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PubMed1996

Hemodynamic responses to cold stress in blacks: effect of application site.

Black Americans have been shown to exhibit increased blood pressure responses to a variety of physical stressors. However, few investigators have examined hemodynamic responses to cold stress. Additionally, no studies have compared blood pressure responses to forehead and foot stress in blacks. Therefore, in this study, hemodynamic responses to cold pressor tests were compared in 30 blacks (15 males, 15 females) utilizing two application sites. Baseline comparisons of systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), forearm blood flow (FBF) and forearm vascular resistance (FVR) were not different prior to forehead and foot cold stress. Following baseline measurements, ice was applied separately to the forehead and foot for 90 seconds with hemodynamic measurements being recorded at 45 and 90 seconds. During application of ice to the forehead, FVR-90 was significantly higher (P < .002, 97.0 units vs. 66.4 units) compared to the foot. The application of ice to the foot resulted in significantly greater SBP-45 responses (P < .0001, 147 mmHg vs. 139 mmHg), HR-45 responses (P < .0043, 80, b.min-1 vs. 69 b.min-1). HR-90 responses (P < .0001, 78 b.min-1 vs. 64 b.min-1), and FBF-45 responses (P < .05, 2.74 ml.min-1.100ml-1 vs. 1.98 ml.min-1.100ml-1). These findings suggest that blacks exhibit disparate patterns of reactivity in response to cold stress as a function of application site. Therefore, investigators should consider the application site when interpreting studies examining a biracial cohort.

Adult↗

PubMed1981

Enhancement of calorigenic response to cold and to norepinephrine in physically trained rats.

Calorigenic response to cold and to norepinephrine (NE: 4 microgram . kg-1 . min-1) in physically fit (SW) rats was compared with control (CT) and cold-acclimated (CA) rats. Physical fitness was obtained by daily 3-hr swimming in water at 36 degree C for 6-8 weeks. Resting heart rate (HR) was significantly less in SW rats. Cold immersion (in water at 18 degree C up to the neck) increased oxygen consumption (VO2) significantly in CA and SW compared to CT rats (p less than 0.01). Cold immersion decreased colonic temperature (Tco1) in all groups. Despite the increased calorigenic response, SW rats cooled as quickly as CT rats in cold water. Body weight and skinfold thickness were significantly less in SW than in CT rats (p less than 0.01). Compared with CT rats, average weight of the interscapular BAT was significantly less in SW rats (p less than 0.05). Infusion of NE significantly increased VO2, Tco1, HR and mean aortic pressure in anesthetized rats. The increase in VO2 was significantly greater in CA (p less than 0.01) and SW (p less than 0.05) than in CT rats. Tco1 increased significantly in CA (p less than 0.05) and slightly in SW compared to CT animals.

Adaptation, Physiological↗

PubMed1999

Cold shock response in mammalian cells.

Compared to bacteria and plants, the cold shock response has attracted little attention in mammals except in some areas such as adaptive thermogenesis, cold tolerance, storage of cells and organs, and recently, treatment of brain damage and protein production. At the cellular level, some responses of mammalian cells are similar to microorganisms; cold stress changes the lipid composition of cellular membranes, and suppresses the rate of protein synthesis and cell proliferation. Although previous studies have mostly dealt with temperatures below 20 degrees C, mild hypothermia (32 degrees C) can change the cell's response to subsequent stresses as exemplified by APG-1, a member of the HSP110 family. Furthermore, 32 degrees C induces expression of CIRP (cold-inducible RNA-binding protein), the first cold shock protein identified in mammalian cells, without recovery at 37 degrees C. Remniscent of HSP, CIRP is also expressed at 37 degrees C and developmentary regulated, possibly working as an RNA chaperone. Mammalian cells are metabolically active at 32 degrees C, and cells may survive and respond to stresses with different strategies from those at 37 degrees C. Cellular and molecular biology of mammalian cells at 32 degrees C is a new area expected to have considerable implications for medical sciences and possibly biotechnology.

Adaptation, Physiological↗

PubMed1988

Sympathetic nervous system responses to cold exposure and diet in rat skeletal muscle.

