of the warm-adapted, control group within 4 weeks of exposure to cold. In contrast, chronic treatment with captopril prevented the elevation of blood pressure. Rats were killed after 4 months of exposure to cold. At death, the heart, kidneys, adrenal glands, and interscapular brown fat pad were removed and weighed. Although captopril prevented the elevation of blood pressure in cold-treated rats, it did not prevent hypertrophy of the kidneys, heart, and interstitial brown adipose tissue that characteristically accompanies exposure to cold. Thus, chronic treatment with captopril prevented the elevation of blood pressure when administered at the time exposure to cold was initiated. It also reduced the elevated blood pressure of cold-treated rats when administered after blood pressure became elevated. This suggests that the renin-angiotensin system may play a role in the elevation of blood pressure during exposure to cold.

Animals↗
PubMed1990

Cytochemical studies of responses of corticotropes and thyrotropes to cold and novel environment stress.

Cold stress stimulates the release of both ACTH and TSH from the pituitary. More striking changes in ACTH content have been seen in the intermediate lobe after cold stress. Therefore, this study was designed to test responses of individual anterior lobe corticotropes to cold exposure. Male rats were exposed to either 30 min of cold (+3-5 C), 30 min of a novel, temperate environment (+24 C) or were unstressed (+24 C). Pituitaries were fixed and embedded in preparation for immunolabeling for ACTH or TSH-beta at the light (semithin sections) and electron microscopic levels. The semithin sections were used to measure areas of corticotropes and thyrotropes with Bioquant image analysis equipment. Separate groups of pituitaries were dissociated and the cells were cultured for 2 or 15 h. Then the cells were stimulated for 5-10 min with biotinylated analogs of corticotropin-releasing hormone (bio-CRH) or arginine vasopressin (bio-AVP) to detect the target cells cytochemically. A third group of dissociated cells were fixed for immunolabeling for ACTH, 16K fragment of pro-opiomelanocortin, beta-endorphin, or TSH-beta. Cold exposure resulted in a 1-4-fold increase in the levels of serum ACTH over that of unstressed rats. This was correlated with a 40% increase in the percentage of cells that contained 16K fragment and a 30-40% increase in percentages of cells storing ACTH or beta-endorphin. Cold stress also increased the percentage of cells that bound bio-CRH or bio-AVP by 45%. Analyses of semithin sections showed that areas of corticotropes increased by 21% following cold stress. The number of rows of immunolabeled (ACTH) secretion granules also increased in corticotropes from cold-stressed rats. Exposure to a novel environment for 30 min resulted in no significant increase in serum ACTH over that of unstressed rats. There was, however, a 20% increase in percentages of cells that stored 16K fragment, beta-endorphin, or target cells that bound bio-CRH. However, the corticotropes were not significantly larger. Many of the cells exhibited reduced numbers of immunolabeled secretory granules. Other corticotropes resembled those from cold-stressed rats. When TSH cells were studied, their percentages increased from 8 +/- 3% to 15.8 +/- 4% and their areas increased by 22% following exposure to cold. After exposure to a novel environment, percentages of cells that stored TSH-beta increased to 11 +/- 2%, however, no changes in areas of TSH cells were measured. These studies demonstrated that the anterior lobe corticotrope is clearly activated by exposure to both cold and novel environment.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed2003

Characterization of calreticulin as a phosphoprotein interacting with cold-induced protein kinase in rice.

