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PubMed1997

Differential roles of neurokinin 1 and neurokinin 2 receptors in the development and maintenance of heat hyperalgesia induced by acute inflammation.

1. Following induction of acute inflammation by intraarticular injection of kaolin and carrageenan into the knee joint in rats, there was a significant decrease in the withdrawal latency to radiant heat applied to the paw (i.e. heat hyperalgesia), an increased joint circumference and increased joint temperature. 2. A neurokinin1 (NK1) receptor antagonist (CP-99,994, 10 mM) had no effect on the paw withdrawal latency when it was administered spinally through a microdialysis fibre before the induction of inflammation. Pretreatment with a NK2 receptor antagonist (SR48968, 1 mM) administered spinally through the microdialysis fibre prevented the heat hyperalgesia from developing in the early stages of the inflammation. 3. Post-treatment through the microdialysis fibre with the NK1 receptor antagonist (0.01-10 mM) was effective in reversing the heat hyperalgesia. In contrast, post-treatment spinally with the NK2 receptor antagonist (0.01-1 mM) had no effect on the heat hyperalgesia. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia. 4. Pretreatment systemically with the NK1 receptor antagonist (30 mg kg-1) had no effect on the heat hyperalgesia or pain-related behaviour ratings where 0 is none and 5 is non weight bearing and complete avoidance of limb contact. Pretreatment with a NK2 receptor antagonist (10 mg kg-1) systemically prevented the heat hyperalgesia and pain-related behaviour ratings from developing in the early stages of the inflammation. The inactive stereoisomers of NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia. 5. Post-treatment systemically with either the NK1 (0.1-30 mg kg-1) or the NK2 (0.1-10 mg kg-1) receptor antagonist resulted in a dose-dependent reversal of the heat hyperalgesia. Pain-related behaviour ratings were reduced by post-treatment only with the NK1 receptor antagonist. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the behavioural responses. 6. Direct pretreatment of the knee joint with either the NK1 (30 mg) or the NK2 (10 mg) receptor antagonist prevented the heat hyperalgesia from developing without affecting joint swelling. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia. 7. There appears to be a differential role for the spinal tachykinin receptors in the development and maintenance of the heat hyperalgesia associated with acute joint inflammation. The NK2 receptors appear to be activated early in the development of the heat hyperalgesia and NK1 receptors are involved in the maintenance of the heat hyperalgesia. 8. Peripherally, both NK1 and NK2 receptors are involved in the development of heat hyperalgesia and pain-related behaviour ratings induced by acute inflammation.

Animals↗
PubMed1989

Application of the relative summary climatic indices during work in heat for ergonomic purposes.

A new method was elaborated for the evaluation of work-heat load. Two indices of heat stress were introduced, the so-called 'climatic heat'--Hcl (a sum of convective, radiation, respiration and maximum evaporation heat), and the 'total heat'--Htot (a sum of metabolic and climatic heat). It is an adapted thermal balance equation in which the evaporation heat was replaced with maximum evaporation heat. This enabled the quantification of climatic load also in the normothermic region, where stored heat S=0. The applicability of these indices is given by the fact that so-called heat heart rate (HRh) is in good correlation with them. The above mentioned indices were used in the relative values of the 'quotient of heat stress' (Qdif,H) and of the 'grade of heat strain' (Gdif,H). These variables are basically a relation between real load and 'permissible' load to which a healthy adult male can be exposed for 8 h without an increase in his body temperature. In this paper, equations for calculation of those relative values according to heat stress indices are introduced. The relative indices show how many times is the real HRh larger (or smaller) than its permissible value (= 20 min(-1)). By joining the relative heat stress indices with the relative work load indices (Qdif,W and Gdif,W, respectively) the index of work-heat load is obtained. The permissible work heart rate (= 30 min(-1)), which corresponds with the energetic output in males (approximately 250 W). The work-heat strain grade (Gdif,WH) can be used for the quantification of load, for the determination of the rest allowance, of the necessary recovery time and for the determination of a suitable regime of work and rest in general. The permissible values of climatic elements under a given physical load, and the admissible duration of exposure under different climatic conditions and different muscle load intensities can be determined.