Norepinephrine (NE) turnover measured in individual skeletal muscles of the rat assessed sympathetic responses to cold (4 degrees C) and diet. Acute cold exposure increased NE turnover slightly (15-50%) in all muscles examined, including gastrocnemius, tibialis anterior, tensor fascia lata, and soleus, in contrast, cold-accelerated NE turnover in heart by one- to twofold and in interscapular brown adipose tissue (IBAT) by more than threefold. Similar results in skeletal muscle and heart were obtained after 1 wk of cold exposure. Examination of dietary effects on NE turnover, comparing rats fed a sucrose-supplemented diet for 3 days with those fasted for 2 days, indicated that sympathetic activity in skeletal muscle was unresponsive to dietary intake. In heart and IBAT, on the other hand, NE turnover in sucrose-fed rats was twice that obtained in fasted animals. Taken together, the lesser effect of cold and the undetectable response to diet indicate that sympathetic outflow to skeletal muscle is regulated differently than that to heart or IBAT and imply that skeletal muscle is not a major site for sympathetically mediated thermogenic responses to cold exposure or to dietary alteration, such as fasting and sucrose feeding.

Acclimatization↗

PubMed1996

Eucapnic hypoxia lowers human cold thermoregulatory response thresholds and accelerates core cooling.

Hypoxia lowers the basic thermoregulatory responses of animals and humans. In cold-exposed animals, hypoxia increases core temperature (Tco) cooling rate and suppresses shivering thermogenesis. In humans, the experimental effects of hypoxia on thermoregulation are equivocal. Also, the effect of hypoxia has not been separated from that of hypocapnia consequent to hypoxic hyperventilation. To determine the isolated effects of hypoxia on warm and cold thermoregulatory responses and core cooling during mild cold stress, we examined the Tco thresholds for sweating, vasoconstriction, and shivering as well as the core cooling rates of eight subjects immersed in 28 degrees C water under eucapnic conditions. On 2 separate days, subjects exercised on an underwater cycle ergometer to elevate Tco above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects inspired humidified room air during the control trial. For the eucapnic hypoxia trial, they inspired 12% O2-balance N2 with CO2 added to maintain eucapnia. Eucapnic hypoxia lowered the Tco thresholds for vasoconstriction and shivering by 0.14 and 0.19 degrees C, respectively, and increased core cooling rate by 33% (1.83 vs. 1.38 degrees C/h). These results demonstrate that eucapnic hypoxia enhances the core cooling rate in humans during mild cold stress. This may be attributed in part to a delay in the onset of vasoconstriction and shivering as well as increased respiratory heat loss during hypoxic hyperventilation.

Adult↗

PubMed2005

Involvement of GIGANTEA gene in the regulation of the cold stress response in Arabidopsis.

The Arabidopsis GIGANTEA (GI) gene has been shown to regulate several developmental processes, including photoperiod-mediated flowering, phytochrome B signaling, circadian clock, and carbohydrate metabolism. However, little is known about the role of GI gene in mediating the cold stress response. Here, we show that GI gene is involved in mediating the cold stress response. GI gene was induced by cold stress, but not by salt, mannitol, and abscisic acid. Moreover, gi-3 plants showed an increased sensitivity to freezing stress. However, no significant differences were detected in the transcript levels of CBF genes CBF1, CBF2, and CBF3 as well as their targeted genes RD29A, COR15A, KIN1, and KIN2 between wild-type and gi-3 plants in response to cold stress. These results suggest that GI gene positively regulates freezing tolerance via a CBF-independent pathway. In addition, intermittent cold treatments had a greater effect on flowering time in gi-3 plants than that in wild-type plants, suggesting that there may be a link between flowering time and cold stress response through GI in Arabidopsis.

Abscisic Acid↗

PubMed1989

Raynaud's phenomenon in patients treated with cisplatin, vinblastine, and bleomycin for germ cell cancer: measurement of vasoconstrictor response to cold.

The prevalence of Raynaud's phenomenon (RP) was studied in patients treated with cisplatin, vinblastine, and bleomycin. Thirty-two patients with germ cell cancer were followed for a median of 78 months (range, 49 to 106 months). All had obtained complete remission during treatment; none had relapsed at last follow-up examination. All blood samples, including serum magnesium, were normal. The arterial vasoconstrictor response to cold in the finger was measured by cuff- and strain-gauge techniques at 30, 15, and 10 degrees C. Blood pressure (BP) was measured auscultatorily, using a 12-cm broad cuff on the ipsilateral upper arm. Fourteen patients (44%) had developed anamnestic RP, and all showed an exaggerated response to cold; arterial closure was provoked in nine patients. Eighteen patients (56%) were without finger symptoms. These patients had an exaggerated response to cold in comparison with controls, and in two patients, RP was provoked. None of the patients had an increased systolic pressure gradient from arm to finger when compared with a control group. Thus, an exaggerated cold response was found to be a prolonged vasospastic side effect not only in patients with RP, but also in patients without finger symptoms.

