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PubMed1996

Hypothermic general cold adaptation induced by local cold acclimation.

To study relationships between local cold adaptation of the lower limbs and general cold adaptation, eight subjects were submitted both to a cold foot test (CFT, 5 degrees C water immersion, 5 min) and to a whole-body standard cold air test (SCAT, 1 degree C, 2 h, nude at rest) before and after a local cold acclimation (LCA) of the lower limbs effected by repeated cold water immersions. The LCA induced a local cold adaptation confirmed by higher skin temperatures of the lower limbs during CFT and a hypothermic insulative general cold adaptation (decreased rectal temperature and mean skin temperature P < 0.05) without a change either in metabolic heat production or in lower limb skin temperatures during SCAT after LCA. It was concluded that local cold adaptation was related to the habituation process confirmed by decreased plasma concentrations of noradrenaline (NA) during LCA (P < 0.05). However, the hypothermic insulative general cold adaptation was unrelated either to local cold adaptation or to the habituation process, because an increased NA during SCAT after LCA (P < 0.05) was observed but was rather related to a "T3 polar syndrome" occurring during LCA.

Acclimatization↗
PubMed2006

Major differences observed in transcript profiles of blueberry during cold acclimation under field and cold room conditions.

Our laboratory has been working toward increasing our understanding of the genetic control of cold hardiness in blueberry (Vaccinium section Cyanococcus) to ultimately use this information to develop more cold hardy cultivars for the industry. Here, we report using cDNA microarrays to monitor changes in gene expression at multiple times during cold acclimation under field and cold room conditions. Microarrays contained over 2,500 cDNA inserts, approximately half of which had been picked and single-pass sequenced from each of two cDNA libraries that were constructed from cold acclimated floral buds and non-acclimated floral buds of the fairly cold hardy cv. Bluecrop (Vaccinium corymbosum L.). Two biological samples were examined at each time point. Microarray data were analyzed statistically using t tests, ANOVA, clustering algorithms, and online analytical processing (OLAP). Interestingly, more transcripts were found to be upregulated under cold room conditions than under field conditions. Many of the genes induced only under cold room conditions could be divided into three major types: (1) genes associated with stress tolerance; (2) those that encode glycolytic and TCA cycle enzymes, and (3) those associated with protein synthesis machinery. A few of the genes induced only under field conditions appear to be related to light stress. Possible explanations for these differences are discussed in physiological context. Although many similarities exist in how plants respond during cold acclimation in the cold room and in the field environment, there are major differences suggesting caution should be taken in interpreting results based only on artificial, cold room conditions.

Acclimatization↗
PubMed2002

Cold tolerance: behavioral differences following single or multiple cold exposures.

Previous research has demonstrated that repeated exposure to cold water results in cold tolerance. The present set of experiments examined whether spontaneous behavioral activity and the rate of rewarming differed between cold tolerant and nontolerant rats. Animals receiving six cold exposures (one per day) were compared to subjects receiving a single cold exposure but cooled to match the final day temperature of the six-exposure group. Immediately following the final or only cold exposure, activity was measured by an activity monitor (Exp. 1) or was videotaped and scored by an independent observer (Exp. 2). Furthermore, rats' temperatures were monitored for 90 min (Exp. 2) and 60 min (Exp. 3) following the activity measurement. The results indicated that cold-tolerant rats exhibited activity similar to normal, noncooled subjects, whereas the activity in the single exposure group was impeded. Moreover, rats in the multiple exposure groups rewarmed more quickly than subjects in the single exposure condition. The third experiment also examined if the procedures of Experiments 1 and 2 resulted in associative cold tolerance. Experiment 3 replicated earlier findings, which have shown that exposure to the same cold stimulus in an altered context resulted in a loss of tolerance. These findings suggest that the processing of contextual stimuli is necessary for the acquisition of cold tolerance and that behavioral activity and rewarming rates can be used as alternative measures of cold tolerance.

Animals↗
PubMed2002

Cold induces catalytic iron release of cytochrome P-450 origin: a critical step in cold storage-induced renal injury.

