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PubMed2006

Population-based case-control study of the common cold during pregnancy and congenital abnormalities.

The common cold is the most frequent maternal disease during pregnancy. The possible association between different congenital abnormalities and the common cold in pregnant women was evaluated in the data set of the Hungarian Case-Control Surveillance of Congenital Abnormalities between 1980 and 1996. Of 22,843 cases with congenital abnormalities, 3,827 (16.8%) had mothers with the common cold, while of 38,151 population controls without congenital abnormalities, 5,475 (14.4%) (adjusted prevalence odds ratio: POR: 1.26 with 95% CI: 1.20-1.32). Of 834 malformed controls with Down syndrome, 114 (17.3%) had mothers with the common cold (POR: 0.96 with 95% CI: 0.80-1.16). Nearly half of mothers with the common cold had secondary complications with antifever therapy. The comparison of cases with 25 congenital abnormalities and population control mothers with medically recorded common cold during the second and third months of gestation showed that five congenital abnormality groups: congenital hydrocephaly (3.6, 1.3-9.7), cleft lip+/-palate (2.3, 1.5-3.6), posterior cleft palate (2.3, 1.2-4.1), limb deficiencies (2.2, 1.1-4.1) and multiple CAs (2.0, 1.4-2.9) had adjusted POR 2 or more. The comparison of cases with different congenital abnormalities and malformed controls (including offspring with Down syndrome) as referent, indicated a higher prevalence of the common cold during the second and third month of gestation only in the mothers of cases with cleft lip+/-palate (adjusted POR: 1.7 with 95% CI: 1.2-2.5), however, congenital hydrocephaly, neural-tube defects and multiple CAs had also mothers with a somewhat higher occurrence of the common cold. The possible association between the common cold during early pregnancy and the above mentioned congenital abnormalities may be connected mainly with the indirect effect of secondary complications of maternal common cold, particularly high fever because antifever drugs were able to prevent the possible teratogenic effect of the common cold.

Analgesics, Non-Narcotic↗
PubMed1986

Cold exposure as a potentiating factor of pineal actions in nonhibernating mammals.

Twenty-eight-day-old male rats were used in three experiments to study whether cold exposure potentiates pineal actions in nonhibernating mammals. The following questions were considered: (a) Can cold exposure increase the antigonadal effects of light deprivation? (b) Are the effects induced by blindness plus cold exposure pineal dependent? (c) Can cold exposure modify the response of the endocrine-reproductive axis to exogenously administered melatonin? Blind cold-exposed rats showed a significant loss in body weight as well as in weights of pituitary and reproductive tract organs compared with either intact or blind animals kept at 22 degrees C, or intact rats exposed to cold; serum testosterone levels were also lowest in blind cold-exposed rats. These effects were not present in blind cold-exposed animals that were pinealectomized at the beginning of the experiment. When intact animals placed at 22 or 10 degrees C were treated with daily injections of melatonin (50 micrograms) there was a reduction of body weight and weights of the hypophyso-gonadal axis organs. Those effects of melatonin were, however, significantly greater in cold-exposed rats than in rats placed at 22 degrees C. These results suggest that cold exposure should be considered as another state which potentiates the pineal-dependent actions of light deprivation. Cold exposure probably acts by increasing the sensitivity of sites at which pineal melatonin exerts its actions.

Acclimatization↗
PubMed1992

Enhancement of cellular immune function during cold adaptation of BALB/c inbred mice.

The cell-mediated immune function of cold-adapted BALB/c inbred mice was studied in experiments of splenic lymphocyte blastogenesis, indicated by tritium-labeled deoxythymidine incorporation and SDS-PAGE autoradiography of synthetic proteins in lymphocytes. Male BALB/c inbred mice were randomly divided into two groups: control (living at 25 degrees C) and cold-exposed (living at 2 degrees C). Results are as follows: in contrast with the control group, there was an obvious fluctuation of cell-mediated immune function in the cold-exposed group at initial cold exposure because of transient stress to cold; then cell-mediated immune function gradually recovered to control level. From Day 15, the cell-mediated immune function of the cold-exposed group was remarkably enhanced. On Day 15, the lymphocyte blastogenesis rate was increased by 20.66% (P less than 0.05), which implies the onset of cold adaptation; on Days 21 and 31, the rates increased by 80.15% (P less than 0.05) and 40.36% (P less than 0.05), respectively. Two to six months later, with continuing cold exposure, the murine lymphocyte blastogenesis rate in the cold-exposed group remained higher than that in the control group. The lymphocyte protein synthesis of the cold-exposed group, indicated by tritium-labeled leucine incorporation, apparently increased on Day 15 and the stimulated rate was 101.47% (P less than 0.05). SDS-PAGE autoradiography of synthetic proteins in lymphocytes demonstrated that after 2 weeks of cold exposure, protein bands were enriched in both quantity and quality. These results are identical to the results obtained from lymphocyte blastogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed2026

