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At least 19 recordsLinked to original sources

PubMed1991

Assessment of cold stress.

Cold stress may be present in terms of a risk for skin surface cooling (wind chill), extremity cooling and whole body cooling. Measures of cold stress differ for the various situations. The most common approach, however, has been to apply more or less complex formulas for heat balance calculations. The combined effect of several climatic factors (air temperature, mean radiant temperature, humidity and air velocity) and the activity level determines the cooling power of the environment. The cooling power can be easily converted into a required insulation value, that applies both to parts of the body and to the body as a whole. The value provides information about cold stress in two ways; (a) by specifying necessary behavioural adjustments in terms of required activity level and clothing insulation level, and (b) by quantifying the thermal imbalance and tolerance time, when protection worn does not provide sufficient insulation.

Body Temperature Regulation↗

PubMed2006

Protective role of caffeic acid phenethyl ester in the liver of rats exposed to cold stress.

Cold exposure can induce a form of environmental stress. Cold stress (CS) alters homeostasis, results in the creation of reactive oxygen species and leads to alterations in the antioxidant defense system. The caffeic acid phenethyl ester (CAPE), an active component of propolis, has an antioxidant capacity. We investigated the effect of CS on oxidative stress and antioxidant defense system and the possible protective effect of CAPE in rat liver tissue. Twenty-four female Wistar Albino rats were divided into four groups: Control, CAPE-treated, CS, and CAPE-treated CS (CS + CAPE) group. Catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were measured. In addition, histological changes in liver tissue were examined by light microscopy. SOD, CAT and GSH-Px activities and total GSH level were significantly declined in the CS group. In the CS + CAPE group, the activities of these three enzymes and GSH level significantly raised with regard to the CS group. MDA levels increased in the CS group and decreased in the CS + CAPE group. The tissues of the CS group showed some histopathological changes such as necrosis, hepatocyte degeneration, sinusoidal dilatation, hemorrhage and vascular congestion and dilatation. In the CS + CAPE group, the histopathological evidence of hepatic damage was markedly reduced. Histological parameters were consistent with biochemical parameters. In this study, CS increased oxidative stress in liver tissue. CAPE regulated antioxidant enzymes, inhibited lipid peroxidation and reduced hepatic damage.

Animals↗

PubMed1982

[Changes of the function of the heart of SART stressed (repeated cold stressed) mice and the action of neurotropin on these changes].

Electrocardiography (ECG) was performed for SART stressed (repeated cold stressed) mice which had changes in blood pressure and blood flow to examine the effects of this treatment on heart function. In the ECG of mice subjected to SART stress for 5 days, potentiations of the R and T voltage, a shortening of the PQ interval, a prolongation of the QRS interval, and a slight increase of the heart rate were observed; and such changes in the ECG were maintained for several days. Recovery from all these changes was observed after a single dose or consecutive administration of propranolol. From these results, it is considered that sympathetic nerve activity may be increased in the function of the heart in SART stressed mice, as contrasted to the partial vagotonia in the duodenum. Neurotropin (NSP), a nerve sedative, was then administered to mice once daily for 5 days during the sart stress. NSP prevented the changes of the PQ and QRS interval in SART stressed mice, but could not prevent the potentiation of the R and T voltage and the heart rate increase. In particular, the potentiations of the R and T voltages were thought to be induced by the increase of sympathetic nerve activity; therefore, it is thought that NSP may not have direct actions at least on the sympathetic nerve sites in autonomic nervous systems.

Animals↗

PubMed1979

[Decrease of ACh response in isolated duodenum from SART stressed (repeated cold stressed) mice (author's transl)].

ACh response in the isolated duodenum from SART stressed (repeated cold stressed) mice was remarkably decreased in comparison to normal mice 5 days after onset of loading SART stress, and maximal contraction in SART stress mice duodenum was about 37% of that in non-stressed mice. Pilocarpine and KCl responses were also considerably decreased, but BaCl2 response was much the same as in the controls. Thus, the contraction system of the muscle is apparently not damaged by SART stress. Though body weights decreased, the daily intake of food incressed in SART stressed mice. Length of small intestine from SART stressed mice was much the same as in controls, but wet weights of small intestines were larger than in controls. Autonomic agonists, antagonists, tranquilizers and other drugs were given intraperitoneally to mice once daily during SART stress, and the ACh responses in the isolated duodenum were investigated. Pretreatment with adrenergic and anticholinergic drugs inhibited the decrease of ACh response, but antiadrenergic and cholinergic drugs had no effects. Pretreatment with tranquilizers such as reserpine, chlorpromazine, carpipramine and imipramine inhibited the decrease of ACh response in the isolated duodenum, but diazepam, meprobamate and benadryl had no influence. Pretreatment of neurotropin, a neurosedative had good inhibitory effects. Our results suggest that SART stressed mice may be in a state of unbalance regarding sympathetic and parasympathetic nerves, particularly with regard to abnormal tension in the parasympathetic nervous system, in part of duodenum. Pretreatment with most of the above drugs had no influence on loss of body weight in SART stressed mice while pretreatment with neurotropin inhibited body weight to a considerable extent.