Calreticulin is an abundant endo/sarcoplasmic reticulum Ca2+-binding protein. To investigate whether calreticulin (CRO1) is involved in the cold-stress response in rice, a transgenic plant was constructed. The transcriptional level was decreased within 30 min and recovered within 2 h of a cold treatment. The calreticulin protein was shifted from a soluble fraction to an insoluble fraction by cold stress. Endogenous abscisic acid (ABA) is an important factor in cold response, and the synthesis of ABA was strongly induced in CRO1-sense transgenic rice, the same as in cold-sensitive rice. The phosphorylation of calreticulin increased after cold treatment. Over-expression of calreticulin enhanced the activities of 47 kDa Ca2+-dependent protein kinase (CDPK) that had been induced by cold treatment. The 47-kDa CDPK activity increases more in the cold sensitive variety IR36 and the sense transgenic rice than it does in other varieties. The synthesis of ABA, phosphorylation of calreticulin and 47-kDa CDPK activity induced in sense transgenic rice were the same as in cold-sensitive rice and the phosphorylation of antisense transgenic rice was similar to that of cold-tolerant rice. These results suggest that the calreticulin is involved in the signaling pathway leading to response to cold stress.

Calreticulin↗
PubMed1997

[Effects of phenylalanine and tyrosine on cold acclimation in mice].

The effects of phenylalanine (PHE) and tyrosine (TYR) on cold acclimation were studied in mice of the ddY strain. At 5 weeks of age, mice were maintained at 4 degrees C for 4 weeks. Test groups of mice were supplied with a 0.05% (w/v) solution of PHE or TYR as drinking water in addition to water. We measured changes in body weight, intake of water and food, rectal temperature upon acute exposure to -20 degrees C, weight of interscapular brown adipose tissue (BAT) and the levels of glucose, nonesterified fatty acids (NEFA) and 3H-butyrate in the blood prior to and after exposure to the lower temperature of -20 degrees C. Chronic exposure to cold (4 degrees C) reduced body-weight gain for the first two weeks but weight gain recovered within the next two weeks. PHE and TYR partially inhibited the gain in body weight under exposing to cold. TYR reduced the gain of body weight under room temperature. Exposure to cold stimulated the daily consumption of food. Both PHE and TYR somewhat enhanced the food intake when exposed to cold. Exposure to cold rendered mice resistant to severe cold (-20 degrees C). Both PHE and TYR did not reduce this resistance except in the early state in the case of TYR. Exposure to cold increased the weight of BAT but both PHE and TYR prevented this increase. The effect of TYR was determined in the case fed under room temperature. Cold exposure changed the utilization of glucose, NEFA and 3H-butyrate in the blood when exposed to severe cold (-20 degrees C). Both PHE and TYR prevented the change in NEFA. It remains to be confirmed whether the growth of brown adipocytes is always necessary when mice acclimate to cold.

Acclimatization↗
PubMed1997

[Effects of adenosine and adenine on cold acclimation in mice].

The effects of adenosine (ADO) and adenine (ADE) on cold acclimation were studied in mice of the ddY strain. At 5 weeks of age, mice were maintained at 4 degrees C for 4 weeks. Test groups of mice were supplied with a 0.05% (w/v) solution of ADO or ADE as drinking water in addition to water. We measured changes in body weight, intake of water and food, rectal temperature upon acute exposure to -20 degrees C, weight of interscapular brown adipose tissue (BAT) and the levels of glucose, nonesterified fatty acids (NEFA) and 3H-butyrate in the blood prior to and after exposure to the lower temperature of -20 degrees C. Chronic exposure to cold (4 degrees C) reduced body-weight gain for the first two weeks but weight gain recovered within the next two weeks. ADO partially but selectively inhibited the gain in body weight. This effect was marked in mice maintained at room temperature. Such an inhibitory effect was the case of ADE in the room temperature. Exposure to cold stimulated the daily consumption of food. ADO further and selectively enhanced food intake, but ADE enhanced that in room temperature. Cold increased in daily intake of water. Both ADO and ADE accelerated the intake of water. This effect was marked in mice maintained at 4 degrees C and the effect of ADE was considerable. Mice chose to drink the water that contained ADO, while the choice of water that contained ADE was apparent only during exposure to cold. Exposure to cold rendered mice resistant to severe cold (-20 degrees C). ADO and ADE partially reduced this resistance. Exposure to cold increased the weight of BAT but ADO selectively prevented this increase. Cold did not change the levels of the various compounds measured in the blood. In mice exposed to 4 degrees C for 4 weeks, acute exposure to severe cold decreased the glucose level and increased the levels of NEFA and 3H-butyrate. ADO selectively prevented the changes in the levels of NEFA and 3H-butyrate. It remains to be confirmed whether the growth of brown adipocytes is always necessary when mice acclimate to cold.