Adult↗

PubMedDate not supplied

Cardiovascular and hormonal responses to cold pressor test in insulin-dependent diabetic adolescents with microalbuminuria.

Cardiovascular responses to cold pressor test and associated changes in blood concentrations of renin, aldosterone, and catecholamines were measured in 11 type I diabetic patients with microalbuminuria; 11 type I diabetic patients with normoalbuminuria matched for age, duration of diabetes, metabolic control; and in nine normal control subjects. Heart rate, renin, aldosterone, and catecholamines concentrations in diabetic patients and controls at baseline were similar, but higher mean blood pressure was evident in microalbuminuric than normoalbuminuric patients (p < 0.01) and controls (p < 0.05). Heart rate and mean blood pressure during cold pressor test in control subjects and type I diabetic patients increased significantly but similarly, regardless of the presence of microalbuminuria. Catecholamines, but not renin-aldosterone release, was associated to blood pressure modifications during the test. Peak values of mean blood pressure induced by cold test were positively correlated to baseline values in control subjects (r = 0.658, p < 0.05) and normoalbuminuric (r = 0.725, p < 0.01), but not microalbuminuric diabetics. These data suggest that the higher blood-pressure values at rest observed in microalbuminuric than normoalbuminuric diabetics are not associated with a higher cardiovascular response to cold hypertensive stimulus.

Adolescent↗

PubMed1982

Regional coronary hemodynamic responses to cold stimulation in patients without variant angina.

The responses to cold in patients with exertional chest pain were studied by measuring coronary sinus and great cardiac vein flows, aortic and left ventricular pressure and diameters of epicardial and small (0.4 to 1.0 mm) intramyocardial coronary arteries before and after the left hand of 18 such patients was immersed in ice water. Coronary sinus and great cardiac vein flows were used as indexes of total and anterior left ventricular flows. Coronary sinus flow minus great cardiac vein flow was used as an index of inferior left ventricular flow. Perfusion of left ventricular regions was considered potentially "normal" or "abnormal" according to the presence or absence of 50 percent or greater stenosis of luminal diameter in the coronary artery supplying a given region. With cold stimulation, increases occurred in heart rate (6 beats/min), mean aortic pressure (22 mm Hg) and left ventricular end-diastolic pressure (8 mm Hg) (all p less than 0.05). Left ventricular flow in normally perfused regions increased as resistance decreased. Left ventricular flow in abnormally perfused regions increased slightly and resistance increased. Regional left ventricular flow increased more, and changes in resistance differed in normally and abnormally perfused regions. Coronary arterial diameter decreased only minimally (6 percent) in both normal and abnormal left ventricular regions. These data show that cold stimulation increases coronary resistance in abnormally perfused left ventricular regions. Cold stimulation-related increases in coronary resistance do not appear to be caused by coronary arterial "spasm."

Adult↗

PubMed2001

Loss of plasma glucose lowering response to cold stress in opioid mu-receptor knock-out diabetic mice.

Opioid mu-receptor plays an important role in the regulation of glucose homeostasis in diabetic rats lacking insulin. Opioid mu-receptor knockout mice were employed to identify the essential role of this receptor in the present study. Western blotting analysis characterized the deletion of opioid mu-receptor in liver of knockout mice as compared to that of normal (wild-type) mice. We found that the plasma glucose concentration of diabetic mice induced by intraperitoneal injection of streptozotocin was markedly decreased after exposure to cold-stress in a cold room for 1 h. However, this plasma glucose lowering response to cold-stress was disappeared in diabetic mice lacking opioid mu-receptor. The important role of opioid mu-receptor in the plasma glucose lowering response to cold stress can thus be considered. Moreover, bilateral adrenalectomy abolished this plasma glucose lowering response to cold stress in diabetic mice with opioid mu-receptor, as compared to the shamed-operated animals. Therefore, activation of opioid mu-receptor by opioid from adrenal gland appears to be responsible for the plasma glucose lowering response to cold-stress in diabetic mice with insulin deficiency.

Adrenal Glands↗

PubMed1997

The effect of blood alcohol on the initial responses to cold water immersion in humans.