Acetylcholine↗

PubMed1987

Electrocorticogram in rats loaded with SART stress (repeated cold stress).

The electrocorticogram (ECoG) in a SART (specific alternation of rhythm in temperature)-stressed (repeatedly cold-stressed) rat, which is regarded as an experimental model for clinical vagotonic-type dysautonomia, was investigated in the present study by the power spectral technique. 1) Analysis of ECoG in SART-stressed rats during the resting-arousal state indicated a decrease in total power and a decrease in relative power in the delta band, and also an increase in relative power in the theta, alpha and beta bands. 2) In the slow-wave sleeping state, the ECoG of SART-stressed rats indicated a marked increase in total power, an increase in the delta band and decreases in theta, alpha and beta bands. 3) Electric stimulation of the posterior-hypothalamic area evoked alterations of ECoG similar to those caused by SART stress. ECoG response to electric stimulation in SART-stressed rats was less than that in unstressed rats. 4) Lesioning of the posterior-hypothalamic areas prevented SART stress-induced ECoG alterations. SART-stressed rats thus appear to be at a higher consciousness level on awakening but to sleep more soundly. They seem to exhibit greater fluctuation in brain activity than normal rats. There is also the possibility that the posterior-hypothalamic area is responsible to some degree for ECoG alterations in SART-stressed rats.

Animals↗

PubMed1995

Immunomodulation by cells of mononuclear phagocyte lineage in acute cold-stressed or cold-acclimatized mice.

Immunoregulatory states in acute cold-stressed or cold-acclimatized mice were investigated. When male C57BL/6 mice were exposed to environmental temperature of 5 degrees for 24 hr (acute cold stress), the spleen cells showed depressed proliferative responses to stimulation with concanavalin A (Con A) or lipopolysaccharide (LPS) compared with control mice (reared at 25 degrees). The proportion of Thy-1.2+ cells increased significantly in spleens from these acute cold-stressed mice. The Con A responses of T-enriched cells from acute cold-stressed mice were restored to the normal level by adding plastic-adherent cells from control mice. Further, adherent cells from acute cold-stressed mice markedly suppressed the Con A responses of control spleen cells. Thus, the plastic-adherent cells appeared to be responsible for the suppressed Con A responses. On the other hand, proliferative responses to Con A or LPS were elevated in spleen cells from mice exposed to 5 degrees for 3 weeks (cold acclimatization). A significant decrease of Thy-1.2+ cells was detected in these spleens. It was shown that the enhanced proliferative responses were attributable to functional alterations of the plastic adherent cell population but not to those of lymphoid cell population. These findings indicate that the low or high responsiveness of spleen cells to Con A observed in cold-stressed or cold-acclimatized mice, respectively, may be due to a mechanism including the contrary modulations of functions of cells of mononuclear phagocyte lineage.

Adaptation, Physiological↗

PubMedDate not supplied

[Evaluation of the effectiveness of the protective effect of arginine in cold stress].

Cold exposition within 3 days at 2-4 degrees caused destabilization of rat erythrocyte membranes. Content of blood serum hemoglobin, total peroxidase activity and the glucose-6-phosphate dehydrogenase activity were increased. Resistance of the animals against high oxygen pressure was reduced. Administration of arginine within 3 days into the animals led to stabilization of membranes and to elevation of rat resistance towards high oxygen pressure.

Adaptation, Physiological↗

PubMed2002

The histidine kinase Hik33 perceives osmotic stress and cold stress in Synechocystis sp PCC 6803.

