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Noradrenaline-induced secretions of pancreatic hormones in cold- and heat-acclimated rats.

Effects of noradrenaline on the portal and aortic plasma pancreatic hormone concentrations were studied in the cold- and heat-acclimated rats in order to know possible roles of these hormones in temperature acclimation. Noradrenaline (NA) infusion (2 micrograms/min, i.v., 30 min) effected greater elevation of colonic temperature (Tc) in the cold-acclimated rats (CA) than in the warm controls (WC), and did not influence Tc in the heat-acclimated rats (HA) under hexobarbital anesthesia. Portal and aortic glucagon levels increased in the NA-infused CA and HA, but no changes were observed in the NA-infused WC. NA-infusion did not affect the portal and aortic insulin levels in WC and CA, but increased aortic insulin level in HA. Aortic glycerol and free fatty acid (FFA) levels increased in all NA-infused groups. Portal and jugular vein FFA levels increased in NA-infused WC, but did not in NA-infused CA and HA. Neither NA infusion, nor glucagon was related to the elevation of Tc in HA. These results suggest that temperature acclimation modifies a glucagon-releasing action of NA and the NA-released glucagon could cooperate with NA to enhance nonshivering thermogenesis in the cold.

Acclimatization↗

Effect of cold acclimation on glucagon receptors of rat white adipocytes.

In order to determine the role of glucagon in cold acclimation, the changes in glucagon receptor were investigated in white adipocytes from cold-acclimated rats by establishing a glucagon radioreceptor assay method for isolated white adipocytes. The following conditions were found to be appropriate for specific glucagon receptor binding assay; cell concentration of about 1 X 10(5) cells/ml, 15 min preincubation with glucagon and 30 min-reaction at 25 degrees C in the presence of bacitracin (1 mg/ml). Cold acclimation decreased the size and increased the number of epididymal white adipocytes. Cold acclimation increased the number of glucagon receptors of white adipocytes, resulting in 140% in terms of unit cell, and 260% increase per unit surface area and 210% increase per whole tissue. However, the affinity of the binding site for glucagon was not affected. The results suggested that an enhanced metabolic response of cold-acclimated rats to glucagon could be partly explained by the increased number of glucagon receptor in white adipocytes.

Adaptation, Physiological↗

Effect of cold acclimation on the broiler chicks' resistance to dietary aflatoxin.

The effect of acclimation to environmental temperatures of 10 to 12 or 28 to 30 C on the resistance of broiler chicks to dietary aflatoxin was examined. Broiler chicks were acclimated from day-of-age for 2 wk to environmental temperatures of 10 to 12 or 28 to 30 C. On Day 14, a single oral dose of aflatoxin (8 mg per kg of body weight) was administered to 50 chicks in each environment. An increase in aflatoxin resistance, as assessed by survival rate, was conveyed by acclimation to cold temperatures. In each environmental chamber, a separate group of chicks was maintained for 2 additional wk, but those groups received 5 mg of aflatoxin per kg feed. By the end of the study, aflatoxicosis was characterized by: 1) a significant (P less than or equal to .05) decrease in body weight; 2) increases in spleen weight, liver weight, liver lipid, and liver dry-matter content; 3) changes in the serum levels of total protein, albumin, glucose, cholesterol, uric acid, potassium, phosphorus, iron and calcium; and 4) increased hepatic hyperplasia. Acclimation to 10 to 12 C was characterized by: 1) an increase in body weight, liver weight, spleen weight and bursa weight; 2) changes in the serum glucose and potassium levels; and 3) a decrease in glutamic-oxaloacetic transaminase activity. Significant aflatoxin by temperature interactions were evident only in serum levels of glucose and phosphorus, and in the serum activity of glutamic-oxaloacetic transaminase. These data suggest that acclimation to cool temperatures does not play a significant role in the resistance by broiler chickens to chronic aflatoxin exposure.

Adaptation, Physiological↗

Effect of acute hypoxia and hypoxic acclimation on hemorheological behavior in rats with frostbite.

It was found that cold injury in rats acclimated to hypoxia was more serious than that in nonacclimated ones. In order to go further into the cause, blood rheological parameters in rats of frostbite at normoxia (FN), frostbite during acute hypoxia (FAH) and frostbite during hypoxia after hypoxic acclimation (FHAC) groups were observed before and after freezing. Before freezing, systemic hematocrit (Hct), blood viscosity, RBC aggregation index and RBC rigidity of FHAC group were higher and RBC deformability index (DI) of FHAC group was lower distinctly than those of FN and FAH groups. After frostbite, the aforesaid changes aggravated prominently, plasma viscosity of FHAC group reduced and was lower than that of FN and FAH groups. The results suggest that the hemorheological behavior is deteriorated in rats acclimated to hypoxia or subjected to freezing, and worsens in hypoxic acclimation rats after freezing. The changes in hemorheological behavior may be one of the causes that would make the frostbite damage more severe in rats acclimated to hypoxia.