Acclimatization↗
PubMed2001

Adult female Drosophila pseudoobscura survive and carry fertile sperm through long periods in the cold: populations are unlikely to suffer substantial bottlenecks in overwintering.

To assess whether, while overwintering, natural populations of Drosophila pseudoobscura are likely to experience substantial bottlenecks in their numbers and genotypes, laboratory tests of the cold sensitivities of each stage of the life history and reproduction were undertaken. Three genetically distinctive lineages established from flies caught at high elevation were used for testing in temperatures likely to persist in protected pockets of fermenting deciduous leaf fall in overwintering sites. Sensitivities to cold of each stage in development were measured as frequencies of survival to adulthood following a period in 5 degrees C in a particular stage. The cold sensitivity of adults was measured as the survival in and following cold stays in adulthood. It was found that cold sensitivity decreases as development progresses, but that only adults (females more than males) are able to withstand long periods in the cold. The cold sensitivity of reproductive capacity of males was scored as their success in mating following a two-month cold stay, and of females as the numbers laying fertile eggs following periods of months in the cold. Both males and females maintain reproductive capacity. Of particular significance, however, is that even after six months in the cold females are able to restart production of eggs and these eggs may be fertilized by the sperm of matings prior to their cold stay. Thus, a substantial proportion of overwintering genomes must be those of adult females and those of the sperm carried by females from matings in the previous summer. This simple finding strongly suggests that populations are not likely to suffer substantial bottlenecks while overwintering. Further, it indicates how arrays of genetic variation may be maintained through winters and largely avoid winter selective pressures. Frequent migration between populations is therefore not required to maintain the variation commonly found in populations throughout the species range.

Animals↗
PubMed1982

Thermal and metabolic responses of temperature-acclimated rats during cold and heat exposures.

Some endocrine and metabolic responses to acute cold and heat exposures were observed in rats acclimated to cold, heat, or both cold and heat. Rats exposed to both cold (12 hr, 5 degrees C) and heat (12 hr, 34 degrees C) for 4 to 5 weeks (CHA) showed less fall of colonic temperature (Tc) in the cold (-5 degrees C) than heat-acclimated rats (34 degrees C, 4 to 5 weeks) (HA) and warm controls (WC), but a greater fall than cold-acclimated rats (5 degrees C, 4 to 5 weeks) (CA). CHA possessed a larger quantity of interscapular brown adipose tissue and showed greater cold-induced oxygen consumption (VO2) than WC and HA but less than CA. Blood glycerol levels rose similarly in all groups in the cold, while the increase in blood free fatty acids (FFA) levels was significantly greater in HA and smaller in CA than in WC and CHA. Acute cold exposure caused the elevation of plasma glucagon level in WC and HA, but not in CA and CHA. It lowered plasma insulin levels in HA, and the insulin/glucagon molar ratio (I/G) in WC, HA, and CHA. All groups showed the same increases in Tc during acute heat exposure (34 degrees C). However, the heat-induced increase in VO2 was greater in WC than in HA, CA, and CHA. Blood metabolite levels were not affected by acute heat exposure in all groups. Plasma glucagon levels decreased in CHA, while plasma insulin levels increased in WC and CA. I/G increased in WC and CHA. These results indicate that thermal and metabolic responses would be modified by previous exposures to cold, heat, and cold-heat.

Acclimatization↗
PubMed2002

Effects of long-term cold exposure on contractile muscles of rats.

