Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Rewarming”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed1962

Cold injury in civil disaster.

Patients exposed to cold environment following a disaster may be suffering from local cold injury or from systemic cold injury (accidental hypothermia). The treatment of the former is well established and consists of rapid rewarming of the frozen parts and physical therapy; early amputation is not advisable. Recommendations for the assessment and treatment of total body cooling, based on case reports of accidental hypothermia, on the results of animal experiments and on the clinical experience with induced hypothermia, are not well established and are controversial. Since, at temperatures below 30 degrees C., death may be caused by cardiac arrhythmias and since, at this low level, spontaneous rewarming may not be possible, active rewarming is recommended at this stage. At a higher temperature level, vigorous warming is dangerous, and the patient's own regulatory mechanisms should be allowed to restore the temperature.

Animals↗
PubMed1996

Hemofiltration in very severe hypothermia with favorable outcome.

Hypothermia is a dangerous situation. It is defined by a core temperature of less than 35 degrees C. Aggressive rewarming is used if it is lower than 30 degrees C, comprising extracorporeal therapies. A case of a 63 year old lady is reported whose temperature was 21.8 degrees C, circulation was unstable, respiratory insufficiency prevailed and severe neurological dysfunction. Serum potassium was 2.9 mmol/l and pH corrected for temperature 7.61. The patient was rewarmed by hemofiltration (HF) over 6 hours with substitution of 18 l of a solution containing a concentration of potassium of 5 mmol/l. Though potassium levels declined initially and than slowly normalized in 9 hours there were no arrhythmias documented. The ECG showed prolongation of the PQ-, QRS-, and especially the QT-times. All clinical and neurological sequelae had disappeared after four days. HF thus seems to be a safe method of rewarming in very severe hypothermia.

Electrocardiography↗
PubMedDate not supplied

Does it make sense to heat gases higher than body temperature for the treatment of cold water near-drowning or hypothermia? A point of view paper.

There appears to be several areas of concern relating to the continued use of heating gases higher than body temperature for the treatment of cold water near-drowning. The use of heated gases as a primary means to rewarm a hypothermic patient does not seem to be any more effective than doing nothing at all. These low rewarming rates translate into some very long resuscitations. Even Dr. Nemiroff, who was a strong advocate of using heated humidified gases for treating cold water near-drowning, did not consider the use of warm inspired gases to be a primary rewarming technique. He referred to the use of heated humidified gases as a, "stabilization technique". However, does it make sense to use a technique that is several times slower than other methods of similar complexity? Does it make sense to use a protocol that may in fact lower a hypothermic patient's basal metabolic rate? There are some major patient safety issues raised by heating gases to high levels. However, there have not been many patients with documented airway damage. I have several hypothesis about why this is so. Few people seem to know how to significantly heat their patient's circuit. If they devise a system that gets to the therapeutic range they usually have second thoughts when the bag-valve-mask is too hot to hold, or the plastic wide bore tubing begins to melt, they will reduce the system temperature on that basis alone. Many of the hypothermic patients who are intubated simply do not have good survival rates, and so we may underestimate the degree of airway damage that occurs. Spontaneously breathing patients will tend to refuse to breathe hot gases which limits their potential for airway damage. However, is this a risk we need to run? Would it not make more sense to heat the inspired gases to close to body temperature and avoid the problem? I feel that the time has come for the Respiratory Therapy community to come together and work on this problem. The researchers have done their jobs in providing us with reasonable data on which to base a clinical decision. It would seem to me that if a Clinical Practice Guideline for cold water near-drowning or hypothermia were in place it might provide the other groups impetus for updating their guidelines. The bottom line is that patients deserve the best care that we know how to provide, and a clear set of guidelines is an essential first step.

Attitude of Health Personnel↗
PubMed1998

The convective afterdrop component during hypothermic exercise decreases with delayed exercise onset.