Earlier experimental studies have suggested a role for iron in cold-storage-induced organ injury. Whether the cytochrome P-450 enzymes, shown to be a source for iron in several injury models, contribute to cold-induced iron release is not known. Storage of human proximal tubular epithelial (RPTE) cells at 4 degrees C in the University of Wisconsin (UW) solution caused a significant and time-dependent increase in bleomycin-detectable iron (BDI). To identify the cellular source of BDI, RPTE cells were subfractionated and stored at 4 degrees C for 4 h. Bleomycin-detectable iron release was highest in the microsomes, next in the cytosol and none in the mitochondria. As microsomes are rich in iron-containing cytochrome P-450 enzymes, microsomes were cold stored with P-450 inhibitors, cimetidine and piperonyl butoxide. P-450 inhibitors significantly reduced cold-induced BDI release. Furthermore, cimetidine and iron chelator deferoxamine (DFO) significantly reduced cold-induced cell injury, suggesting a role for P-450-derived iron in cold-induced cell injury. In rat kidney experiments, BDI and LDH release were significantly higher in cold-stored kidneys than in control kidneys. Inclusion of cimetidine and DFO in the cold-storage solution significantly suppressed the BDI and LDH release, and reduced the ultrastructural changes. Our data demonstrate for the first time that cold-induced catalytic iron release may be at least in part of microsomal cytochrome P-450 origin, and that it participates in cold-storage-induced renal injury. In the clinical setting, sequestering free iron released during cold storage is possible and may prove to be useful in limiting organ injury.

Adenosine↗
PubMed1990

Release of cold-induced burning pain by block of cold-specific afferent input.

While the pure sensation of cold is evoked by activation of a specific set of afferent channels, an additional set is believed to be activated by noxious low-temperature stimuli evoking cold pain. At primary afferent level, the channels concerned with the cold fraction of cold pain are served by myelinated A delta cold-specific fibres, whereas those concerned with the pain fraction are served by unmyelinated C nociceptors. In the present study, interaction between the two types of afferent input underlying cold pain was investigated by selectively blocking conduction in myelinated fibres. When doing so to the point of abolishing cold sensation, ramps of low-temperature stimuli eventually evoked a first sensation of burning pain. In addition to, and contemporaneous with, this change in quality, a significant decrease in pain threshold (reduction in required stimulus energy) was recorded when applying a noxious low-temperature stimulus. Such exaggeration in magnitude of low temperature-induced pain and the unmasking of its burning quality by A fibre block imply release of central sensory transmission due to removal of inhibitory primary afferent input. Myelinated fibres transmitting either tactile, cold sensations or both could exert this inhibition. Previous evidence of suppression of pain by low-temperature stimuli indicates that it is the cold-specific input that normally exerts this central gating on nociceptor input. The present results may also offer an explanation for the occurrence of a syndrome of burning pain on cold exposure in neuropathic patients with impaired ability to perceive cold.

Adult↗
PubMed2002

Arabidopsis transcriptome profiling indicates that multiple regulatory pathways are activated during cold acclimation in addition to the CBF cold response pathway.

Many plants, including Arabidopsis, increase in freezing tolerance in response to low, nonfreezing temperatures, a phenomenon known as cold acclimation. Previous studies established that cold acclimation involves rapid expression of the CBF transcriptional activators (also known as DREB1 proteins) in response to low temperature followed by induction of the CBF regulon (CBF-targeted genes), which contributes to an increase in freezing tolerance. Here, we present the results of transcriptome-profiling experiments indicating the existence of multiple low-temperature regulatory pathways in addition to the CBF cold response pathway. The transcript levels of approximately 8000 genes were determined at multiple times after plants were transferred from warm to cold temperature and in warm-grown plants that constitutively expressed CBF1, CBF2, or CBF3. A total of 306 genes were identified as being cold responsive, with transcripts for 218 genes increasing and those for 88 genes decreasing threefold or more at one or more time points during the 7-day experiment. These results indicate that extensive downregulation of gene expression occurs during cold acclimation. Of the cold-responsive genes, 48 encode known or putative transcription factors. Two of these, RAP2.1 and RAP2.6, were activated by CBF expression and thus presumably control subregulons of the CBF regulon. Transcriptome comparisons indicated that only 12% of the cold-responsive genes are certain members of the CBF regulon. Moreover, at least 28% of the cold-responsive genes were not regulated by the CBF transcription factors, including 15 encoding known or putative transcription factors, indicating that these cold-responsive genes are members of different low-temperature regulons. Significantly, CBF expression at warm temperatures repressed the expression of eight genes that also were downregulated by low temperature, indicating that in addition to gene induction, gene repression is likely to play an integral role in cold acclimation.