The stress imposed on living organisms by hyperosmotic conditions and low temperature appears to be perceived via changes in the physical state of membrane lipids. We compared genome-wide patterns of transcription between wild-type Synechocystis sp. PCC 6803 and cells with a mutation in the histidine kinase Hik33 using a DNA microarray. Our results indicated that Hik33 regulated the expression of both osmostress-inducible and cold-inducible genes. The respective genes that were regulated by Hik33 under hyperosmotic and low-temperature conditions were, for the most part, different from one another. However, Hik33 also regulated the expression of a set of genes whose expression was induced both by osmotic stress and by cold stress. These results indicate that Hik33 is involved in responses to osmotic stress and low-temperature stress but that the mechanisms of the responses differ.

Cell Division↗

PubMed2004

Effect of duration of cold stress on plasma adrenal and thyroid hormone levels and immune responses in chicken lines divergently selected for antibody responses.

There is increasing evidence that stress affects various immune processes. Some of these changes are due to hormonal changes involving corticosterone (CORT), triiodothyronine (T3), and thyroxine (T4). Effects of stress depend on the nature of specific stressors (e.g., thermal extremes, diet, pollutants), and stress-modifiers (e.g., genetic make-up, duration and severity of the stressors). We studied the effects of a specific stress (cold stress) with stress-modifiers (duration of stress and genotype of the bird) on immune responses and plasma adrenal and thyroid hormone levels in 3 layer-type chicken lines. Two lines were divergently selected for high (H line) or low (L line) antibody responses to SRBC, and the third line was a randombred control (C) line. Growing chicks (3- to 4-wk-old) of the 3 lines were feed-restricted at 80% of ad libitum consumption, and subjected to cold stress (CS) at 10 degrees C continuously for 7, 5, 3, 1, or 0 d before immunization with keyhole limpet hemocyanin (KLH). Specific antibody titers to KLH, and in vitro lymphocyte proliferation (LP) upon mitogen stimulation were measured. In addition, adrenal and thyroid hormone levels were measured in the plasma samples collected at the end of CS. No significant effect of duration of CS on specific antibody titers was found in the 3 lines. A significant enhancing effect of CS was found on LP. A significant dose-dependent suppressive effect of CS was found on plasma CORT levels. One day of CS had a significant enhancing effect on T3 levels. There was no significant effect of duration of CS on T4 levels. We conclude that CS does not affect specific antibody responses, but may have a modulating effect on cellular immunity and plasma CORT levels, depending on the duration of the stress. The present study suggests an inverse relationship between LP and CORT. This is the first study that reveals an absence of significant differences in adrenal and thyroid hormone levels in the described selection lines.

Animals↗

PubMed1990

Effects of exercise stress and cold stress on glutathione and gamma-glutamyltransferase in rat liver.

Effects of acute and chronic stress (exercise and cold) on glutathione and gamma-glutamyltransferase (gamma GT) in the rat liver were investigated. Such stress, except for in the case of acute exercise, had no definite influence on the glutathione level. On the other hand, gamma GT activity in both the extramicrosomal and microsomal fractions varied substantially, suggesting that acute exercise increases the release ability of the microsomal membrane of the rat liver, and that swimming training and long-term cold exposure stabilize the membrane. Immunoreactive gamma GT, however, did not always correlate with the enzyme activity, especially in the extramicrosomal fraction. Cross-adaptation appeared to exist between swimming training and chronic cold exposure.

Animals↗

PubMed1979

Effects of noradrenaline and carbachol on temperature regulation of cold-stressed and cold-acclimated rats.

1 Noradrenaline (20 micrograms) and carbachol (1 microgram) injected into the anterior hypothalamus of rats at an ambient temperature of 23 degrees C evoked significant falls in core temperature and increases in tail temperature. 2 When rats were cold-stressed (4 degrees C for 90 min) or cold-acclimated (4 degrees C for 4 weeks) and the above amine injections repeated, only carbachol evoked significant falls in core temperature and neither amine increased tail temperature. 3 Central injections of noradrenaline and carbachol also evoked increases in plasma glucose concentrations but not plasma non-esterified fatty acid (NEFA) concentrations in control, acutely cold-stressed and cold-acclimated rats. 4 Although concentrations of plasma glucose and blood lactate of rats were unaffected by cold exposure to 4 degrees C for 1 to 28 days, glucose oxidation rate of both cold-stressed and cold-acclimated rats was significantly greater than in rats at 23 degrees C. Concentrations of plasma NEFA were increased after 1 to 28 days of cold exposure.

Acclimatization↗

PubMed1997

Relationship between cold tolerance and generation of suppressor macrophages during acute cold stress.