Hot vs cold knife for endoscopic ablation of posterior urethral valves: a systematic review by the EAU-YAU paediatric urology working group.

INTRODUCTION: Posterior urethral valves (PUV) are the most frequent cause of congenital lower urinary tract obstruction in males. Despite early surgical ablation, up to 22% of patients develop chronic kidney disease and 11% progress to end-stage renal disease. Multiple endoscopic modalities have been described for valve ablation but the optimal technique remains uncertain. This systematic review aims to determine whether cold or hot knife ablation provides superior effectiveness for primary endoscopic treatment of PUV in a single surgical session. MATERIAL AND METHODS: A systematic search of PubMed and Embase databases was conducted to identify studies comparing cold and hot knife techniques for endoscopic ablation of PUV in children, covering all publications up to December 2025. The review was performed in accordance with PRISMA 2020 guidelines and was prospectively registered in PROSPERO (ID CRD420251180556). Original studies including patients <18 years who underwent primary valve ablation with postoperative cystoscopy or VCUG and &#x2265;6 months of follow-up were included. Quality assessment was done using RoB 2.0 for randomized trials and MINORS for observational studies. RESULTS: A total of 1581 studies were identified, of which 26 met the inclusion criteria, comprising one randomized controlled trial, five prospective, and 20 retrospective studies constituting a sum of 1725 paediatric patients. The overall methodological quality of included studies was moderate, with marked heterogeneity in design, follow-up duration, and outcome reporting, limiting direct comparisons across series. Thus statistical analysis was not possible. Of these, 829 (48.1%) underwent cold valve ablation and 896 (51.9%) underwent hot ablation techniques. Within the cold group, most patients were treated with a cold knife (80.2%), followed by balloon dilatation (7%), the Mohan valvotome (6.5%), cold hook (5%), and, rarely, a modified venous valvulotome (1.3%). Among hot techniques, 32.8% of procedures were performed by electro-fulguration with a resectoscope, 29.4% using a Bugbee electrode, 23.8% with a hook electrode and 14% with laser-based systems. Follow-up ranged from 6 months to 22 years across studies. Single-session success rates for valve ablation ranged from 22% to 100% in the cold resection group and from 71.4% to 100% in the hot resection group. Reintervention for residual valves was reported in 0%-78% of cold cases and in 0%-28.6% of hot resections. Urethral stricture rates ranged from 0% to 11.1% after cold incision and from 0% to 23.8% after hot techniques. Reporting of postoperative outcomes such as urinary tract infection, incontinence, bladder dysfunction, vesicoureteral reflux (VUR) resolution, hydronephrosis improvement, and renal function varied widely among studies and was assessed using different methodologies. CONCLUSIONS: Both cold and hot ablation techniques for PUV achieved high single-session success rates and low complication rates. Cold resection appeared slightly safer, although this finding should be interpreted cautiously given the heterogeneity and observational nature of the available data.

Humans↗
PubMed2006

Comparison of three models of neuropathic pain in mice using a new method to assess cold allodynia: the double plate technique.