HYPOTHESIS: Following cold water immersion, the post-cooling decrease in esophageal temperature (Tes) (i.e., afterdrop) is 3 times greater during exercise than during shivering, presumably due to increased muscular blood flow and convective core-to-periphery heat loss with exercise (J. Appl. Physiol. 63:2375, 1987). We felt that if exercise were to commence once the afterdrop period during shivering is complete, the threat of a further decrease in Tes (i.e., a second afterdrop) during the subsequent exercise would be minimized because much of the convective capacity for core cooling would already be dissipated. METHODS: Six subjects were each cooled three times in 8 degrees C water, until Tes decreased to 35.3 +/- 0.7 degrees C, and rewarmed by either shivering alone, exercise, or exercise commencing once a shivering afterdrop period was complete. RESULTS: The initial afterdrop was greater during Exercise only (1.1 +/- 0.4 degrees C) than Shivering only (0.35 +/- 0.3 degrees C) and Shivering-Exercise (0.45 +/- 0.2 degrees C) (p < 0.05). In contrast, exercise caused a secondary afterdrop of only 0.38 +/- 0.3 degrees C during Shivering-Exercise (p < 0.05). The initial rewarming rate during Exercise only (3.45 degrees C.h-1) was greater than the initial (2.7 degrees C.h-1) and second (2.4 degrees C.h-1) rewarming rates during Shivering-Exercise (p < 0.05), but not significantly greater than during Shivering only (2.99 degrees C.h-1) (p < 0.1). DISCUSSION: It is likely that during the Shivering-Exercise protocol, continued blood flow to shivering muscles: a) contributes to the initial afterdrop, and thus b) diminishes the convective capacity (or heat sink) available for further cooling during subsequent exercise.

Adult↗
PubMed1998

Hypothermia in trauma patients.

Accidental hypothermia (AH) can be defined as an unintentional decrease in core temperature below 35 degrees C during cold exposure by individuals without intrinsic thermoregulatory dysfunction. Pathophysiological changes can be attributed both to the severity of hypothermia and to co-morbid factors such as trauma, submersion, intoxication and underlying diseases. In trauma victims stratified according to the Injury Severity Score, the factor hypothermia is considered to be a poor prognostic sign for survival. In these patients rewarming therapy should be applied as soon as possible. In the Utrecht University Hospital, adult patients with AH are managed according to an algorithm based on their presenting hemodynamic conditions. Patients with perfusing cardiac rhythms and systolic pressures over 80 mmHg will receive continuous arteriovenous rewarming (CAVR). Arrested and hemodynamically instable patients are treated with cardiopulmonary bypass (CPB). In a 3-year period, 22 patients with AH were admitted to the emergency department. Fourteen patients had a trauma as the cause of hypothermia. Twenty patients were treated according to the algorithm (CAVR n = 18, CPB n = 2) and two patients were alternatively managed. Mortality in the CAVR group was 28% and total mortality reached 32%. Complications of CAVR are related to placement and removal of vascular catheters and may be severe in these patients with impaired coagulation. CAVR permits a good access to the (trauma-) patient and rewarming can be continued synchronously with diagnosis and treatment of various injuries.

Adolescent↗
PubMed1978

Surface cooling (20 degrees C) and circulatory arrest in infants undergoing cardiac surgery. Results in ventricular septal defect, complete atrioventricular canal, and total anomalous pulmonary venous connection.

During a six-year period, 46 severely symptomatic infants (average age, 5.1 months) underwent correction of ventricular septal defect (22 patients), total anomalous pulmonary venous connection (13 patients), and complete atrioventricular canal (11 patients), with the use of surface cooling to 20 degrees C. Cardiac repair was performed during circulatory arrest, and rewarming was performed with a pump oxygenator. Ten patients undergoing repair of ventricular septal defects were studied hemodynamically at 21 degrees C, before repair and at 37 degrees C after rewarming. Heart rate, left ventricular systolic pressure, maximum dp/dt, cardiac index, stroke work, and oxygen consumption were reduced substantially at 21 degrees C. Systemic vascualr resistance was increased at 21 degrees C. All changes were reversible with repair and rewarming. A protocol for hemodilution and crystalloid volume loading was devised to maintain urine output after early patients were noted to demonstrate renal dysfunction. With this protocol, survival rates were 89% for patients with ventricular septal defects, 67% for those with atrioventricular canal defects, and 85% for those with total anomalous pulmonary-venous connection.

