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Maternal administration of reserpine (100 microgram/kg/day) from day 8 of pregnancy until weaning of the pups produced no change in litter size, birth weight or weaning weight. At 70 to 80 days of age the offspring of reserpine treated dams were less able to maintain body temperature in response to cold stress with physical restraint. Similarly treated offspring exhibited a smaller rise in urinary free norepinephrine levels during the initial stages of cold exposure and they incorporated significantly less 14C from tyrosine into heart norepinephrine during acute cold exposure. No differences in incorporation of 14C into norepinephrine from tyrosine were evident when the animals were not subjected to cold stress. These data are consistent with the hypothesis that maternal administration of reserpine produces a permanent alteration in the ability of the offspring to respond to cold stress and that this deficit is related to an alteration in adrenergic nervous system development.
A DNA microarray-based global transcript profiling of Escherichia coli in response to cold shock showed that in addition to the known cold shock-inducible genes, new genes such as the flagellar operon, those encoding proteins involved in sugar transport and metabolism, and remarkably, genes encoding certain heat shock proteins are induced by cold shock. In the light of strong reduction in metabolic activity of the cell after temperature downshift, the induction of sugar metabolism machinery is unexpected. The deletion of four csps (cspA, cspB, cspG, and cspE) affected cold shock induction of mostly those genes that are transiently induced in the acclimation phase, emphasizing that CspA homologues are essential in the acclimation phase. Relevance of these findings with respect to the known RNA chaperone function of CspA homologues is discussed.
1. The responses of fifty-five single units to changes in skin temperature were recorded in twenty-three guinea-pigs anaesthetized with urethane. Skin-temperature changes were induced by changing the temperature of the water-perfused support plate of the stereotaxic apparatus and that of the double-walled Perspex jacket that was put on the support plate.2. Thirty-three units were stereotaxically and histologically verified as being within a circumscribed area of the pontine dorsomedial reticular formation (subcoeruleus region). Twenty-one units were located in the surrounding areas, and one unit in the nucleus raphé magnus region.3. Twenty-seven of thirty-three recorded subcoeruleus units were specifically excited by cooling of the abdominal or leg skin, whereas only five units were non-thermoresponsive and one unit was warm-responsive. The cold-responsive units had peak activity at skin temperatures between 22 and 29 degrees C, in accordance with the maximum activity in cutaneous cold-receptors.4. A markedly different distribution of units was found in the surrounding areas. Only four units were cold-responsive. Thirteen units were non-thermoresponsive, and four units were warm-responsive.5. The cold-responsive subcoeruleus units were situated in regions which are known to contain accumulations of noradrenergic cell bodies, and to project to hypothalamic neurones. Electrical stimulation of these regions is known to cause excitatory metabolic responses in unanaesthetized guinea-pigs. It is concluded that part of the cutaneous cold-afferents projects to hypothalamic thermointegrative neurones via noradrenergic pathways that ascend from these subcoeruleus regions.
The review is an attempt to analyze the data available in the literature concerning the response of mesophilic bacteria to cold shock at the level of DNA transcription, translation, and chromosome dynamics, i.e., in terms of cell biology. The review considers relevant molecular mechanisms and particular regulatory systems within the framework of a general cell response to cold shock. It is suggested that a short-term response to cold shock is necessary for bacteria to transit to a viable but nonculturable state and/or for their physiological and genetic adaptation to psychrotrophic life. It is emphasized that cell responses to cold and heat shocks are different and that DNA dynamics (i.e., its supercoiling, multiple bending, and condensation) and the rearrangement of the protein-synthesizing apparatus of cells (including the induction of alternative translational mechanisms) may play a central role in cell response to cold shock. The role of molecular chaperones in cold shock response is presumably of less importance than it is in the case of heat shock.
All organisms examined to date, respond to a sudden change in environmental temperature with a specific cascade of adaptation reactions that, in some cases, have been identified and monitored at the molecular level. According to the type of temperature change, this response has been termed heat shock response (HSR) or cold shock response (CSR). During the HSR, a specialized sigma factor has been shown to play a central regulatory role in controlling expression of genes predominantly required to cope with heat-induced alteration of protein conformation. In contrast, after cold shock, nucleic acid structure and proteins interacting with the biological information molecules DNA and RNA appear to play a major cellular role. Currently, no cold-specific sigma factor has been identified. Therefore, unlike the HSR, the CSR appears to be organized as a complex stimulon rather than resembling a regulon. This review has been designed to draw a refined picture of our current understanding of the CSR in Bacillus subtilis. Important processes such as temperature sensing, membrane adaptation, modification of the translation apparatus, as well as nucleoid reorganization and some metabolic aspects, are discussed in brief. Special emphasis is placed on recent findings concerning the nucleic acid binding cold shock proteins, which play a fundamental role, not only during cold shock adaptation but also under optimal growth conditions.