Adaptation, Biological↗

[The reaction of acclimated isolated gill epithelium of mollusc to a short-term superoptimal heating].

Thermoresistance (TR) of isolated gill epithelium of molluscs Anodonta anatina L. (n = 20) acclimated for 72 h at 24 degrees C was studied. In 1, 2, 12, 24, 36, 48, 60, and 72 h, the gills were submitted to a provoking action: a 10-minutes heating at 36 degrees C. As a criterion of the tissue TR level served a logarithmic index of the time of survival at 40 degrees C. During 24 h, negative correlation (about 0.50) was revealed between the acclimated epithelium TR level and the value and direction (sign) of its change under the provoking action. In 36 h, this coefficient fell to 0.13. As a result, the range of interorganism variability of the tissue TR level enlarged. Meanwhile, a decrease in the acclimated tissue mean TR level occurred as late as in 60 h of the experiment, being equal to 21%. In 72 h, it reached 30%, which traditionally indicates a deterioration of the functional state of tissue cells and a subsequent death. However, we believe that the deterioration of this state actually had happened earlier, in 36 h, when the range of the interorganism variability of the tissue TR level became enlarged. It was at this moment that the acclimated tissue lost its ability to regulate the shift in stability with the TR level at this period of acclimation.

Acclimatization↗

[Effect of thermal acclimation on the expression of gene coding for lactate dehydrogenase A4 in loach skeletal muscle].

Acclimation of Misgurnus fossilis to 5 and 18 degrees C induced considerable changes in LDH-A gene expression in white skeletal muscle. Qualities of total and messenger RNA isolated from weighted portions of muscle are considerably higher after acclimation to 18 degrees C as compared to 5 degrees C. However, a PCR assay of cDNA synthesized from these mRNA and equalized by optical density demonstrated that the level of LDH-A gene expression was indistinguishable for high and low acclimation temperatures, while expression of other genes (glyceraldehyde-3-phosphate dehydrogenase and alpha-actin) considerably increased at 18 degrees C as compared to 5 degrees C. The specific enzymatic activity of LDH from white skeletal muscle of the fish acclimated to low temperature is by 20% higher than that for high-temperature acclimation. Structural analysis of the PCR products synthesized on cDNA-5 degrees C and cDNA-18 degrees C has revealed no differences. However, there are indirect indications of the differences in the C-thermal region of the LDH-A molecule. Northern hybridization reveals the differences at the RNA level: one (1400 bp) or two (about 1600 and 1400 bp) hybridization signals have been found in mRNA-5 degrees C and mRNA-18 degrees C, respectively. The presence of two fractions in the mRNA-18 degrees C indicates alternative splicing.

Adaptation, Physiological↗

[Reorganization of the tubulin and actin cytoskeleton under acclimation and abscisic acid treatment of Triticum aestivum L. plants].

Only scanty and contradictory data are available concerning effects of low temperatures and ABA on the structural organization of microtubules (MTs) and microfilaments (MFs), and no information exists on the interaction of these parameters at cold acclimation of plants. Therefore, in cold acclimate and ABA-treated winter wheat plants, a comparative study was made of the state (localization, orientation, structure) and stability of actin and tubulin cytoskeleton in root cells taken from different zones, using indirect immunofluorescent microscope. The plant cold acclimation caused MT aggregation, the rise of MT and MF fluorescence, and the increase of their stability (a decrease of oryzalin effect) mainly in the root differentiation zone, that may testify to the strengthening of contacts between MTs and MFs. Like the cold acclimation, ABA induced the formation of MT bunches only in meristem and elongation zone cells. However in the zone of differentiation, the hormone stimulated the increase of tubulin structure stability, well correlating with a decrease in MT content, aggregation degree, and immunofluorescence, and, in addition with a complete depolymerization of MFs. Low temperatures removed the hormone effect on the structural organization of tubulin and actin cytoskeleton in the zone of differentiation. It is suggested that MT destruction, the decrease of instable MT populations, and the increase of stable MT populations may slow down growth processes in ABA-treated plants, similarly as in seedlings being on the initial stages of cold acclimation. By the end of this process, the induction of plant growth is determined evidently by the increase in the number of instable, highly labile MT populations, and in the status of MF polymerization.