The recent identification of receptors sensitive to cold stimuli increased the significance of using mice to study cold allodynia, one of the important features of neuropathic pain. However, commonly used techniques (simple cold plate and acetone technique) may be inappropriate to study cold allodynia in mice because of problems of interpretation. We have developed a new method for assessing aversion to a cold non-noxious stimulus. It consists of calculating the time that mice spend on a non-noxious cold plate during their explorative behavior versus a thermoneutral one. We used three different models of neuropathic pain: chronic constriction injury of the sciatic nerve (CCI), partial sciatic nerve ligation (PSL) and chronic constriction of the saphenous nerve (CCS) with their respective sham groups and naive animals to assess the double plate in comparison to the acetone drop technique. All operated mice displayed cold allodynia with both methods. The response to acetone and the time spent on the cold plate were correlated (r=-0.93) and we also showed that the CCI mice were more sensitive to cold. Pharmacological validation of this technique showed that CCI induced cold allodynia was alleviated by gabapentin. In conclusion, the double plate technique provides a new, relevant method for assessing cold allodynia in mice. The advantages and drawbacks with the other techniques are discussed.

Animals↗
PubMed1979

Cold blood as the vehicle for potassium cardioplegia.

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.

Adenosine Diphosphate↗
PubMed1998

Temporal and qualitative properties of cold pain and heat pain: a psychophysical study.

Dorsal horn neurons that respond to noxious cold also respond to noxious heat, suggesting the hypothesis that pain evoked by temperature extremes, whether hot or cold, may be processed similarly in the CNS. In this study, we tested perceptual consequences of this hypothesis by comparing characteristics of heat and cold pain, as well as of innocuous warm and cool. Eight healthy subjects performed psychophysical tasks involving hot and cold cutaneous stimuli. Using a 9-cm2 contact thermode, temperatures from -5 degrees to 48 degrees C were each applied for 30 s to the thenar eminence. Subjects gave continuous ratings of perceived temperature and pain intensity, using an electronic VAS. After each stimulus, subjects also reported the maximum stimulus intensity and unpleasantness, and chose appropriate words from a list of qualitative verbal descriptors. We found that larger temperature differences were needed in the noxious cold than in the noxious heat range to produce equal perceptual differences. Further, in the heat range, stimulus-response functions were steeper for noxious than for innocuous temperatures, whereas in the cold range, the opposite held true. The relative unpleasantness of heat pain did not differ from that of cold pain, but subjects used a wider range of qualitative words to describe cold pain. Perceived stimulus intensity was compared to temperature recordings from intradermal and skin surface thermocouples. Heat pain, cool and warmth appeared to depend on surface temperature, whereas cold pain was related to subcutaneous temperature, suggesting different receptors for noxious heat and noxious cold. These data, combined with results of human brain imaging and primate electrophysiological studies, suggest that the unpleasantness associated with both heat pain and cold pain is processed similarly in the CNS, whereas differential information about stimulus quality is preserved in the cerebral cortex.

Adult↗
PubMed2003

Cold transduction in rat trigeminal ganglia neurons in vitro.

Three sub-populations of sensory neurons may be distinguished based on responses to a decrease in temperature: one has a relatively low threshold for activation (cool fibers), a second has a high threshold for activation (cold nociceptors), and the third is unresponsive to a decrease in temperature. Results from several recent studies suggest that the ability to detect a decrease in temperature reflects an intrinsic property(ies) of sensory neurons and therefore may be characterized via the study of the sensory neuron cell body in vitro. However, while three unique ionic mechanisms of cold transduction have recently been identified (i.e. activation of the transient receptor potential channel M8 [TRPM8] or an epithelial Na(+) channel [ENaC] or inhibition of two pore K(+) channel [TREK-1]), the possibility that these "mechanisms" may be differentially distributed among sensory neurons in a manner consistent with predictions based on in vivo observations has not been investigated. To investigate this possibility, we have characterized the influence of cooling on isolated trigeminal ganglion (TG) neurons from adult rats in vitro with Ca(2+) microfluorimetry in combination with a series of pharmacological interventions. We report that neurons responded to a decrease in temperature from approximately 34 degrees C to approximately 12 degrees C in one of two ways: 1) with a low threshold (30.1+/-0.6 degrees C) for activation demonstrating an increase in fluorescence with a minimal decrease in bath temperature (12.3%); 2) with a high threshold for activation (21.5+/-0.6 degrees C), demonstrating an increase in fluorescence only after a substantial decrease in bath temperature (13.3%); 74.4% did not respond to a decrease in temperature with an increase [Ca(2+)](i). These responses also were distinguishable on the basis of their rate of activation and degree of desensitization in response to prolonged application of a cold stimulus: low threshold responses were associated with a rapid (tau=12.0+/-5.7 s) increase in [Ca(2+)](i) and a time constant of desensitization of 85.8+/-20.7 s while high threshold responses were associated with a slow (tau=38.1+/-8.2 s) increase in [Ca(2+)](i) and demonstrated little desensitization over 4 min of stimulation. We refer to low threshold and high threshold cold responsive TG neurons as LT(cool) and HT(cool) neurons, respectively. LT(cool) and HT(cool) neurons were distributed among two distinct subpopulations of TG neurons distinguishable on the basis of cell body size and isolectin B4 staining. Both ENaC and TRPM8 appear to contribute to cold transduction, but neither is sufficient to account for all aspects of cold transduction in either population of TG neurons. Furthermore, inhibition of Ba(2+) and/or Gd(3+) sensitive two-pore K(+) channels (i.e. TREK-1 and TRAAK) was insufficient to account for cold transduction in HT(cool) or LT(cool) neurons. Our results suggest that cold transduction in sensory neurons is a complex process involving the activation and inhibition of several different ion channels. In addition, there appear to be both similarities and differences between mechanisms underlying cold transduction in LT(cool) and HT(cool) neurons. Identification of specific mechanisms underlying cold transduction in LT(cool) and HT(cool) neurons may enable the development of novel therapeutic interventions for the treatment of pathological conditions such as cold allodynia.