OBJECTIVES: We sought to determine whether abnormal myocardial blood flow (MBF) responses to the cold pressor test (CPT) in patients with various risk factors may involve different mechanisms that could lead to varying responses of short- and long-term administration of antioxidants. BACKGROUND: There is a growing body of evidence that increased vascular production of reactive oxygen species markedly reduces the bioavailability of endothelium-derived nitric oxide, leading to impaired vasodilator function. It is unknown whether increased oxidative stress is the prevalent mechanism underlying endothelial dysfunction in patients with different coronary risk factors. METHODS: Fifty patients with normal coronary angiograms were studied. The MBF responses to CPT was determined by means of positron emission tomography before and after intravenous infusion of 3 g vitamin C or saline (placebo), as well as after 3 months and 2 years of 2 g vitamin C or placebo supplementation daily. RESULTS: In hypertensive patients, the change in MBF (DeltaMBF) was not modified significantly by short-term vitamin C administration challenges (0.20 +/- 0.20 ml/g/min; p = NS) but was significantly increased after three months and two years of treatment with vitamin C versus baseline (0.58 +/- 0.27 and 0.63 +/- 0.17 vs. 0.14 +/- 0.18 ml/g/min; both p < or = 0.001). In smokers, DeltaMBF in response to CPT was significantly increased after short-term vitamin C infusion and long-term vitamin C treatment (0.52 +/- 0.10, 0.54 +/- 0.13, 0.50 +/- 0.07 vs. -0.08 +/- 0.10 ml/g/min; all p < or = 0.001). In hypercholesterolemic patients, no improvement in DeltaMBF during CPT was observed after short- and long-term vitamin C treatment (0.05 +/- 0.14, 0.08 +/- 0.18, 0.02 +/- 0.19 vs. 0.08 +/- 0.16 ml/g/min; p = NS). The CPT-induced DeltaMBF in hypertensive patients and smokers after follow-up was significant as compared with placebo and control subjects (p < or = 0.001). CONCLUSIONS: The present study revealed marked heterogeneous responses in MBF changes to short- and long-term vitamin C treatment in patients with various risk factors, which highlights the quite complex nature underlying abnormal coronary vasomotion.
The cold-shock response of Escherichia coli describes a specific pattern of gene expression in response to abrupt shifts to lower temperatures. This pattern includes the induction of cold-shock proteins, synthesis of proteins involved in transcription and translation, and repression of heat-shock proteins. The identified cold-shock proteins are involved in various cellular functions from supercoiling of DNA to initiation of translation. The major cold-shock protein, CspA, has high sequence similarity with three other E. coli proteins--CspB, CspC, and CspD. Using translational lacZ fusions, cspB was found to be cold-shock inducible at the level of transcription like cspA, while cspC and cspD were not. The Csp proteins, which share sequence similarity with other prokaryotic proteins and with the 'cold-shock domain' of eukaryotic Y-box proteins, may have a function in activating transcription or unwinding or masking RNA molecules. Because the cold-shock response can also be induced by the addition of certain inhibitors of translation, it has been proposed that the state of the ribosome is the physiological sensor for the induction. In addition to E. coli, cold-shock proteins have also been found in other prokaryotic and eukaryotic organisms.
INTRODUCTION: Residence at high altitude modifies thremoregulatory responses to cold stress upon return to lower altitude. These changes are difficult to explain since several stresses related to high altitude may interact, including hypoxia, cold, solar radiation, and physical exertion. We hypothesized that adaptation to hypoxia without cold exposure would produce at least part of the observed changes. METHODS: Five men underwent acclimation to intermittent hypoxia (AIH) in a hypobaric chamber (8 h daily for 4 d, and 6 h on the last day, 4500 to 6000 m) at 24 degrees C. Cold stress responses were tested during a whole-body standard cold air test (1 degrees C, 2 h at rest at sea level) both before and after AIH. RESULTS: Increased reticulocyte counts and percentages confirmed acclimation to hypoxia after AIH. Changes in thermoregulation during the cold test included lower mean skin temperature after 60-80 min (18.8 +/- 0.7 degrees C vs. 19.4 +/- 0.7 degrees C); higher mean metabolic heat production (127 +/- 8 W x m(-2) vs. 118 +/- 6 W x m(-2)); and lower heat debt (7.7 +/- 1.3 kJ x kg(-1) vs. 10.3 +/- 1.2 kJ x kg(-1)), without significant change in rectal temperature. Time to onset for continuous shivering decreased after AIH (12 +/- 5 min vs. 21 +/- 6.3 min), and shivering activity occurred at higher mean skin but not rectal temperatures. CONCLUSION: AIH in comfortable ambient temperature leads to a normothermic-insulative-metabolic general cold adaptation. We conclude that AIH modifies the thermoregulatory responses to cold at sea level without cold exposure leading to a cross-adaptation.