Acclimatization↗
PubMed1996

RbfA, a 30S ribosomal binding factor, is a cold-shock protein whose absence triggers the cold-shock response.

The cold-shock response, characterized by a specific pattern of gene expression, is induced upon a downshift in temperature and in the presence of inhibitors of ribosomal function. Here, we demonstrate that RbfA of Escherichia coli, considered to be involved in ribosomal maturation and/or initiation of translation, is a cold-shock protein. Shifting the rbfA mutant to a lower temperature resulted in a constitutive induction of the cold-shock response accompanied by slower growth at low temperatures, while shifting the rbfA mutant that overproduces wild-type RbfA resulted in an increase in total protein synthesis accompanied by faster growth adaptation to the lower temperature. Furthermore, the cold-shock response was also constitutively induced in a cold-sensitive 16S rRNA mutant at low temperatures. Accompanying the transient induction of the cold-shock response, we also report that shifting E. coli from 37 degrees C to 15 degrees C resulted in a temporary inhibition of initiation of translation, as evidenced by the transient decrease in polysomes accompanied by the transient increase in 70S monosomes. The accumulative data indicate that the inducing signal for the cold-unadapted non-translatable ribosomes which are converted to cold-adapted translatable ribosomes by the association of cold-shock proteins such as RbfA. Therefore, the expression of the cold-shock response, and thus cellular adaptation to low temperature, is regulated at the level of translation. The data also indicate that cold-shock proteins can be translated by ribosomes under conditions that are not translatable for most mRNAs.

Bacterial Proteins↗
PubMed1994

Cold-induced perturbation of cutaneous blood flow in the rat tail: a model of nonfreezing cold injury.

Cold-induced alteration of cutaneous blood flow, measured with laser-Doppler flowmetry, was studied in a rat tail model of nonfreezing cold injury (NFCI). The NFCI-inducing condition consisted of prolonged tail immersion in 1 degree water. Before exposure to the injury condition, tail blood flow (laser Doppler flux) during brief 3 degrees immersion showed cold-induced cycles of vasoconstriction followed by cold-induced vasodilation (CIVD). Tail temperature exhibited cyclic patterns similar to blood flow in response to cold water immersion. Cold exposures to 1 degree for 1 or 3 hr induced no systematic change; however, cold exposures of 6 or 9 hr induced profound and long-lasting blood flow and temperature deviations. Following the cold injury condition, CIVD was completely absent and remained absent for several weeks, suggesting that CIVD loss is an important component in development of NFCI. Cold-induced disturbances of cutaneous blood flow in the rat tail consisted of a sequence of distinctive stages analogous to those described in human NFCI. These stages were evidenced initially by several days of reduced blood flow and thermal sensitivity, followed in a week by a hyperemia stage, and later by enhanced vascular and thermal sensitivity. The cutaneous blood flow alterations and sequence of variations following prolonged cold exposure suggest that the rat tail may be a valid model of human NFCI.

Animals↗
PubMed2005

Enhanced cold tolerance in transgenic tobacco expressing a chloroplast omega-3 fatty acid desaturase gene under the control of a cold-inducible promoter.

A new cold-inducible genetic construct was cloned using a chloroplast-specific omega-3-fatty acid desaturase gene (FAD7) under the control of a cold-inducible promoter (cor15a) from Arabidopsis thaliana. RT-PCR confirmed a marked increase in FAD7 expression, in young Nicotiana tabacum (cv. Havana) plants harboring cor15a-FAD7, after a short-term exposure to cold. When young, cold-induced tobacco seedlings were exposed to low-temperature (0.5, 2 or 3.5 degrees C) for up to 44 days, survival within independent cor15a-FAD7 transgenic lines (40.2-96%) was far superior to the wild type (6.7-10.2%). In addition, the major trienoic fatty acid species remained stable in cold-induced cor15a-FAD7 N. tabacum plants under prolonged cold storage while the levels of hexadecatrienoic acid (16:3) and octadecatrienoic acid (18:3) declined in wild type plants under the same conditions (79 and 20.7% respectively). Electron microscopy showed that chloroplast membrane ultrastructure in cor15a-FAD7 transgenic plants was unaffected by prolonged exposure to cold temperatures. In contrast, wild type plants experienced a loss of granal stacking and disorganization of the thylakoid membrane under the same conditions. Changes in membrane integrity coincided with a precipitous decline in leaf chlorophyll concentration and low survival rates in wild type plants. Cold-induced double transgenic N. alata (cv. Domino Mix) plants, harboring both the cor15a-FAD7 cold-tolerance gene and a cor15a-IPT dark-tolerance gene, exhibited dramatically higher survival rates (89-90%) than wild type plants (2%) under prolonged cold storage under dark conditions (2 degrees C for 50 days).