Blood Pressure↗
PubMed2001

Induction of apoptosis in human colon carcinoma cells HT29 by sublethal cryo-injury: mediation by cytochrome c release.

Cryosurgery is an emerging treatment for human solid tumors, notably colorectal liver metastasis. Cryosurgical procedures generate a thermal gradient of from at least -50 degrees C at the center of the tumor being treated to about 0 degrees C at the periphery. Cell death occurs by necrosis in the center, while the peripheral zone of frozen tumor harbors a mix of viable and dead tissue. In order to understand the mechanisms of cell death and survival in this peripheral area at risk for tumor recurrence, we have established an in vitro freezing system that mimics in vivo conditions of sublethal injury. HT29 colon cancer cells were subjected to freezing temperatures from -6 degrees C to -36 degrees C, thawed at room temperature for 30 min and rewarmed at 37 degrees C for a period of time. Post-freeze-thaw, cryolytic cells were evaluated by trypan blue exclusive assay. We also identified apoptotic cells after rewarming by cell shrinkage, nucleic condensation, TUNEL assay, DNA fragmentation and PARP degradation. The intensity of cryolysis and apoptosis was increased by lowering the freezing temperature. At -36 degrees C, all cells were dead immediately after freeze-thaw. A kinetic analysis of cryo-induced apoptosis showed that the commitment to enter apoptosis occurred right after the freeze-thaw period and lasted less than 8 hr after rewarming. We further demonstrated that freezing triggers one of the caspase cascade involved in apoptosis: release of cytochrome c from mitochondria to cytosol, followed by activation of caspase-9 and degradation of PARP. These results indicate the death of cancer cells under cryo-treatment at sublethal freezing temperature can be attributed 2 different modes, cryolysis as well as apoptosis. HT29 cells carrying p53 mutant have very quick response for induction of apoptosis by cryo-treatment and contain an intact pathway of caspase cascade. Further studies will address if mechanisms in cells with wild-type p53 will differ.

Apoptosis↗
PubMed2005

Changes in tyrosine phosphorylation associated with true capacitation and capacitation-like state in boar spermatozoa.

Capacitation is defined as a series of events that render boar sperm competent to fertilize, either in vivo or in vitro. Moreover, preliminary stages of cryopreservation of spermatozoa involving cooling to 5 degrees C have been shown to induce capacitation-like changes in boar spermatozoa. Capacitation of boar spermatozoa is accompanied by protein phosphorylation, however the relationship between both processes is poorly understood. Capacitation status was assessed by chlortetracycline (CTC) staining. Changes in protein tyrosine phosphorylation were examined in pre-cleared whole cell lysates using a specific anti-phosphotyrosine monoclonal antibody. Our results in boar spermatozoa show a significant positive correlation between p32 tyrosine phosphorylation levels and percentage of capacitated (CTC pattern B) spermatozoa. Moreover, incubation of boar spermatozoa with two unrelated tyrosine kinase inhibitors induces a significant reduction in the percentages of capacitated and acrosome-reacted (AR) boar spermatozoa and a reduction in the p32 tyrosine phosphorylation. In our conditions, cooling boar spermatozoa to 5 degrees C and rewarming to 39 degrees C in a noncapacitating medium results in similar CTC staining patterns to those obtained after incubation of boar sperm for 1 or 4 hr at 39 degrees C in a capacitating medium. However, cooled-rewarmed fails to induce an increase in p32 tyrosine phosphorylation in boar spermatozoa. Moreover, CTC staining patterns of cooled-rewarmed spermatozoa do not change after incubation with a tyrosine kinase inhibitor. In conclusion, our results show a direct relationship between capacitation and tyrosine phosphorylation and suggest that p32 tyrosine phosphorylation levels could be used as a marker of the true capacitation changes observed in boar spermatozoa. Moreover, our results show that true capacitation and capacitation-like changes induced after cooling involve alternative intracellular tyrosine phosphorylation pathways in boar spermatozoa.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1977

A histofluorescence study of events accompanying accumulation and migration of norepinephrine within locally cooled nerves.