Abscisic Acid↗

[Protein synthesis during acclimation of cold-blooded animals to various temperatures].

It was shown that the intensity of protein synthesis in cells of frogs, acclimated to 5 degrees C, is maintained at a high level, which is only 1.5-2 folds lower than that in animals acclimated to 20 C. In the process of acclimation to cold the intensity of synthesis decreases rapidly and already after 5 hours comprises one half of the value, which is characteristic of "warm" frogs, and the intensity of the process decreases more rapidly than the temperature of organs. On acclimation to warmth the intensity of protein synthesis increases and is getting stabilized at the level, characteristic of "warm" amphibia in 10-15 hours. It was shown that under various temperature conditions or conditions of acclimation specific proteins were synthesized against a background of the main groups of proteins.

Adaptation, Physiological↗

Acclimation of activated sludge to degrade toxic levels of 2,4-dinitrophenol.

Biodegradation of 75 and 100 mg/l of 2,4-dinitrophenol (DNP) by activated sludge acclimated in a Sequencing Batch Reactor (SBR) consistently required less than 6 hours although a lag at the beginning of every 48-hour SBR cycle was observed. Other investigators have reported that DNP levels of 100 mg/l and higher are significantly toxic even to acclimated bacteria. The activated sludge acclimated to 75 mg/l initial DNP had over 100 times the DNP-degrading bacteria than an SBR acclimated to 10 mg/l DNP, although the MLSS concentration in both reactors was similar. Results suggest that two mechanisms are responsible for activated sludge acclimation to toxic levels of DNP: maintenance of DNP-degrading biomass sufficiently large to reduce initial DNP to non-toxic levels, allowing for subsequent rapid degradation; and extension of the aeration period well beyond the time required for degradation to prevent gradual accumulation of any by-product which might also be toxic.

2,4-Dinitrophenol↗

Time course of recovery and heat acclimation ability of prior exertional heatstroke patients.

Our understanding of the time course of recovery from exertional heatstroke (EH) and the heat acclimation ability of prior EH patients is limited. This manuscript reviews previous findings regarding recovery from EH and presents original research involving the heat acclimation ability of 10 prior EH patients (PH) and 5 control subjects. Heat acclimation, by definition, distinguishes heat-intolerant from heat-tolerant prior heatstroke patients. Nine PH exhibited normal heat acclimation adaptations (40.1 degrees C, 7 d, 90 min.d-1), thermoregulation, sweat gland function, whole-body sodium and potassium balance, and blood values at 61 +/- 7 d after EH. One PH (subject A) did not adapt to exercise in the heat, was defined heat intolerant, but subsequently was declared heat tolerant (11.5 months post-EH). Three PH exhibited large, unexpected increases in serum CPK levels, which resolved upon subsequent testing, and were probably related to their detrained state and the exercise which they performed. It was concluded that: 1) sleep loss and generalized fatigue were the most common predisposing factors for PH; 2) recovery from EH was idiosyncratic and may require up to 1 year in severe cases; 3) PH were not hereditarily heat intolerant, prior to EH; 4) no measured variable predicted recovery from EH, or heat acclimation responses; 5) heat intolerance occurs in a small percentage of prior heatstroke patients, and may be transient or persistent.

Acclimatization↗

Saturable urea transport pathway across the urinary bladder of Bufo viridis and salt acclimation.

Urea fluxes across the urinary bladder of Bufo viridis were studied in vitro after modification of the mounting technique. The fluxes increased as a function of the bath urea concentration, saturating near 200 mmol/l. The apparent Km was 88 mmol/l in the bladders from tapwater-acclimated toads, and 107 mmol/l in toads acclimated to 500 mOsm NaCl. The Vmax which was 300 mumol.h-1.cm-2 at room temperature in bladders from tapwater acclimation, changed to more than 1500 mumol.h-1.cm-2 upon salt acclimation. It is suggested that urea movement across the urinary bladder of this species occurs by facilitated diffusion and that salt acclimation induces an increase in the density of this pathway, but not of its characteristics (Km).

Acclimatization↗

Effect of food intake on oxygen consumption in cold-acclimated rats.