Animals↗
PubMed2001

Cold adaptive thermogenesis in small mammals from different geographical zones of China.

The mechanisms of thermogenesis and thermoregulation were studied in the tree shrew (Tupaia belangeri) and greater vole (Eothenomys miletus) of the subtropical region, and Brandt's vole (Microtus brandti), Mongolian gerbil (Meriones unguiculatus), Daurian ground squirrel (Spermophilus dauricus) and plateau pika (Ochotona curzoniae) of the northern temperate zone. Resting metabolic rate (RMR) and non-shivering thermogenesis (NST) increased significantly in T. belangeri, E. miletus, M. brandti and M. unguiculatus after cold acclimation (4 degrees C) for 4 weeks. In T. belangeri, the increase in RMR and thermogenesis at liver cellular level were responsible for enhancing the capacity of enduring cold stress, and homeothermia was simultaneously extended. Stable body temperature in M. brandti, E. miletus, M. unguiculatus and O. curzoniae was maintained mainly through increase in NST, brown adipose tissue (BAT) mass and its mitochondrial protein content, and the upregulation of uncoupling protein (UCP1) mRNA, as well as enhancement of the activity of cytochrome C oxidase, alpha-glycerophosphate oxidase and T(4) 5'-deiodinase in BAT mitochondria. The RMR in O. curzoniae and euthermic S. dauricus was not changed, while NST significantly increased during cold exposure; the former maintained their stable body temperature and mass, while body temperature in the latter declined by 4.8 degrees C. The serum T(3) concentration or ratio of T(3)/T(4) in all the species was enhanced after cold acclimation. Results indicated that: (1) the adaptive mechanisms of T. belangeri residing in the subtropical region to cold are primarily by increasing RMR and secondly by increasing NST, and the mechanisms of thermogenesis are similar to those in tropical mammals; (2) in small mammals residing in northern regions, the adaptation to cold is chiefly to increase NST; (3) the mechanism of cold-induced thermogenesis in E. miletus residing in subtropical and high mountain regions is similar to that in the north; (4) a low RMR in warm environments and peak RMR and NST in cold environments enabled M. unguiculatus to tolerate a semi-desert climate; (5) O. curzoniae has unusually high RMR and high NST, acting mainly via increasing NST to adapt to extreme cold of the Qinghai-Tibet Plateau; (6) the adaptation of euthermic S. dauricus to cold is due to an increase in NST and a relaxed homeothermia; and lastly (7) the thyroid hormone is involved in the regulation of cold adaptive thermogenesis in all the species studied.

Adaptation, Physiological↗
PubMed2001

Cold-activation of Brassica napus BN115 promoter is mediated by structural changes in membranes and cytoskeleton, and requires Ca2+ influx.