Glyoxylic acid was used to induce fluorescence in sections of rabbit sciatic nerve. In fresh nerves treated with this agent there were scattered finely beaded axons with a weak blue-green fluorescence. During local cooling, blue-green fluorescence accumulated steadily at the proximal boundary of the cooled region but never at its distal boundary. This accumulation gave rise to dilated axons that often swelled into brilliantly fluorescent balloon-like structures up to 10 microgram in diameter. Axonal fluorescence was probably specific for norepinephrine, being enhanced by inhibition of the metabolism and diminished by inhibition of the synthesis or storage of this neurotransmitter. After local cooling of nerves for 1.5 hr, specific fluorescence was confined within 0.8 mm of the cooled region. Rewarming led to rapid removal of fluorescence from the cooled region and to disappearance of most of the balloon-like swellings. Simultaneously, rewarming caused brightly fluorescent fibers that were neither dilated nor swollen to appear in distal regions of nerve. As this wave of fluorescence migrated distally with increasing duration of rewarming, it was spread over increasingly broad regions of nerve, which suggests that axonal transport of norepinephrine may invole some kind of dispersive process.

Animals↗
PubMed1993

Cytoprotective effect of glycine in cold stored canine renal tubules.

Reperfusion injury has been suggested to cause delayed graft function in renal transplantation. Methods to reduce reperfusion injury could lead to improved clinical renal transplantation. Glycine has been shown to suppress reperfusion injury in rabbit renal tubules and rat hepatocytes. In this study we have determined the effects of glycine on viability of isolated canine renal tubules. Renal tubules were cold stored at 4 degrees C under hypoxic conditions for up to 96 h in the UW solution and rewarmed to 37 degrees C for up to 2 h under oxygenated conditions to simulate reperfusion of an organ after cold static storage. Short-term storage (24 to 48 h) did not cause membrane injury (leakage of lactate dehydrogenase (LDH)) on rewarming. However, after 72 and 96 h cold storage reperfusion injury was evident and LDH leakage increased from about 25% to 59 +/- 3% and 71 +/- 2% at 72 and 96 h cold storage, respectively. The presence of 3 mM glycine in the reperfusion medium suppressed injury to cold-stored renal tubules. After cold storage for 72 and 96 h LDH leakage was reduced to control concentrations (31 +/- 3% and 29 +/- 1%, respectively). After cold storage for 72 h there was a reduction in ATP concentration in rewarmed renal tubules (3 nmol/mg protein at 48 h to 1.25 nmol/mg protein at 72 h). Also, there was a loss of mitochondrial functions including decreased stimulation of oxygen consumption by uncoupling of oxidative phosphorylation. Although glycine suppressed LDH leakage in renal tubules cold stored for 72 h it had no effect on the regeneration of ATP or mitochondrial functions, which remained depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

Prostaglandin E2, interleukin-1 alpha, and potassium release from artificial human skin after freeze-thaw injury.

Living skin equivalent (LSE) was used to identify nonvascular aspects of freeze-thaw injury to human skin cells. Pairs of transwell cell culture inserts, containing LSE, were washed twice for 30 min in maintenance media at 37 degrees C in a CO2 incubator and placed in two wells of a six-well assay tray (containing assay media). One specimen was maintained at room temperature. The other was cooled at 1 degrees C/min to -15 degrees C and rapidly rewarmed. Both were incubated for 24 h on fresh maintenance media at 37 degrees C in a CO2 incubator. This process was repeated producing 12 per group. Prostaglandin E2 (PGE2), interleukin-1 alpha (IL-1 alpha), and K+ were measured (mean +/- SE) in the assay medium, after the rewarming interval, and in the maintenance media after the 24-h incubation. Specimens were then processed for electron microscopy. After the rewarming interval, PGE2 (164.0 +/- 23.2 pg/0.1 ml), IL-1 alpha (24.3 +/- 2.2 pg/0.1 ml), and K+ (6.47 +/- 0.41 mM) released from frozen LSE were significantly increased compared to controls (PGE2 = 22.2 +/- 4.6 pg/0.1 ml, IL-1 alpha = 5.7 +/- 1.0 pg/0.1 ml, K+ = 4.32 +/- 0.02 mM). After the 24-h incubation, PGE2 and IL-1 alpha released by frozen LSE (PGE2 = 1126 +/- 208 pg/0.1 ml; IL-1 alpha = 80.6 +/- 6.8 pg/0.1 ml) remained significantly higher than controls (PGE2 = 229.0 +/- 45 pg/0.1 ml; IL-1 alpha = 4.9 +/- 0.7 pg/0.1 ml). At this time, K+ leakage from frozen LSE (4.39 +/- 0.03 mM) had returned to a normal range (control = 4.65 +/- 0.02 mM). Keratinocytes and, to a lesser extent, fibroblasts showed ultrastructural freeze-thaw damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Artificial Organs↗
PubMed1999