The feeding response to cold exposure of male Sprague-Dawley rats bearing Walker 256 carcinosarcoma has been measured at 5 degrees, 13 degrees, and 17 degrees exposure. The cold-specific feeding response of the host is estimated taking account of the food cost of the tumor and of changes in food intake induced by weight change of host produced by both cold exposure and tumor growth. The cold-specific feeding response to cold exposure is depressed by about 30% by presence of tumor but is only marginally influenced by tumor size. This tumor-induced impairment of feeding response contrasts with the eventual total abolition and tumor size dependency of feeding response of tumour bearers to caloric density of food.
Changes in polyol, sugar and free amino acid (FAA) body contents were investigated in the aquatic, subterranean (i.e. hypogean) crustaceans Niphargus rhenorhodanensis and Niphargus virei and in a morphologically close aquatic, surface-dwelling (i.e. epigean) crustacean Gammarus fossarum acclimated to 12 degrees C, 3 degrees C and -2 degrees C. With decreasing temperature, G. fossarum significantly increased its alanine and glutamine levels, while trehalose body content was found to increase above control levels only at -2 degrees C. N. virei showed moderate increases of alanine and glycine, and no change in trehalose level was observed in this species. By contrast, N. rhenorhodanensis was the only species showing a significant rise in its total FAA pool, mainly explained by alanine, glycine, arginine and glutamine accumulations. This species also gradually increased its trehalose body content with decreasing temperature. Several cold-hardy ectotherms show metabolic responses to cold that are identical to those observed in N. rhenorhodanensis. A previous comparative study showed that the hypogean N. rhenorhodanensis exhibited a survival time (Lt50) at -2 degrees C that was 26.3 times and 2.6 times higher than the hypogean N. virei and the epigean G. fossarum, respectively. Thus, crustacean levels of FAA and trehalose were correlated with their respective cold tolerances. Such differences in metabolic responses to cold in both hypogean organisms were unexpected since they both live in thermally buffered biotopes. Considering the current distribution areas of the two subterranean crustaceans studied, we assume that the cold hardiness found in the hypogean N. rhenorhodanensis could be correlated with its biogeography history during the quaternary glaciations.
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A comparison of cold pressor response with coronary arteriography and left ventriculography was made in 26 consecutive patients having chest pain suggesting coronary heart disease. Patients with normal coronary arteriograms and normal left ventriculograms showed normal cold pressor responses. Patients with coronary atherosclerosis and normal left ventricular performance showed an exaggerated cold pressor response, whereas patients with severe coronary atherosclerosis and poor left ventricular performance did not exhibit an exaggerated cold pressor response. In patients with inferior wall myocardial infarction having dyskinesia or akinesia of the inferior wall, the cold pressor response was not impaired. In contrast, patients with anterior wall myocardial infarction and dyskinesia or akinesia of the anterior wall showed a marked impairment of the left ventricular performance and no exaggeration of the cold pressor response.
OBJECTIVE: To study the vasomotor response (cold pressor/basal flow) in myocardium perfused entirely by collaterals, using the reflex sympathetic stimulation of cold pressor stress. DESIGN: Regional myocardial blood flow was measured in collateral dependent and in remote myocardium using positron emission tomography with 15O water at basal and at cold pressor stress. Regional ischaemia was measured with 18F-fluorodeoxyglucose (FDG). PATIENTS: Nine patients (mean (SD) age 53 (6) years) with an occluded coronary artery supplied entirely by collaterals from other angiographically normal arteries. RESULTS: In remote myocardium, basal and cold pressor flow were 0.99 (0.26) and 1.46 (0.60) ml/min/g (P < 0.05), respectively, a myocardial vasomotor response of 1.46 (0.45). In collateral dependent myocardium, basal and cold pressor flow were 0.91 (0.20) and 0.87 (0.35) ml/min/g, respectively (the latter value, P < 0.05 v remote region), a myocardial vasomotor response of 0.97 (0.43) (P < 0.05 v remote region). The myocardial vascular resistance (mean arterial pressure/flow) during cold pressor was higher in the collateral dependent than in remote myocardium, at 147.0 (61.1) and 85.6 (32.3) mm Hg.min.g/ml (P < 0.05), respectively, but with no relative increase in FDG uptake. CONCLUSIONS: In contrast to the decrease in myocardial resistance in remote myocardium with cold pressor, an increase was observed in collateral dependent myocardium suggesting a vasoconstrictor response in resistive vessels, without demonstrable myocardial ischaemia.