The objective of the present study was to determine the relative importance of thermoregulatory and energy conservation mechanisms in cold-exposed, food-restricted rats at thermoneutrality. Oxygen consumption was measured at 25 degrees C and 10 degrees C in rats acclimated at 30 degrees C and fed ad libitum and in animals acclimated at 10 degrees C and either fed ad libitum or subjected to food restriction. Rectal temperature was taken before and after each oxygen consumption measurement. Rats from all three groups showed a similar oxygen consumption measured at 10 degrees C. At 25 degrees C, the cold-acclimated rats on ad libitum intake displayed a higher oxygen consumption than did non-acclimated animals. The food-restricted rats at thermoneutrality showed an oxygen consumption similar to that of non-acclimated animals. Rectal temperature did not change significantly under any type of condition. It is concluded that the energy conservation mechanism in food-restricted rats is present only when the thermoregulatory drive is not too strong.

Acclimatization↗

Human vascular fluid responses to cold stress are not altered by cold acclimation.

Repeated cold water immersion can induce the development of an insulative type of cold acclimation in man. This investigation determined if repeated cold water immersion produced changes in vascular fluid responses to cold stress in addition to the previously reported changes in thermoregulation. Seven male subjects performed a standardized cold air and cold water exposure before and again after a cold acclimation program. The cold acclimation program consisted of daily immersion (90 min) in cold water (18 degrees C, stirred) repeated 5 times/wk for 5 consecutive wk. Cold acclimation did not alter the responses of plasma volume or electrolyte concentrations, nor urinary flow or electrolyte excretion during either cold air or cold water exposure. The percent reduction in plasma volume was larger (P less than 0.01) in cold water (-17%) than in cold air (-12%). Cold water immersion resulted in greater (P less than 0.01) diuresis than cold air exposure. Plasma K+ concentration increased (P less than 0.01) during cold (both air and water) exposure, whereas plasma Na+ concentration was unchanged. Calculated renal clearance and urinary excretion rate of both Na+ and K+ increased during cold (both air and water) exposure. The magnitude of plasma volume reduction during cold exposure was not correlated with either the degree of body cooling or diuresis. It is concluded that a) insulative cold acclimation does not influence vascular fluid responses to cold stress, and b) although vascular fluid shifts, body cooling and diuresis are all greater in cold water than in air, a consistent relationship among these parameters could not be established for an individual's response.

Acclimatization↗

Effects of exercise-heat acclimation on fluid, electrolyte, and endocrine responses during tilt and +Gz acceleration in women and men.

Plasma fluid, electrolyte, protein, renin, and vasoactive hormone (epinephrine, norepinephrine, vasopressin) responses were measured in six women (21-23 yr) and four men (21-38 yr) before and immediately following an orthostatic tolerance test (70 degrees head-up tilt) and a +Gz (head-to-foot) acceleration tolerance test (0.5 G X min-1 linear ramp to grayout). These tests were conducted before and after 12 consecutive days of exercise-heat acclimation when the subjects exercised on a cycle ergometer at a relative oxygen uptake of 44% to 49% peak oxygen uptake in a hot environment (Ta = 40 degrees C, 42% rh). During acclimation plasma volume increased by 10.6% (p less than 0.05) in the women and by 11.9% (p less than 0.05) in the men; in both groups exercise heart rate decreased significantly. After acclimation, acceleration tolerance was unchanged in both groups (range 3.1 to 3.4 G); the women's tilt tolerance was unchanged (range 33.6 to 39.5 min), but the men's tilt tolerance increased from 30.4 min before to 58.3 min (delta = 91%, p less than 0.05) after acclimation. Since the pattern of fluid, electrolyte, and protein shifts and acceleration tolerances in the women and men were virtually the same, the hormone responses were highly variable, and the men's tilt tolerance increased significantly after acclimation, it is clear that responses to tilting cannot be used to predict responses to acceleration. Analysis of data from the present study and the literature suggests that current exercise training regimes should be unrestricted for astronauts who have not previously been highly endurance trained.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗

Time for loss of increased cardiac responsiveness to isoproterenol in cold-acclimated rats after removal from cold.

Female rats exposed to air at 5 +/- 1 degree C for 12 weeks had a greater increase in heart rate in response to s.c. administration of d,l-isoproterenol (8 microgram/kg body weight) than warm-acclimated controls when both were tested in air at 25 +/- 1 degree C. After removal from cold for 24, 48, or 72 h, cold-acclimated rats still showed a greater responsiveness of heart rate to s.c. administration of isoproterenol (8 microgram/kg body weight) when compared with warm-acclimated controls. However, by 96 h after removal from cold, the responsiveness of heart rate to isoproterenol in the cold-treated group no longer differed from that of the warm-acclimated group. Hence, the increased beta-adrenergic responsiveness of heart rate in cold-acclimated rats was lost at some time between 72 and 96 h after removal from cold.