Many drowning victims have alcohol in their blood, but it is not clear whether there is a causal relationship. This study examined the effect of moderate alcohol consumption on the initial responses to cold water immersion. Sixteen subjects wearing swimming costumes undertook two, 3-min head-out seated immersions in water at 15 degrees C. One hour before immersion, subjects drank either 3.7 ml.kg body water-1 of 40% v:v alcohol as vodka, or an equivalent volume of water (control) mixed with squash. On immersion, the average blood alcohol concentration was 23 mmol.l-1 (105 mg.100 ml-1) after alcohol consumption and zero in the control condition. Respiratory frequency in the first 20 s of immersion was found to be reduced (P < 0.05) by 10% (a total of 2-3 breaths) after alcohol consumption compared to the control immersion. Tidal volume, heart rate, rectal temperature and skin temperatures did not differ significantly between immersions. It is concluded that moderate alcohol consumption does not attenuate the initial "cold shock" responses to a practically significant extent and is thus unlikely to reduce the risk of drowning on immersion in cold water.

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↗

PubMed1982

Onset of thermogenesis in response to cold in newborn mice.

The onset of thermogenesis in response to cold exposure in individual mice was studied using a sensitive close circuit system for measuring their rate of oxygen consumption. On the day of birth, exposure to a cool environment did not stimulate an increase in oxygen consumption, but 48 h later the majority of mice respond by doubling their metabolic rate in response to a fall from 36 to 31 degrees C in ambient temperature. When 5 mice huddled together an ambient temperature drop from 36 to 23 degrees C was required to provoke the same response. Brown adipose tissue is present at birth but the cells are relatively small and contain little fat. By the second day they are three times larger and contain far more fat. The onset of thermogenesis appears to await the development of brown adipose tissue.

Adipose Tissue, Brown↗

PubMed1997

Role of Escherichia coli cspA promoter sequences and adaptation of translational apparatus in the cold shock response.

A shift in growth temperature from 37 degrees C to 15 degrees C leads to a dramatic increase in the level of CspA, the major cold shock protein of Escherichia coli. To investigate the molecular basis of this induction, we considered the relevance of transcriptional and posttranscriptional controls by analyzing the steady-state levels of transcripts and the expression of reporter genes in cells carrying a set of cspA promoter fragments of variable length fused to lacZ or cat genes. We demonstrate that: (i) the core cspA promoter (from -40 to +16) responds to cold shock and a mutation at -36 increases the relative activity of the promoter at low temperature by threefold; (ii) the sequences upstream of -40 have a positive effect on expression at 37 degrees C, but no effect on the cold shock response; (iii) by virtue of their influence on mRNA stability, the downstream sequences (from +81 to +165) reduce expression at 37 degrees C and increase the intensity of the cold shock response; (iv) mutations in the GCACATCA and CCAAT motifs, present at +1/-4 and between the -10 and -35 elements, respectively, do not affect the cold shock response of the cspA promoter; (v) following cold shock, a modification of the protein synthetic machinery takes place that allows preferential translation of cspA mRNA relative to the non-cold shock cat and lacZ mRNAs. The quantitatively modest transcriptional activation shown by the core promoter of cspA following cold shock suggests that transcriptional activation can significantly contribute to cold shock induction only when coupled to posttranscriptional controls, such as alterations in mRNA stability and the translational apparatus.

Adaptation, Physiological↗

PubMed1998

Metabolic and endocrine responses to cold exposure in chronically incubated extrauterine goat fetuses.

To investigate developmental aspects of metabolic and endocrine responses to cold exposure in fetuses, we conducted experiments on six goat fetuses, three aged 95-116 d of gestation (dGA; group I), and three aged 122-134 dGA (group II), using an extrauterine fetal incubation system that provided arterio-venous extracorporeal membrane oxygenation (A-V ECMO). The fetuses were cannulated via the umbilical vessels, and their blood gas exchange was totally supported by A-V ECMO, while they were maintained in an isothermal incubator containing artificial amniotic fluid. After confirming that fetuses were in metabolically stable condition in the extrauterine incubation system, fetal core temperature was lowered by 2 degrees C over 2 h by decreasing the temperature of incubating fluid from 39.5 degrees C. During and after cold exposure, fetal heart rate and arterial blood pressure remained unchanged. We observed significant increases in oxygen consumption and plasma concentrations of norepinephrine, epinephrine, adrenocorticotropic hormone, and cortisol in group II but not in group I fetuses. In addition, based on regression analysis, maximal changes of these parameters during cold exposure were linearly correlated with gestational age significantly, and the regression lines were found to intersect the x (gestational age) axis at around 98-106 dGA. These results suggest that metabolic and endocrine responses to cold exposure develop with gestational age in the goat fetus, the responses being manifested around 100 dGA.