Arabidopsis↗
PubMed1976

Induced tolerance in cold urticaria caused by cold-evoked histamine release.

The interrelations between cold sensitivity and release of histamine and other mediators in five patients with cold urticaria undergoing cold tolerance treatment were studied. Tolerance to cold was produced in all patients by repeated cold exposure. In four patients tolerance was maintained by once daily exposures. In the fifth patient 4-hourly exposures were necessary. Cold sensitivity was associated with histamine release in venous blood draining urticated skin. No prostaglandin activity was detected, and low concentrations of kinin activity were found in blood draining the normal and exposed skin of healthy subjects as well as in patients with cold urticaria. After induction of tolerance, no histamine release occurred on challenge by cold. Relapse of sensitivity was associated with reappearance of histamine release on challenge. The conclusion that tolerance is due to depletion of histamine stores in skin after repeated cold exposure was supported by diminished wealing in response to injection of a histamine liberator (compound 48/80) in cold-tolerant skin.

Adolescent↗
PubMed1995

Comparing methods for assessing bronchial responsiveness in children: single step cold air challenge, multiple step cold air challenge, and histamine provocation.

Cold air challenge (CACh) can be applied by either a single step (SSCACh) or a multiple step (MSCACh) protocol. The interrelationship of the responses of the different protocols has not yet been studied. Furthermore, there is contradictory information on the correlation of cold air challenge responses to the outcome of pharmacological provocations. A single and a multiple step cold air challenge and a histamine provocation were performed in random order on three consecutive days on 28 children and adolescents with bronchial asthma, who were currently symptom- and medication-free. Single step cold air challenge consisted of a 4 min isocapnic hyperventilation of dry, -10 degrees C air; the subjects's response was quantified by the induced change in forced expiratory volume in one second (FEV1). Multiple step cold air challenge consisted of a series of 3 min, cold dry air hyperventilation steps from 20 to 80% of maximal voluntary ventilation (MVV); response was expressed as the provocative dose causing a 10% fall in FEV1 (PD10). Histamine provocation consisted of a series of 2 min inhalations of stepwise increasing histamine concentrations from 0.03 to 8.0 mg.mL-1; response was expressed as the provocative concentration of histamine causing a 20% fall in FEV1 (PC20). Change in FEV1 (delta FEV1) (SSCACh) correlated closely with PD10 (MSCACh); scatter around the regression line was minimal. With one exception, both types of CACh identified the same subjects as hyper- and normoresponsive. delta FEV1 (SSCACh) correlated significantly to PC20 (histamine), but scatter around the regression line was substantial. The correlation of PD10 (MSCACh) to PC20 (histamine) failed to reach statistical significance. These results indicate that the stimulus applied and the bronchoconstrictor mechanism activated, and not the challenge protocol, determine the outcome of a cold air challenge. In clinical practice, a brief single step cold air challenge can substitute for a more time-consuming multiple step cold air challenge. As nonpharmacological challenges seem to measure a different type of bronchial responsiveness, neither a single step nor a multiple step cold air challenge can substitute for a pharmacological provocation.

Adolescent↗
PubMed2000

Dependence of cold-related coronary and respiratory symptoms on age and exposure to cold.