The effects of 20-week cold exposure on contractile properties of soleus and extensor digitorum longus (EDL) muscles and plasma hormone levels were studied in rats. Twenty male Wistar rats (5 week old) were randomly divided into 2 groups (n = 10 each): cage-control and cold-exposed. The rats in the cold-exposed group were immersed in shoulder-deep water (approximately 18 degrees C) for 1 h/d, 5 d/week, for 20 weeks. The temperature and humidity of the animal room with 12:12 h light-dark cycle were maintained at approximately 23 degrees C and 55%, respectively. The rats were pair-fed powdered diets. The electromyogram activities in soleus and EDL were elevated by cold exposure. The body weight and absolute soleus wet weight of the cold-exposed group were significantly less than controls at the end of experiment. The one-half relaxation time and contraction time of EDL were significantly longer in the cold-exposed group than in the control group. The rate of twitch tension development, normalized by the maximum twitch tension, in EDL of the cold-exposed group was less than in the control group. Further, the fatigue resistance of EDL, but not of soleus, in response to train stimulation at 10 Hz was improved by cold exposure. The plasma levels of thyroid hormones, 3,5,3'-triiodothyronine and thyroxine, were significantly greater in cold-exposed group. Similar changes were also seen in the plasma catecholamine levels in the cold-exposed group (p > 0.05). It is suggested that long-term cold exposure causes a shift of the contractile properties of fast-twitch EDL muscle toward the slow-twitch type. The results also indicated that the characteristics of muscles responded more strongly to an increased activity level than to the elevation of plasma hormones.

Adrenal Glands↗
PubMed1990

Factors affecting cold-induced hypertension in rats.

A 3- to 4-week exposure of rats to a cold environment (5 +/- 2 degrees C) induces hypertension, including elevation of systolic, diastolic, and mean blood pressures and cardiac (left ventricular) hypertrophy. The studies described here were designed to investigate some factors affecting both the magnitude and the time course for development of cold-induced hypertension. The objective of the first study was to determine whether there was an ambient temperature at which the cold-induced elevation of blood pressure did not occur. The objective of the second experiment was to determine whether body weight at the time of exposure to cold affected the magnitude and time course for development of hypertension. To assess the first objective, male rats were housed in a chamber whose temperature was maintained at 5 +/- 2 degrees C while others were housed in an identical chamber at 9 +/- 2 degrees C. After 7 days of exposure to cold, the rats exposed to the colder temperature had a significant elevation of blood pressure (140 +/- 2 mm Hg) compared with the group maintained at 9 degrees C (122 +/- 3 mm Hg). The rats exposed to 9 degrees C had no significant elevation of systolic blood pressure at either 27 or 40 days after initiation of exposure to cold. At the latter time, the temperature in the second chamber was reduced to 5 +/- 2 degrees C. By the 25th day of exposure to this ambient temperature, the rats had a significant increase in systolic blood pressure above their levels at 9 degrees C. Thus, there appears to be a threshold ambient temperature for elevation of blood pressure during exposure to cold. That temperature appears to lie somewhere between 5 and 9 degrees C. The second objective was assessed by placing rats varying in weight from approximately 250 to 430 g in air at 5 degrees C. There was a highly significant direct relationship (r = 0.96) between body weight at the time of introduction to cold and the number of days required to increase systolic blood pressure by 10 mm Hg above pre-cold exposure level. The third objective was to make an initial assessment of potential differences among strains of rats with respect to development of cold-induced hypertension. To this end, rats of the Fischer 344 strain were used. Systolic blood pressures of these rats also increased during chronic exposure to cold.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

[Influence of environmental temperature (cold exposure) on nasal resistance].