Previous studies on cold-triggered events leading to Ca2+ influx during cold acclimatization have been conducted on either unicellular cyanobacterium Synechocystis or plant cell suspensions, and used transcript levels of cold-induced genes as end-point markers. Whether the results of these studies are valid for intact plants or their organs is not known. Here we examine cold signaling in transgenic Brassica napus seedlings carrying, in addition to the endogenous cold-inducible BN115 gene, the beta-glucuronidase (GUS) gene placed under control of the BN115 promoter. The activity of BN115 promoter was monitored at the transcriptional and translational levels by determining accumulation of BN115 transcripts and by histochemical assay of GUS activity. Cold-activation of BN115 was strongly inhibited by the membrane fluidizer benzyl alcohol, but mimicked at 25 degrees C by the membrane rigidifier dimethylsulfoxide (DMSO). The cold induction of BN115 was also inhibited by stabilizers of microtubules and actin microfilaments, taxol and jasplakinolide, respectively, but was mimicked at 25 degrees C by microtubule destabilizer oryzalin or colchicine, or by microfilament destabilizer latrunculin B. Gd3+ or ruthenium red prevented the cold activation of BN115, but Ca2+ ionophore A23187 or cyclic ADP-ribose activated it at 25 degrees C. Inhibitors of tyrosine kinases, protein kinase C and phosphoinositide kinases prevented the cold activation of BN115, but inhibitors of protein phosphatases (PP) 1 and 2 A activated BN115 at 25 degrees C. Constitutively expressed GUS activity in another transgenic line of the same cultivar of B. napus, was not affected by cold or any of the chemical treatments used in the experimentation. Activation of BN115 at 25 degrees C by DMSO, Ca2+ ionophore, cADPR, and by inhibitors of PP1 and 2A was accompanied by an increased freezing tolerance. It was concluded that the cold-activation of BN115 requires membrane rigidification, cytoskeleton reorganization, Ca2+ influx and action of several types of protein kinases.

Brassica↗
PubMed1992

Energy metabolism during cold exposure.

Recent advances on the influence of cold exposure on energy metabolism in animals and humans are summarized. Although the cold-induced enhancements in carbohydrate metabolism have been the focus of numerous studies, it was only recently that pieces of evidence from animal studies have suggested that cold exposure exerts an insulin-like effect on peripheral tissue glucose uptake, which appears to proceed primarily via insulin-independent pathways. Interestingly, this phenomenon was observed in insulin-sensitive tissues of warm- a well as cold-adapted rats. Whereas previous human studies have concentrated on the cold-induced changes in basal levels of hormones and metabolic substrates, recent work from our laboratory has demonstrated that exposure to cold at rest shifts substrate utilization from mainly lipids at thermal neutrality to carbohydrates, representing the main fuel for shivering thermogenesis. Further investigation has revealed that the marked increment in carbohydrate oxidation in cold-exposed humans is derived from a greater utilization of both circulating glucose and intramuscular glycogen. With respect to lipid metabolism, recent studies have shown that the cold-induced increase in lipid oxidation in man is fuelled primarily by the fatty acids released from white adipose tissue triglycerides (TG) and possibly intramuscular TG, not plasma TG. One practical application of this work on energy metabolism in the cold resides in the pharmacological approach to improve cold tolerance, where pharmacological agents that alter energy metabolism and substrate utilization could be used to enhance cold thermogenesis and produce warmer body temperatures.

Animals↗
PubMed2003

Treatment of cold injury-induced brain edema with a nonspecific matrix metalloproteinase inhibitor MMI270 in rats.