Effects of solute methoxylation on glass-forming ability and stability of vitrification solutions

The effects of replacing hydroxyl groups with methoxyl (OCH(3)) groups in the polyols ethylene glycol (EG), propylene glycol (PG), glycerol, and threitol were studied by differential scanning calorimetry (DSC) during cooling of aqueous solutions to -150 degrees C and subsequent rewarming. For 35% (w/w) PG, 40% EG, and 45% glycerol, a single substitution of a terminal hydroxyl group with a methoxyl group reduced the critical cooling rate necessary to avoid ice on cooling (vitrify) from approximately 500 to 50 degrees C/min. This reduction was approximately equivalent to increasing the parent polyol concentration by 5% (w/w). The critical warming rate calculated to avoid formation of ice on rewarming (devitrification) was also reduced by methoxyl substitution, typically by a factor of 10(4) for dilute solutions. Double methoxylation (replacement of both terminal hydroxyls) tended to result in hydrate formation, making these compounds less interesting. An exception was threitol, for which substituting both terminal hydroxyls by methoxyls reduced the critical rewarming rate of a 50% solution by a factor of 10(7) without any hydrate formation. These glass-forming and stability properties of methoxylated compounds, combined with their low viscosity, enhanced permeability, and high glass transition temperatures, make them interesting candidate cryoprotective agents for cryopreservation by vitrification or freezing. Copyright 1999 Academic Press.

Journal Article↗
PubMed2000

Effect of cooling on the motility and function of human spermatozoa.

Human spermatozoa were cooled from 37 to 0 degrees C at 10 degrees C min(-1) in 5 degrees C steps with 1 min equilibration at each step, the temperature control was +/- 0.1 degrees C. Spermatozoa were held at 0 degrees C for 5 min and then rewarmed at the same rate. No significant effect of cooling on the straight-line velocity was found using computer-aided semen analysis. The physiological function of spermatozoa was also examined before and after cooling using hypoosmotic swelling, ionophore-provoked acrosome reaction, and binding to fragments of human zonae pellucidae. Spermatozoa were cooled either in seminal plasma or in conventional IVF medium with or without fractionation by centrifugation through a discontinuous Percoll gradient. When spermatozoa were cooled and rewarmed in seminal plasma there was no significant change in either the ionophore-induced acrosome reaction or the binding to zona pellucida fragments. When spermatozoa were fractionated by centrifugation through Percoll an increased response in both was seen. However, following cooling and rewarming, a significant decline in the response of both occurred. We suggest that motility alone is not a reliable predictor of changes in other physiological functions of spermatozoa following cooling. Furthermore, short-term cooling appears to have no significant detrimental effect on normozoospermic samples and cold shock may be avoided in the clinical context by controlled cooling and warming.

Acrosome↗
PubMed1999

Moderate posttraumatic hypothermia decreases early calpain-mediated proteolysis and concomitant cytoskeletal compromise in traumatic axonal injury.