Cold causes cardiopulmonary stress often perceived as shortness of breath or chest pain, and causes exacerbation of these symptoms in persons suffering heart or lung disease. We investigated the prevalence of these symptoms and their association with sex, age and cold exposure in a population-based sample of 1,785 persons who lived in three areas of Finland. The exposure to cold was measured by the annual number cold days (mean daily temperature below 0 degree C) in the resident locality and weekly hours spent in the cold in winter. Shortness of breath was 25% and chest pain 52% more common in females than in males, and their prevalence increased by 24% and 77%, respectively, for every 10 years of age. The prevalence of shortness of breath increased by 5% and chest pain by 6% for every 10 cold days in the resident locality, and by 6% and 7% for every 10 hours spent in the cold, respectively. We suggest that environmental cold, measured by the number of cold days throughout the year and weekly hours spent in the cold, may provoke cardiopulmonary symptoms independent of sex and age.

Adult↗
PubMed1988

Respiratory and cardiovascular responses to cold stress following repeated cold water immersion.

The effects of cold acclimation (CA) on the cardiorespiratory responses to cold air and water stress tests (CST) were studied in 7 males before and after a CA program of daily 90-min cold water (18 degrees C) immersions repeated 5 times a wk for 5 consecutive wk. The CST consisted of a 90-min resting exposure to cold air (5 degrees C, 30% relative humidity) or water (18 degrees C) during which rectal temperature, oxygen consumption (VO2), carbon dioxide production (VCO2), minute ventilation (VE), heart rate, cardiac output (Q), and blood pressure (BP) were periodically measured. In cold air following CA, the VO2 at 10 min was lower (P less than 0.02) post- than pre-CA, however, no differences were found in cold water. The VE increased (P less than 0.01) during CST as a function of VCO2. The CA did not affect the VE-VCO2 relationship or the pattern of breathing during CST in cold air or water. The CA had no effect on Q or (a-v) O2 difference, which both increased (P less than 0.01) during the first 45 min of CST, then remained stable. BP increased significantly during the first cold water exposure, but not during the last cold water immersion. These data indicate that CA attenuated the onset of metabolic heat production during CST in air but did not alter its ultimate magnitude or the relationships between the cardiorespiratory variables and metabolic requirements. Also, the thermoregulatory adjustments associated with CA altered the control of blood pressure during acute cold stress.

Acclimatization↗
PubMed1998

[Influence of stress and stress-protecting factors on rat tolerance to cold and efficiency of rat adaptation to cold].

The adaptive characteristics of the body, including the specific features of increased cold resistance upon repeated exposures to cold, are determined not only by the properties of thermogenic structures themselves, but largely depend on the contribution of the central mechanisms which control the processes of habituation and mobilization of functions. The experiments revealed an increase in cold resistance in rats after preexposure to cold. Immobilization stress prior to training cold significantly decreased rapid cold resistance in the animals, but increased the training effect of the first cooling. On the contrary, chlordiazepoxide increased cold resistance during the first cooling. Testing of the untreated animal showed no effect of training. No adaptive changes in cold resistance occurred in rats with impaired amygdaloid complex. Analyzing adrenal catecholamines revealed a significant elevation of dopamine concentrations in the rats exposed to cold. Hypothalamic catecholamines did not change with cold and serotonin in intact rats and 5-hydroxyindoleacetic acid in amygdalectomized rats substantially increased.

Adaptation, Physiological↗
PubMed1967

Chronic hemolytic anemia due to cold agglutinins: the mechanism of resistance of red cells to C' hemolysis by cold agglutinins.

The red cells of patients with chronic hemolytic anemia due to cold agglutinins are agglutinated by antiglobulin serum in a nongamma reaction due to the coating of beta-globulins, C'4 and C'3. The red cells of such patients are abnormally resistant to C' hemolysis by cold agglutinin. Normal red cells can be made equally resistant to C' hemolysis by incubation with cold agglutinin and normal serum at temperatures which allow transient reactions between the red cells and cold agglutinins. The development of resistance to C' hemolysis was related to increasing susceptibility to agglutination in anti-beta(1c)- and anti-beta(1e)-sera and by increasing uptake of (131)I activity from labeled anti-beta-globulin serum containing antibodies for both globulins. There was decrease in the adsorption of (131)I-labeled cold agglutinin during the development of resistance to C' hemolysis and reduced susceptibility to agglutination by cold agglutinins. Since cold agglutinins have been demonstrated to dissociate from the red cell, leaving fractions of C' globulin attached, it is postulated that repeated transient reactions produce the accumulation of incomplete C' complexes. Steric hindrance by the adsorbed C' complexes is probably responsible for the inhibition of the reaction with cold agglutinin. There is evidence that the adsorbed C' complexes also interfere with the hemolytic action of C' even when cold agglutinin has become reattached to the red cells. The accumulation of C' complexes by cold agglutinins appears to be the most important factor in the abnormal resistance to C' hemolysis exhibited by the patient's red cells. Other factors, such as the heterogeneity within a population of normal cells, appear to be of minor significance.