Blood-brain barrier (BBB) disruption is a critical event leading to vasogenic brain edema and secondary brain damage after cold injury-induced brain trauma. Matrix metalloproteinases (MMPs), a family of proteolytic enzymes which degrade the extracellular matrix, are implicated in BBB disruption in this model. The purpose of this study was to examine the effects of MMI270 (N-hydroxy-2(R)-[(4-methoxysulfony) (3-picolyl)-amino]-3-metylbutaneamide hydrochloride monohydrate), a synthetic nonspecific MMP inhibitor, on cold injury-induced brain edema in rats. Cold injury was induced by applying a copper probe cooled with liquid nitrogen on the parietal skull for 30 sec in 38 rats. Treatment with MMI270, a bolus injection at a dose of 30 mg/kg, was started immediately after the induction of cold injury and was continued for 24 h at a dose of 40 mg/kg/day using an intraperitoneal osmotic minipump (n = 7). In the untreated control group (n = 7), rats were administered a vehicle and implanted with a vehicle-containing osmotic pump. Two percent Evans Blue (EB) in saline (1 mL/kg) was administrated intravenously immediately after the cold injury in another group of rats, six of which were untreated and six of which were treated with MMI270 at the above dose. At 24 h after the cold injury, the brain water content and the BBB permeability to EB were determined. To assess the protective effect of MMI270 on secondary brain lesion after the cold injury, the MMI270-treated rats received a bolus injection at a dose of 30 mg/kg, followed by a continuous administration of MMI270 for 7 days at a dose of 40 mg/kg/day using an osmotic minipump (n = 6). In the untreated control group (n = 6), the rats were administered the vehicle and implanted with a vehicle-containing osmotic pump. At 7 days after cold injury, the secondary brain lesion was assessed using hematoxylin and eosin (H-E) staining. Compared with the untreated control group, treatment with MMI270 significantly reduced the brain water content in the ipsilateral core and intermediate areas (p < 0.05 and p < 0.01) and protected the BBB integrity to EB in the ipsilateral core area (p < 0.05) at 24 h after the cold injury. The secondary lesion was significantly smaller in the MMI270-treated animals compared with the untreated animals (p < 0.05) a 7 days after the cold injury. O kur results indicate that treatment with MMI270 in rats exhibits protection in acute brain edema formation and secondary brain damage by attenuating the BBB permeability after cold injury.

Animals↗
PubMed2004

Cold adaptation in budding yeast.

We have determined the transcriptional response of the budding yeast Saccharomyces cerevisiae to cold. Yeast cells were exposed to 10 degrees C for different lengths of time, and DNA microarrays were used to characterize the changes in transcript abundance. Two distinct groups of transcriptionally modulated genes were identified and defined as the early cold response and the late cold response. A detailed comparison of the cold response with various environmental stress responses revealed a substantial overlap between environmental stress response genes and late cold response genes. In addition, the accumulation of the carbohydrate reserves trehalose and glycogen is induced during late cold response. These observations suggest that the environmental stress response (ESR) occurs during the late cold response. The transcriptional activators Msn2p and Msn4p are involved in the induction of genes common to many stress responses, and we show that they mediate the stress response pattern observed during the late cold response. In contrast, classical markers of the ESR were absent during the early cold response, and the transcriptional response of the early cold response genes was Msn2p/Msn4p independent. This implies that the cold-specific early response is mediated by a different and as yet uncharacterized regulatory mechanism.

Adaptation, Physiological↗
PubMed1996

Genetic influences on blood pressure with the cold-pressor test: a twin study.

OBJECTIVES: To determine the genetic and environmental contributions to resting blood pressure, the level of blood pressure during the cold-pressor test and the increase in blood pressure with the cold-pressor test in an adult cohort of normotensive twins. DESIGN AND METHODS: Ninety-one monozygotic and 41 dizygotic normal twin pairs were recruited by advertisement. The mean age was 34 +/- 14 years (mean +/- SD). Systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate were measured continuously at the finger (using a Finapres device) and verified at the upper arm oscillometrically (using a Dinamap device) every minute. The cold-pressor test was conducted by immersing the non-dominant hand into cold (< 4 degrees C) water for 2 min. Statistical analysis was performed by using the SPSS program; parameters of the quantitative genetic models were estimated by path-analysis techniques using the LISREL 8 program. RESULTS: Heritability estimates of additive genetic effects were statistically significant for SBP and DBP but not for heart rate during rest and during the cold-pressor test. Furthermore, the path analysis indicated shared as well as specific genetic components both for the blood pressure level at rest and for that during the cold-pressor test. However, the genetic influences on the blood pressure level at rest and on the increase in blood pressure during the cold-pressor test (the blood pressure level during the cold-pressor test minus that during rest) were entirely independent of one another. CONCLUSIONS: A significant genetic covariation exists for SBP and DBP during rest and during the cold-pressor test, as well as a significant genetic variation that is specific to the cold-pressor stress condition. These findings suggest that different genes or sets of genes contribute to blood pressure regulation during rest and to blood pressure reactivity to cold-pressor stress.