This study sought to determine whether spontaneously hypertensive rats (SHR) on a high-NaCl diet have an enhanced pressor response to acute cold exposure and to define the peripheral mechanisms involved in the enhanced pressor response. SHR and normotensive Wistar-Kyoto (WKY) rats that had been on 1 and 8% NaCl diets for 3 wk were subjected to cold exposure. After a 30-min control period, animals were exposed to cold (6 +/- 2 degrees C) for 90 min. Mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured continuously. In a separate group of SHR on 1 and 8% NaCl diets, an arginine vasopressin (AVP) V1 receptor antagonist (10 micrograms/kg iv) was given before cold exposure, and MAP was measured throughout cold exposure. Plasma AVP was measured before and during cold exposure in a separate group of SHR. During cold exposure, there was a significant increase (P less than 0.05) in MAP (25 mmHg) in SHR on the 8% NaCl diet only. In contrast, HR and LSNA increased similarly during cold exposure in both SHR and WKY on the two diets. AVP was similar in both SHR groups (7.1 pg/ml for 1% vs. 6.1 pg/ml for 8%) before cold exposure, but during cold exposure it increased in the 8% NaCl SHR only, reaching 17.6 pg/ml at 90 min. The AVP V1 antagonist completely abolished the cold stress-induced rise in MAP in SHR. Thus SHR on a high-NaCl diet have an enhanced pressor response to acute cold exposure compared with SHR on a normal NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)
This study presents a global transcriptional analysis of the cold shock response of Shewanella oneidensis MR-1 after a temperature downshift from 30 degrees C to 8 or 15 degrees C based on time series microarray experiments. More than 700 genes were found to be significantly affected (P < or = 0.05) upon cold shock challenge, especially at 8 degrees C. The temporal gene expression patterns of the classical cold shock genes varied, and only some of them, most notably so1648 and so2787, were differentially regulated in response to a temperature downshift. The global response of S. oneidensis to cold shock was also characterized by the up-regulation of genes encoding membrane proteins, DNA metabolism and translation apparatus components, metabolic proteins, regulatory proteins, and hypothetical proteins. Most of the metabolic proteins affected are involved in catalytic processes that generate NADH or NADPH. Mutational analyses confirmed that the small cold shock proteins, So1648 and So2787, are involved in the cold shock response of S. oneidensis. The analyses also indicated that So1648 may function only at very low temperatures.
The hypothesis that the initial responses to cold water immersion could be attenuated by repeated cold showers was tested. Eighteen (13 men, 5 women) non-habituated subjects undertook two 3-min head-out seated immersions into stirred water at 10 degrees C wearing swim wear. The immersions were separated by 4 days during which time they took six cold showers. The subjects were randomly split into three groups with different showering regimes: 3 min at 10 degrees C on the back (10B); 3 min at 15 degrees C on the back (15B); and 30 s at 10 degrees C on the back followed by 30 s on the front (10BF). Over the first 30 s of immersion respiratory frequency ( f (R)) was reduced by 21% in groups 10B and 10BF from 54 (14) to 44 (16) breaths.min(-1) ( P <0.05), and 33 (8) to 26 (10) breaths.min(-1) ( P <0.05) respectively, following repeated showers. Group 15B showed no change in f (R). The tachycardia induced on immersion in water at 10 degrees C was not reduced by repeated showers except in group 15B during the last 150 s [from 119 (23) to 105 (25) beats.min(-1), P <0.05]. Repeated showering in water at 10 degrees C reduced the respiratory drive (as measured by f (R)) during head-out immersion in water at the same temperature. No such habituation was observed with repeated showers in warmer water (15 degrees C). It is concluded that when the body surface area cooled is the same, the rate of change of skin temperature is an important factor in determining the degree of habituation produced.
Seventy-nine units in the striatal region were examined in 48 urethan-anesthetized rats. When these units were classified by their thermal responsiveness, proportions of the cold-responsive, warm-responsive, and thermally unresponsive units were 25.4, 35.4, and 39.2%, respectively, of the total units tested. Either microiontophoretically or systemically administered apomorphine (a dopamine agonist) and haloperidol (a dopamine antagonist) affected (inhibited and/or excited) most (86.5-100%) cold-responsive units. In contrast, only a small percentage of the warm-responsive (28.6-43.8%) or thermally unresponsive (0-19.2%) units were affected by both apomorphine and and haloperidol. Furthermore it was found that most (73-100%) cold-responsive units were inhibited by apomorphine but excited by haloperidol; the inhibitory responses of the unit activity induced by apomorphine were antagonized by haloperidol. The reciprocal relationships between apomorphine and haloperidol were not observed in most warm-responsive (76.2-85.7%) or thermally unresponsive (80.8-100%) units. The data demonstrate that many striatal neurons are influenced by thermal afferent activation in the scrotum. The results also provide a neuronal basis for the hypothesis that the dopaminergic receptors located in the cold-responsive neurons of the striatum have effects on metabolic heat production in rats.