Traumatic brain injury (TBI) in animals and man generates widespread axonal injury characterized by focal axolemmal permeability changes, induction of calpain-mediated proteolysis, and neurofilament side-arm modification associated with neurofilament compaction (NFC) evolving to axonal disconnection. Recent observations have suggested that moderate hypothermia is neuroprotective in several models of TBI. Nevertheless, the pathway by which hypothermia prevents traumatic axonal injury (TAI) is still a matter of debate. The present study was conducted to evaluate the effects of moderate, early posttraumatic hypothermia on calpain-mediated spectrin proteolysis (CMSP), implicated in the pathogenesis of TAI. Using moderate (32 degrees C) hypothermia of 90 min duration without rewarming, the density of CMSP immunoreactive/damaged axons was quantified via LM analysis in vulnerable brain stem fiber tracts of hypothermic and normothermic rats subjected to impact acceleration TBI (90 min postinjury survival). To assess the influence of posthypothermic rewarming, a second group of animals was subjected to 90 min of hypothermia followed by 90 min of rewarming to normothermic levels when CMSP was analyzed to detect if any purported CMSP prevention persisted (180 min postinjury survival). Additionally, to determine if this protection translated into comparable cytoskeletal protection in the same foci showing decreased CMSP, antibodies targeting altered/compacted NF subunits were also employed. Moderate hypothermia applied in the acute postinjury period drastically reduced the number of damaged axons displaying CMSP at both time points and significantly reduced NFC immunoreactivity at 180 min postinjury. These results suggest that the neuroprotective effects of hypothermia in TBI are associated with the inhibition of axonal/cytoskeletal damage.

Animals↗
PubMed1997

Mild preischemia hypothermia adversely affects postischemic myocardial function in the neonatal piglet heart.

BACKGROUND: During cardiac surgery, operative hypothermia has been shown to be beneficial in certain situations, although in children perioperative hypothermia has been associated with several physiologic alterations that have proven detrimental to their postoperative function. Little attention has been given to the effects of mild (34.5 degrees C) perioperative hypothermia on postischemic myocardial function in the pediatric population. It was hypothesized that mild hypothermia would be detrimental to postischemic ventricular function in the neonatal heart. METHODS: Neonatal (0-2 days old) piglets were subjected to mild perioperative hypothermia without rewarming (HT-only, n = 6), hypothermia followed by rewarming (HT-RW, n = 6), or continuous normothermia (NT, n = 8). The hearts were rapidly excised, suspended on an isolated perfusion apparatus, and allowed to spontaneously beat while being perfused with an asanguinous solution. All hearts were subjected to 20 min global, normothermic, zero-flow ischemia followed by 45 min oxygenated crystallite buffer reperfusion (I-R). RESULTS: Compared to that of NT piglets, there were significant (P < 0.05) reductions in recovery of left ventricular (LV) diastolic and systolic function following ischemia and reperfusion in HT-RW animals. When the hearts were rendered ischemic without first rewarming, the degree of myocardial dysfunction was not as severe. In contrast to the NT piglets, HT-RW animals demonstrated significant (P < 0.05) reductions in the final recovery of LV developed pressure (71 +/- 6 vs 105 +/- 6 in NT), LV rate pressure product (52 +/- 4 vs 102 +/- 9 NT), and LV end diastolic pressure (32 +/- 7 vs 3 +/- 1 in NT) following I-R. When compared to the HT-RW group, HT-only piglets did not exhibit significant differences in systolic function, although diastolic function was minimally altered initially as evidenced by the slight elevation of LV end diastolic pressure at 5 min, with reperfusion in the HT-only group (P < 0.05). CONCLUSIONS: In this newborn piglet model, mild hypothermia significantly reduces recovery of systolic and diastolic left ventricular function when followed by an episode of global myocardial ischemia-reperfusion only when the animals are returned to normothermia prior to the ischemic insult. When hypothermia is immediately followed by the ischemic event, left ventricular function is unaffected.

Animals↗
PubMed1985

Skeletal muscle activity of alcohol-treated rabbits in immersion hypothermia: adenine nucleotide concentrations and phosphorylation state.