Acclimatization↗

Deconditioning-induced exercise responses as influenced by heat acclimation.

Five young men were tested on a bicycle ergometer before (Test 1) and after (Test 2) 8 d of heat acclimation (exercise at 50% of Vo2max at 39.8 degrees C DB, 30.0 degrees C WB) and after 8 h of water immersion (Test 3). A control group of five subjects underwent a similar procedure in a temperate environment of 23.8 degrees C. Heat acclimation resulted in the usual decreases in exercise heart rate (30 beats/min) and rectal temperature (0.6 degrees C) and an increase in sweat rate (19%). The control group showed effects of moderate training by decreases in exercise heart rate (11 beats/min), rectal temperature (0.3 degrees C), and sweat rate (24%). Water immersion resulted in substantial diuresis in both groups, despite 1800 ml of water consumed by each subject. In the acclimation group, exercise responses in Test 2 were better than in Test 1, with little improvement shown by the control group. The acclimation group maintained exercise responses in Test 3 as in Test 1, with more adverse responses shown by the control group. The results show that heat acclimation provides an effective method to prevent the adverse effects of water-immersion deconditioning on exercise tolerance.

Acclimatization↗

Brown adipose tissue metabolism in cold-acclimated weanling rats with hypothalamic obesity.

Certain aspects of intermediary metabolism of white (epididymal) and brown (interscapular) adipose tissue (BAT) were studied in cold-acclimated weanling rats with hypothalamic obesity. Groups of rats with ventromedial hypothalamic lesions (VMNL rats) and controls were maintained for four weeks at 6 degrees C and 22 degrees C, respectively. Sham-operated rats served as controls. Cold-acclimated VMNL rats showed greater percent BAT but normal percent epididymal fat pad weight, hypophagia, reduced body weight and body weight gains, hyperdipsia, hyperinsulinemia, normoglycemia and normal circulating fatty acid levels, higher carcass lipid and lower carcass protein. They also exhibited a higher rate of epididymal fat pad lipolysis than the controls, but the increment during cold adaptation was less in the VMNL rats compared with the 22 degrees C-maintained VMNL animals. In-vitro metabolism was determined in both the basal and the epinephrine-stimulated state. Basal-state 14C-palmitate oxidation, BAT fatty acid and lipid contents were increased in VMNL rats but protein content, incorporation into phospholipid and triglycerides, BAT lipolysis and glycolysis were normal in cold-acclimated VMNL rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats, but the epinephrine-stimulated increase in lipolysis only in the cold-acclimated VMNL rats. Whereas at 22 degrees C BAT of VMNL rats showed decreased palmitate oxidation and no change of incorporation into phospholipid and triglyceride, during cold acclimation VMNL rats showed normal BAT metabolism and normal response to epinephrine, except for an increase in lipolysis. The data are in agreement with the observation that hypothalamic-obese mature rats have normal cold survival potential and allow us to extend this fact to the normophagic-obese-weanling rat.

Acclimatization↗

[Studies on the creatine metabolism in cold acclimation (author's transl)].

Creatine metabolism in cold-acclimated rats was studied with the aid of [1-14C] creatine as a tracer. Urinary creatine derived from muscle increased in the early stage of cold exposure, and creatine contents of all muscles studied were significantly lower in cold-acclimated rats than in controls. Increased urinary creatine derived from muscle and reduced creatine contents of all muscles were also observed in thyroid hormone, triiodothyronine (T3)-treated rats, while chronic treatment of noradrenaline did not affect urinary creatine derived from muscle and creatine contents of all muscles. Radioactive creatine uptake by skeletal muscle was significantly lower in cold-acclimated rats than in controls, while radioactive creatine uptake by heart and diaphragm of cold-acclimated rats was not different from that of controls. Chronic treatment of noradrenaline produced a similar change in radioactive creatine uptake by skeletal muscle, while the inhibitory effect of T3 on radioactive creatine uptake is not different among the different types of muscle, although the uptakes of radioactive creatine by all muscles studied were lower in T3-treated rats than in controls. These findings indicate that cold acclimation results in reduced creatine contents in all muscles and reduced uptake of creatine in skeletal muscle, possibly reflecting an enhanced ability of nonshivering thermogenesis in skeletal muscle induced by both thyroid hormones and noradrenaline.

Acclimatization↗