Adult↗
PubMed1985

On the regulation of cold-labile cytosolic and of mitochondrial acetyl-CoA hydrolase in rat liver.

The discovery of a cold-labile cytosolic acetyl-CoA hydrolase of high activity in rat liver by Prass et al. [(1980) J. Biol. Chem. 255, 5215-5223] has questioned the importance of mitochondrial acetyl-CoA hydrolase for the formation of free acetate [Grigat et al. (1979) Biochem. J. 177, 71-79] under physiological conditions. Therefore this problem has been reevaluated by comparing various properties of the two enzymes. Cold-labile cytosolic acetyl-CoA hydrolase bands with an apparent Mr of 68000 during SDS/polyacrylamide gel electrophoresis, while the native enzyme elutes in two peaks with apparent Mr of 136000 and 245000 during gel chromatography in the presence of 2 mM ATP. The mitochondrial enzyme elutes under the same conditions with an apparent Mr of 157000. Under conditions where the cold-labile enzyme binds strongly to DEAE-Bio-Gel and ATP-agarose, the mitochondrial enzyme remains unbound. The cold-labile enzyme can be activated 14-fold by ATP, half-maximal activation occurring already at 40 microM ATP. AdoPP[NH]P, AdoPP[CH2]P and GTP have a similar though weaker effect. ADP as well as GDP can completely inhibit the cold-labile enzyme with 50% inhibition occurring for both nucleotides at about 1.45 microM. The binding of ATP and ADP is competitive. Acetyl phosphate and pyrophosphate have no effect on the activity of the cold-labile enzyme. The mitochondrial acetyl-CoA hydrolase is not affected by these nucleotides. CoASH is a strong product inhibitor (approximately equal to 80% inhibition at 40 microM CoASH) of the cold-labile enzyme, but only a weak inhibitor of the mitochondrial enzyme. Under in vivo conditions the activity of the cold-labile cytosolic acetyl-CoA hydrolase can be no more than 7% of the activity calculated for mitochondrial acetyl-CoA hydrolase under the same conditions. Accordingly the mitochondrial enzyme seems to be mainly responsible for the formation of free acetate by the intact liver, especially in view of the fact that the substrate specificity of the mitochondrial enzyme is much higher (activity ratios acetyl-CoA/butyryl-CoA 4.99 and 1.16 for the mitochondrial and the cold-labile enzyme respectively). Alloxan diabetes neither increased the activity of the cold-labile enzyme nor that of the mitochondrial enzyme. No experimental support has been found yet for the hypothesis that the acetyl-CoA hydrolase activity of the cold-labile enzyme represents the side-activity of an acetyl-transferase.

Acetyl-CoA Hydrolase↗
PubMed1980

New intervention in mitral valve prolapse. Use of cold pressor test during echocardiography.

A study was performed in 13 patients with idiopathic mitral valve prolapse and in 21 control subjects to assess the effect of the cold pressor test on systolic motion of the mitral valve. A significant increase in blood pressure occurred in 10 patients with mitral valve prolapse and in 19 controls after immersion of one hand in ice-cold water. M-mode echocardiographic recordings from the mitral valve were obtained in all patients before, during, and after the cold pressor test, together with simultaneous phonocardiograms in selected patients. Nine out of 10 patients with mitral valve prolapse and a hypertensive response to the cold stimulus showed a significant increase in the depth of mitral valve prolapse during the cold pressor test whereas in three patients with mitral valve prolapse and no hypertensive response the depth of mitral valve prolapse did not change during cold stimulation. Three patients with previously demonstrated mitral valve prolapse had equivocal resting echocardiograms but developed diagnostic evidence of mitral valve prolapse during the cold pressor test. No evidence of mitral valve prolapse was seen in any of the control subjects before, during or after the cold pressor test. In four patients with mitral valve prolapse and a hypertensive response to cold stimulation the systolic click was delayed by the cold pressor test, whereas the time of the systolic click remained constant in the three patients whose blood pressure did not increase. It is concluded that the cold pressor test provides a stimulus sufficient to delay the onset and increase the depth of mitral valve prolapse, thereby enhancing the diagnostic sensitivity of echocardiography in this condition.