Acute cold stress induces suppressor macrophages expressing large numbers of receptors to the crystallizable fragment (Fc) portion of immunoglobulin G (MAC-1+ FcgammaRII/IIIbright cells), resulting in the immunosuppression of splenocyte mitogenesis. The generation of MAC-1+ FcgammaRII/IIIbright cells is mediated by the action of glucocorticoids (GCs) through the GC-receptor. In the present study, the generation of MAC-1+ FcgammaRII/IIIbright cells in peritoneal exudate cells was closely related to the decrease of rectal temperature during 3-day exposure to 5 degrees C. We next investigated the effects of improved cold tolerance on the generation of MAC-1+ FcgammaRII/IIIbright cells during acute cold stress. Mice were adapted to cold by exposure to 5 degrees C for 3 wk (cold-acclimated mice) and then reexposed to 5 degrees C for 3 h (acute cold stress) after living at 25 degrees C for 24 h. The rectal temperature of cold-acclimated mice was not decreased by the acute cold stress. In addition, the proportion of MAC-1+ FcgammaRII/IIIbright cells in peritoneal exudate cell population from cold-acclimated mice was unaffected by the acute cold stress. The cold acclimation significantly attenuated the increases in serum corticosterone levels and the expression of the GC-receptor mRNA on peritoneal exudate cells in response to acute cold stress. These results suggest that the altered GC response to acute cold stress by the improvement of cold tolerance inhibits the generation of suppressor macrophages during acute cold stress.

Acclimatization↗

PubMed1986

Total acetylcholine content, and activities of choline acetyltransferase and acetylcholinesterase in brain and duodenum of SART-stressed (repeated cold-stressed) rat.

The cholinergic activities in SART (specific alternation of rhythm in temperature)-stressed (repeated cold-stressed) rats, which are diseased rats with vagotonic-type dysautonomia, were examined with the following results. A decreased content of total acetylcholine (T-ACh) and increased activities of choline acetyltransferase (CAT) and acetylcholinesterase (ACh) in the basal ganglia and an increase in the T-ACh content and decrease in the AChE activity in the duodenum of SART-stressed rats reached the respective plateaus on day 5 of stress, which were maintained thereafter. CAT activity, however, in the hypothalamus was activated most on day 2. These changes in SART-stressed rats were different from those in simple cold-stressed rats. Subdiaphragmatic vagotomy inhibited the appearance of the changes in the duodenum, but not those in the hypothalamus of SART-stressed rats. The sedative analgesic Neurotropin prevented all the changes in SART-stressed rats described above. These results suggest that cholinergic neurons may be activated in both the hypothalamus and basal ganglia of the brain of SART-stressed rats, and the characteristic peripheral changes of the cholinergic system in the duodenum of SART-stressed rats may be under the control of the parasympathetic center.

Acetylcholine↗

PubMed1989

Ergonomic aspects of cold stress and cold adaptation.

In contrast to the simplified, unvarying, and rigidly controlled conditions that characterize laboratory studies of human responses to cold, normal work in cold regions is characterized by a complex and unstable thermal environment, intermittent cold exposure and exercise, and the freedom to adjust clothing and activity for comfort. These "ergonomic" aspects profoundly modify the impact of a cold environment on people's health, comfort, and performance. A review of recent field studies in the Antarctic shows that the supposed "tropical microclimate" of clothed people in the cold is an over-simplification. People tend to be alternately chilled and overheated, and the accompanying exercise of the vascular responses provides a potential stimulus for vasomotor adaptation. Significant and substantial changes in men's responses to standardized whole-body cold exposures, observed on eight Antarctic expeditions, show that general acclimatization to cold develops as an increase in tissue insulation, which is mediated by an enhanced vascular response to cold.

Acclimatization↗

PubMed1993

Possible involvement of oxygen-derived free radicals in abnormal hemostasis induced by SART stress (repeated cold stress) in laboratory animals.

Abnormal hemostatic profiles indicating hemorrhagic tendency have been reported in rodents exposed to prolonged fluctuation in ambient temperature, known as SART (specific alternation of rhythm in temperature)-stressed animals. In this study, investigation was made of possible involvement of oxygen-derived free radicals in the development of stress-induced hemostatic alteration. SART-stressed rats and mice exhibited marked decrease in platelet count, fibrinogen level and factor VIII:C activity. Superoxide dismutase, when administered s.c. twice a day to mice for 7 days of stress exposure, inhibited the above alterations. Catalase given in the same manner, had essentially the same effect, though to a lesser extent. Allopurinol administered orally once daily during stress reduced stress-induced thrombocytopenia, but caused considerable increase in fibrinogen and factor VIII:C activity in stressed and unstressed mice. Lipid peroxide significantly increased in the heart but not in the plasma following stress exposure in rats and mice. Active oxygens would thus appear to be, at least partially, involved in the development of abnormal hemostasis induced by SART stress.