Animals↗

PubMed1992

Effects of hyperoxia on the metabolic response to cold of the newborn rat.

We asked what effects hyperoxia may have on the metabolic response to cold of the newborn rat. Whole body gaseous metabolism (VO2 and VCO2) was measured in 2-day old rats by open flow respirometry at ambient temperatures (Tamb) between 40 and 20 degrees C, changed at a rate of 0.5 degrees C/min during normoxia and hyperoxia (100% O2 breathing). In normoxia, the thermoneutral range was very narrow, at Tamb = 33-35 degrees C. A decrease in Tamb at first stimulated VO2; a further drop in Tamb below 28 degrees C reduced metabolic rate. The metabolic response to cold was not sufficient to maintain body temperature (Tb). In hyperoxia average values of VO2 were above the normoxic values at all Tamb, but the difference was mostly apparent at low Tamb; at 20 degrees C, hyperoxic VO2 averaged 73% more than in normoxia. This metabolic increase determined a significant but small rise of Tb. We conclude that in the 2-days-old rat hyperoxia has a stimulatory effect on metabolism which is Tamb-dependent, being much more apparent in the cold. This supports the concept that the normoxic VO2 of the newborn is limited by the supply of O2. However, the fact that in the cold, even in hyperoxia, VO2 did not reach very high values, and Tb was not maintained, suggests that not only O2 availability, but also the rate of O2 utilization limits the aerobic metabolic response of the newborn.

Animals↗

PubMed1988

Effects of captopril on cold pressor test responses in normotensive and hypertensive subjects.

The aim of this study was to evaluate the effects of short-term captopril administration on the response to cold pressor testing in normotensive and hypertensive subjects. Cold pressor testing was performed in 15 normotensive subjects and 15 hypertensive patients before and 90 minutes after captopril administration. Blood pressure and heart rate were measured before testing and at one-minute intervals from the beginning of cold pressor testing. Systolic time intervals were also assessed before and after testing. Captopril did not affect pressor responses to cold pressor testing in normotensive subjects or hypertensive patients. Basal heart rate (before testing) did not change, despite the decrease in blood pressure and showed a smaller increase in response to cold pressor testing in normotensive subjects, suggesting that captopril might interfere with arterial baroreflexes. The systolic time intervals were not modified by captopril except isometric contraction time; its basal value was reduced by captopril in both normotensive subjects and hypertensive patients. Cold exposure caused a similar increase in isometric contraction time before and after captopril in normotensive subjects, and the increase in isometric contraction time in hypertensive patients was greater. These findings suggest that captopril did not affect cardiac performance, indeed improving it, at least in basal conditions.

Adult↗

PubMed2026

Engineering cold stress resilience in capsicum annuum through functional genomics and precision breeding.

This review synthesizes the molecular mechanisms of cold tolerance in pepper, integrating multi-omics data,genome editing, and precision breeding strategies to accelerate the development of cold-resilient cultivars. Cold stress is a significant environmental factor that affects the growth, productivity, and fruit quality of Capsicum annuum by impairing membrane integrity photosynthesis and cellular redox homeostasis. Although pepper has several endogenous cold-responsive regulators such as CaNAC035 and CabHLH035, along with antioxidant defense systems, its cold tolerance remains limited due to low transcriptional activation of key regulators, functional redundancy among cold-responsive genes, and the polygenicity of cold tolerance. These complexities, combined with low genetic diversity and linkage drag, have hindered the improvement of cold-resistant cultivars through conventional breeding. This review brings together the recent progress in understanding the molecular mechanisms of cold stress perception, signal transduction, transcriptional regulation, metabolic reprogramming, and phytohormone interactions in pepper. Precision Breeding 2.0 is a new innovation that combines the integration of multi-omics-based target identification with next-generation genome-editing techniques, allowing precise and multiplex engineering of complex and interconnected regulatory networks instead of single genes. We cover new approaches such as engineering the DREB/CBF pathway, allele-specific editing and targeted disruption of negative regulators to enhance the pathway(s) involved in cold response. Moreover, we propose a roadmap for integration of transcriptomics, proteomics, metabolomics, high-throughput phenomics, and speed breeding to accelerate the identification, validation, and deployment of superior alleles to boost cold tolerance. This review provides a foundation for developing climate-resilient pepper cultivars by connecting functional genomics with precision genome engineering approaches to maintain productivity under variable environmental conditions.

Capsicum↗