Adult↗
PubMed1995

Vasoconstrictor peptides and cold intolerance in patients with stable angina pectoris.

BACKGROUND: The exact mechanism that explains the phenomenon of cold intolerance in patients with angina remains controversial. Although the response to the effects of a cold environment has been examined in these patients, their response to cold air inhalation has produced conflicting results. In addition, the possible role of vasoactive peptides in the pathophysiology has not been explored. OBJECTIVES: The aims of this study were to examine the response of patients with stable angina to the effects of cold air inhalation during exercise testing, and to investigate the possible role played by the vasoconstrictor peptides endothelin-1 (ET-1) and angiotensin-II (AT-II) in the pathophysiology. METHODS: In a randomised order, 12 men with stable angina, whose medication had been stopped, underwent two separate symptom limited treadmill exercise tests. At one visit the patients exercised while breathing room air and at the other visit they exercised while breathing cold air from a specially adapted freezer. Serial peripheral venous blood samples were taken for ET-1 and AT-II estimations during each visit. RESULTS: Cold air inhalation resulted in a significant reduction in the mean time to angina (232.7 (20.4) s v 274.1 (26.9) s, P = 0.04) and the mean total exercise time (299.5 (27.0) s v 350.3 (23.9) s, P = 0.008), but no significant change in the time to 1 mm ST depression (223.3 (29.0) s v 241.3 (29.2) s, P = 0.25). There was no significant difference between the rate-pressure products at the onset of angina (P = 0.13) and the time to 1 mm ST depression (P = 0.85), but at peak exercise the rate-pressure product was significantly lower in patients breathing cold air as opposed to room air (P = 0.049). There was an equivalent significant decrease in ET-1 concentrations at peak exercise compared with that at rest at both visits (room air 5.0 (0.7) pmol/l v 4.3 (0.7) pmol/l, P = 0.03; cold air 4.4 (0.6) pmol/l v 3.8 (0.5) pmol/l, P = 0.02). There was a significant increase in AT-II concentrations 10 min after peak exercise in patients breathing room air (39.2 (6.1) pmol/l v 32.1 (4.8) pmol/l, P = 0.01) which was not repeated during cold air inhalation (36.6 (3.4) pmol/l v 28.3 (3.4) pmol/l, P = 0.07). CONCLUSIONS: Cold air inhalation in patients with stable angina results in an earlier onset of angina and a reduction in exercise capacity. Both peripheral and central reflex mechanisms appear to contribute to the phenomenon of cold intolerance. Peripheral ET-1 and AT-II do not appear to play a significant role in the pathophysiology.

Aged↗
PubMed1982

Cold acclimation in insulin secretion of isolated perfused pancreas of the rat.

The secretory function of the endocrine and exocrine pancreas in the process of cold acclimation has been studied in rats fed at an ambient temperature of 2 degrees C. In anesthetized rats, plasma glucose decreased immediately after cold exposure and increased again toward the basal level after 20 days of continuous cold exposure. Plasma insulin level in these rats also decreased immediately after cold exposure, and the low level was maintained throughout the whole period of cold exposure. In the isolated perfused rat pancreas, the basal insulin output estimated before the stimulation with glucose decreased immediately after the cold exposure and increased gradually during the continuous cold exposure. In these preparations, the initial and the second phases of insulin output were induced by sustaining stimulation with 16.7 mM glucose. Changes in the glucose-induced initial and second phases showed a diphasic pattern during the course of cold exposure. Thus, there was temporary decrease within a week of cold exposure followed by a gradual increase after 3 wk of this condition. The diphasic insulin output in the preparation isolated from rats fed during cold exposure for 6 wk was twice as much as that in the preparation isolated from the rats fed during exposure to 23 degrees C for 5 wk. In the isolated perfused rat pancreas, a monophasic insulin output was induced by sustaining stimulation with 0.1 microM ACh. The monophasic insulin output showed an increasing tendency during cold exposure, but the increase was insignificant because of a larger individual variation.

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