Animals↗

PubMed2001

Acid stress, starvation, and cold stress affect poststress behavior of Escherichia coli O157:H7 and nonpathogenic Escherichia coli.

The effects of acid shock, acid adaptation, starvation, and cold stress of Escherichia coli O157:H7 (ATCC 43895), an rpoS mutant (FRIK 816-3), and nonpathogenic E. coli (ATCC 25922) on poststress heat resistance and freeze-thaw resistance were investigated. Following stress, heat tolerance at 56 degrees C and freeze-thaw resistance at -20 to 21 degrees C were determined. Heat and freeze-thaw resistance of E. coli O157:H7 and nonpathogenic E. coli was enhanced after acid adaptation and starvation. Following cold stress, heat resistance of E. coli O157:H7 and nonpathogenic E. coli was decreased, while freeze-thaw resistance was increased. Heat and freeze-thaw resistance of the rpoS mutant was enhanced only after acid adaptation. Increased or decreased tolerance of acid-adapted, starved, or cold-stressed E. coli O157:H7 cells to heat or freeze-thaw processes should be considered when processing minimally processed or extended shelf-life foods.

Adaptation, Physiological↗

PubMed1992

Platelet hypoaggregability in rats exposed to SART stress (repeated cold stress).

A prolongation of bleeding time accompanied by thrombocytopenia and abnormalities in coagulation-fibrinolysis systems has been observed in laboratory animals exposed to a chronic form of environmental stress induced by severe fluctuations of air temperature, known as SART (specific alternation of rhythm in temperature) stress. In order to clarify the hemostatic profile under SART stress in more detail, the present study examined platelet aggregability in vitro as well as in vivo in stressed rats. During exposure to stress, thrombocytopenia developed from day 5, and remained up to at least day 14. In vitro aggregation of platelets stimulated by ADP or collagen was markedly decreased in stressed rats, compared with unstressed rats. Furthermore, stressed rats exhibited in vivo hypoaggregability of platelets, as estimated by the magnitude of the drop in circulating platelet counts following intravenous injection of ADP and collagen. Protein and cholesterol content in platelets remained constant after stress exposure. These results indicate that SART-stressed rats exhibit platelet dysfunctions in addition to thrombocytopenia. Considering the previous findings, the hemostatic system under SART stress appears to show a general tendency toward hemorrhage.

Adenosine Diphosphate↗

PubMed1991

Mechanism of hyperalgesia in SART stressed (repeated cold stress) mice: antinociceptive effect of neurotropin.

Exposing mice to 24 and 4 degrees C in alternate 1 hr periods in the day time and maintaining 4 degrees C at night for several days decreases the tail clamp pressure required to evoke pain behavior. This model is referred to as SART (specific alternation rhythm of temperature) stress. An extract from inflamed skin of rabbits inoculated with vaccinia virus (neurotropin) clearly normalized the hyperalgesia in this SART stress model. To clarify the mechanism of the hyperalgesia in SART mice and the mode of the antinociceptive action of neurotropin in this model, the influence of systemically administered neurotransmitter related drugs was studied. 1) Neurotropin, 5-hydroxytryptophan and L-dihydroxyphenylalanine significantly normalized the decrease in nociceptive threshold, and muscimol tended to inhibit it in nociceptive threshold in SART stressed mice. 2) Haloperidol, phenoxybenzamine, reserpine, bicuculline, scopolamine, physostigmine and naloxone alone did not influence the nociceptive threshold in SART stressed mice. 3) The antinociceptive effect of neurotropin was significantly attenuated by p-chlorophenylalanine, haloperidol and phenoxybenzamine; and it was completely inhibited by reserpine. 4) Naloxone, bicuculline, scopolamine and physostigmine had no influence on the antinociceptive effect of neurotropin. These results suggest that hypofunction mainly of the monoaminergic systems contributes to hyperalgesia in SART stressed mice and that neurotropin produces the antinociceptive effect by restoring these neural functions.

5-Hydroxytryptophan↗