Changes in nasal resistance were examined in 33 healthy subjects in order to investigate the physiological reactions of nasal mucosa to cold exposure. Each examinee was exposed to changes in room temperature from 25 degrees C to 15 degrees C with the same humidity in an artificial atmosphere chamber, regulated by an environmental control unit. Nasal resistance was measured by means of the active-anterior method using a rhinomanometer MPR-2200. The same experiments were repeated on different dates in all 18 subjects. The results can be summarized as follows. 1) The average value of nasal resistance significantly increased after room temperature was decreased from 25 degrees C to 15 degrees C. 2) Patterns of nasal resistance responses to cold exposure were classified into two types. One type was increased nasal resistance after cold exposure and the other was maintenance of resistance despite cold exposure. Each individual manifested a different pattern in experiments carried out on different dates. 3) The nasal resistance value in the chamber at 25 degrees C was significantly higher in winter than in summer, and the increase in nasal resistance in response to cold exposure was significantly larger in summer than in winter. This result was assumed to be due to cold adaptation of the nasal mucosa in winter. 4) Heart rate decreased significantly with cold exposure. However, changes of heart rate in response to cold exposure did not correlate with changes in nasal resistance. No correlation between changes in nasal resistance in response to cold exposure and orthostatic loading, which was carried out after the cold exposure experiment, was detected. 5) A nasal cycle was observed in 7 (14%) of the 33 cases. In 6 of these total nasal resistance was maintained despite cold exposure.

Adult↗
PubMed1981

Dipsogenesis in cold-acclimated rats.

Water intakes of control rats kept at 25 degrees C and cold-acclimated rats kept at 6 degrees C for at least 4 weeks were compared when both groups were at 25 degrees C. Cold-acclimated rats exhibited an increase in water intake (thermogenic drink) during the first but not the second hour after removal from the cold. Cold-acclimated rats, administered the dipsogenic agents angiotensin I, angiotensin II, isoproterenol or serotonin, had water intakes not significantly different from control rats. Administration (1% of body weight) of several different doses of hypertonic NaCl (0.25 to 1.00M) intraperitoneally increased water intake to the same level in both control and cold-acclimated rats. Water deprivation for 24 h, initiated either 2 or 24 h after removal of cold-acclimated rats from the cold, resulted in water intakes not significantly different between cold-acclimated and control rats. In spite of an initial thermogenic drink on removal of cold-acclimated rats from cold, cold-acclimation does not appear to alter the dipsogenic responsiveness of rats to either extracellular or intracellular dipsogenic stimuli, or to a dipsogenic stimulus (dehydration) involving both.

Acclimatization↗
PubMedDate not supplied

Effects of thyroid status on cold-adaptive thermogenesis in Brandt's vole, Microtus brandti.

Hyper- and hypothyroidism were induced by subcutaneous injection of thyroxine and by oral administration of methimazol in Brandt's voles. The effects of the two treatments on metabolic thermogenesis at 25 degrees C and 4 degrees C were investigated. The level of resting metabolic rate was closely related to thyroid status: high in the hyperthyroid case and low in the hypothyroid case. However, no increase in resting metabolic rate occurred in either case during further cold acclimation. Hyperthyroidism resulted in an increased nonshivering thermogenesis, which was much enhanced by lower temperature, but hypothyroidism led to a suppressed nonshivering thermogenesis in the cold. The state-4 and state-3 respirations and the activities of cytochrome-c oxidase of liver mitochondria were elevated in hyperthyroid animals but attenuated in hypothyroid ones. However, these levels were scarcely changed after further cold acclimation. Both hyperthyroidism and cold acclimation induced the recruitment of brown adipose tissue, but brown adipose tissue was different biochemically in the two cases: in hyperthyroidism, the total protein was reduced, while fat content increased; in cold acclimation, the total and mitochondrial proteins were increased. However, in hypothyroid voles, the normal adaptive changes in brown adipose tissue were impaired in further cold acclimation. The activity of cytochromec oxidase in brown adipose tissue was increased by hyperthyroidism and enhanced in further cold. In contrast, its activity was inhibited in hypothyroid animals, though activated to some extent in cold. These results demonstrate that normal thyroid function is essential for the cold-induced increase of resting metabolic rate and nonshivering thermogenesis and that there is a synergism between thyroid hormone and cold acclimation in the regulation of nonshivering thermogenesis in Brandt's vole. In addition, the blunted response of brown adipocytes to the cold may be the cytological mechanism for the suppressed nonshivering thermogenesis found with hypothyroidism.

Adaptation, Physiological↗