The effects of alcohol injection (0.5 g . kg-1 i.v.) on the core cooling and rewarming rates, concentration of the adenine nucleotides, and the phosphorylation state of the adenylate system (ATP/ADP X P) were studied in the skeletal muscle of anesthetized rabbits immersed in ice-cold water. NaCl-injected rabbits immersed in ice-cold water were used as cold controls, alcohol-treated animals at room temperature (20 degrees C) as alcohol warm controls, and NaCl-injected animals at room temperature as anesthesia controls, respectively. The fall of core temperature to 32 degrees C in the alcohol-treated rabbits and the cold controls took about 40 min. During this time the temperature of the alcohol warm and anesthesia controls fell by about 1 degree C. No difference in the rewarming rate was observed between the alcohol-treated and cold control rabbits. Serum glucose concentration was elevated in the cold controls (from 5.9 to 8.3 mmol/l) but not in the alcohol-treated rabbits. Cold exposure reduced the phosphorylation state in the skeletal muscle of the alcohol-treated rabbits by 32% (P less than 0.05), but the decrease (6%) was not significant in the cold controls. After rewarming the phosphorylation state decreased in the above groups by 71% and 15%, respectively, as compared with the initial values. No significant changes in the phosphorylation state were found in the warm control animals. The redox state of the cytosol in the skeletal muscle or liver did not change, nor was there any change observed in the arterial pO2 or pCO2 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1996

Biometrical characteristics and physiological responses to a local cold exposure of the extremities.

The aim of this study was firstly to describe the physiological responses observed in 19 subjects during immersion of the arm up to the elbow in water at 5 degrees C (5 min) followed by a 10-min recovery and secondly, to correlate the observed physiological responses with biometrical characteristics of the subjects (maximal oxygen uptake, VO2max, percentage fat content of whole body, BF, and arm, forearm and hand skinfold thickness). The results showed that the time courses of changes in forearm and hand skin temperature were different compared to those of finger skin temperatures both during local cooling and during rewarming (P < 0.05). Cardiovascular responses (heart rate, systolic and diastolic blood pressures) and finger skin temperatures were not related to the biometrical characteristics of the subjects. However, at the end of the immersion, decreased hand skin temperature was correlated to VO2max (r = 0.45, P < or = 0.05) whereas decreased forearm skin temperature was correlated both to VO2max (r = 0.44, P < or = 0.05) and to skinfold thickness (r = -0.44, P < or = 0.05) but not to BF. During the beginning of the recovery period only, outside, inside forearm and hand skin temperatures were related to VO2max (r = 0.54, P < or = 0.05; r = 0.66, P < or = 0.01 and r = 0.45, P < or = 0.05, respectively) and all the skinfold thicknesses (r = -0.47 to -0.71, P < or = 0.05). It was concluded that the local skin temperature profiles differed according to the upper limb segment both during cooling and during early rewarming. Moreover, VO2max and upper limb skinfold thickness but not BF did influence the forearm and hand skin temperature changes during cooling and early rewarming but not the finger skin temperature changes and cardiovascular responses.

Adult↗
PubMed1983

Calcium movements and intracellular calcium distribution in neoplastic GH3 cells.

Experiments were carried out to investigate the nature of the calcium homeostatic mechanisms in neoplastic GH3 rat pituitary cells. GH3 cells grown and maintained in Ham's F10 culture medium contained 35 nmoles calcium/mg cell protein. When stimulated by thyrotropin releasing hormone (TRH) or elevated K+ concentrations, only the latter caused cell calcium levels to rise although both resulted in hormone release. When exposed to EGTA, the GH3 cells lost calcium. When the temperature was lowered to 4 degrees C, the cells gained calcium and when rewarmed were able to extrude the previously accumulated calcium. The increased cell calcium following cold exposure could be blocked by prior treatment with rotenone. If rotenone was added subsequent to the cold exposure, it did not block the extrusion seen upon rewarming. In the absence of glucose in the medium, the GH3 cells took up more calcium upon exposure to 4 degrees C, and upon rewarming the cells could not return to their previous low levels. There are thus significant differences in calcium homeostasis between the neoplastic GH3 cells and their normal pituitary counterparts. When intracellular calcium was localized with the potassium pyroantimonate technique, there was calcium found in/on mitochondria, membrane bound vesicles and plasma membrane. Nuclear staining was sparse, and nucleolar staining was virtually absent. Upon stimulation with TRH, there was a decrease in mitochondrial calcium along with increases in both plasma membrane and nucleolar calcium levels. Since total calcium is unchanged, this indicates a significant calcium redistribution in response to TRH. The increased nucleolar calcium may reflect a calcium dependent increase in mRNA synthesis as has been reported. Since TRH presumably acts at a surface receptor, the increased plasma membrane calcium might be functionally related to receptor activation.

Animals↗