Agglutination↗
PubMed1987

Cold hemagglutinin disease associated with IgG cold-reactive antibody.

Six patients with chronic idiopathic cold hemagglutinin disease were studied whose serum cold agglutinin was not inactivated or was incompletely inactivated with the IgM-reducing agent dithiothreitol. In five of these patients, isolation of the antibodies revealed that two patients had predominantly IgG cold-reactive antibody, which was associated with smaller amounts of IgM in one patient and with IgA in the other; two patients had predominantly IgM cold agglutinin with lesser amounts of cold-reactive IgG; and one patient had an IgG cold agglutinin only. Both patients with predominantly IgG cold-reactive antibodies were treated with splenectomy and subsequently had a rise in more than hemoglobin levels that has been maintained for over 36 months without additional therapy. Two of the other three patients were treated with glucocorticoids only and responded similarly. These data indicate that a subset of patients with cold hemagglutinin disease have IgG cold-reactive antibodies. In contrast to patients with typical cold agglutinin disease, this subset appears responsive to glucocorticoids and splenectomy.

Adolescent↗
PubMed1989

Effects of cold exposure on cyclic AMP concentration in plasma, liver, and brown and white adipose tissues in cold-acclimated rats.

Effects of acute cold exposure on plasma energy substrates and tissue 3',5'-adenosine monophosphate (cAMP) were analyzed in intact rats, to define an involvement of the nucleotide in nonshivering thermogenesis (NST) and resultant cold acclimation. After an acute cold exposure to -5 degrees C, the plasma glucose level increased gradually in warm-kept control rats (C) while it decreased significantly in cold-acclimated rats (CA). However, it was increased considerably by an extreme cold exposure to -15 degrees C in both C and CA. By contrast, plasma levels of free fatty acids (FFA) increased immediately after cold exposure and the release lasted during the period of exposure especially in C. The cold exposure also increased plasma cAMP concentration but no concomitant increase was found in the liver. In both brown (IBAT) and white (WAT) adipose tissues the nucleotide concentration showed a stepwise decrease. The observed correlation between lipolysis and plasma cAMP response after cold exposure suggests an involvement of the adenylate cyclase-cAMP system in NST via lipid metabolism, at least, in the early stages of cold acclimation.

Acclimatization↗
PubMed1978

Effects of reserpine and propranolol on urinary excretion of histamine and 5-hydroxytryptamine in severe cold exposure in normal and cold-acclimated Guinea-pigs.

The effects of cold-acclimation, reserpine and propranolol were investigated on the survival time, rectal temperature and urinary excretion of histamine and 5-HT in guinea-pigs at -20 degrees C. Both reserpine and propranolol shortened survival time by 3 hours and 1.5 hours respectively, the shortest time being in the cold-acclimated reserpine-treated animals. There was a trend in severe cold exposure to increased excretion of histamine both in the non-acclimated and in cold-acclimated animals. Reserpine did not change the excretion but increased the concentration of histamine from 0.08 to 0.25 microgram/ml. Propranolol proved to be a histamine liberator by increasing the excretion in non-acclimated from 0.10 to 1.40 microgram/h and concentration from 0.10 to 4.52 microgram/ml and in cold-acclimated animals the excretion from 0.20 to 2.85 microgram/h and the concentration from 0.08 to 3.23 microgram/ml. Severe cold increased the excretion of 5-HT in the non-acclimated animals from 0.08 to 0.21 microgram/h and cold acclimation increased this to 0.17 microgram/h. Reserpine diminished the excretion from 0.08 to 0.03 microgram/h in the non-acclimated animals, but propranolol had no effect. The results showed that the excretion of histamine and 5-HT into urine are changed in cold and can be modified with drugs. The application of the findings in proving a cold stress deserves further study.

Acclimatization↗