Climate↗
PubMed2002

Heat shock-induced apoptosis in preimplantation bovine embryos is a developmentally regulated phenomenon.

Apoptosis is a form of cell death that can function to eliminate cells damaged by environmental stress. One stress that can compromise embryonic development is elevated temperature (i.e., heat shock). For the current studies, we hypothesized that heat shock induces apoptosis in bovine embryos in a developmentally regulated manner. Studies were performed to 1) determine whether heat shock can induce apoptosis in preimplantation embryos, 2) test whether heat-induced apoptosis is developmentally regulated, 3) evaluate whether heat shock-induced changes in caspase activity parallel patterns of apoptosis, and 4) ascertain whether exposure to a mild heat shock can protect embryos from heat-induced apoptosis. As determined by TUNEL reaction, exposure of bovine embryos > or =16 cells on Day 5 after insemination to 41 or 42 degrees C for 9 h increased the percentage of cells undergoing apoptosis. In addition, there was a duration-dependent increase in the proportion of blastomeres that were apoptotic when embryos were exposed to temperatures of 40 or 41 degrees C, which are more characteristic of temperatures experienced by heat-stressed cows. Heat shock also increased caspase activity in Day 5 embryos. However, heat shock did not induce apoptosis in 2- or 4-cell embryos, nor did it increase caspase activity in 2-cell embryos. The apoptotic response of 8- to 16-cell-stage bovine embryos to heat shock depended upon the day after insemination that heat shock occurred. When 8- to 16-cell embryos were collected on Day 3 after insemination, heat shock of 41 degrees C for 9 h did not induce apoptosis. In contrast, when 8- to 16-cell embryos were collected on Day 4 after insemination and exposed to heat shock, there was an increase in the percentage of cells undergoing apoptosis. Exposure of 8- to 16-cell embryos at Day 4 to a mild heat shock of 40 degrees C for 80 min blocked the apoptotic response to a subsequent, more-severe heat shock of 41 degrees C for 9 h. In conclusion, apoptosis is a developmentally acquired phenomenon that occurs in embryos exposed to elevated temperature, and it can be prevented by induced thermotolerance.

Animals↗
PubMed1995

Heat flow and distribution during epidural anesthesia.

BACKGROUND: Core hypothermia after induction of epidural anesthesia results from both an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors thus evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. METHODS: Twelve minimally clothed male volunteers were evaluated in a approximately 22 degrees C environment for 2.5 control hours before induction of epidural anesthesia and for 3 subsequent hours. Epidural anesthesia produced a bilateral sympathetic block in only six volunteers, and only their results are reported. Shivering, when observed, was treated with intravenous meperidine. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in esophageal or tympanic membrane (core) temperatures, leaving the core hypothermia specifically resulting from redistribution. RESULTS: Arm heat content decreased approximately 5 kcal/h after induction of anesthesia, but leg heat content increased markedly. Most of the increase in leg heat content was in the lower legs and feet. Core temperature increased slightly during the control period but decreased 0.8 +/- 0.3 degrees C in the 1st hour of anesthesia. Redistribution, contributing 89% to this initial decrease, required a net transfer of 20 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 0.4 +/- 0.3 degrees C, with redistribution contributing 62%. Thus, only 7 kcal were redistributed during the 2nd and 3rd hours of anesthesia. Redistribution therefore contributed 80% to the entire 1.2 +/- 0.3 degrees C decrease in core temperature during the 3 h of anesthesia. CONCLUSIONS: Core hypothermia during the 1st hour after induction of epidural anesthesia resulted largely from redistribution of body heat from the core thermal compartment to the distal legs. Even after 3 h of anesthesia, redistribution remained the major cause of core hypothermia. Despite the greater fractional contribution of redistribution during epidural anesthesia, core temperature decreased only half as much as during general anesthesia because metabolic rate was maintained and the arms remained vasoconstricted.

Adjuvants, Anesthesia↗
PubMed1995

The physiology of heat regulation.

Heat regulation is presented as the physiological method of handling metabolic heat, instead of temperature regulation. Experimental evidence of heat regulation from the literature is reviewed, including more than 20 years of calorimetric studies by the author. Changes in heat production are followed by slow exponential changes in heat loss, which produce changes in body heat storage. Heat balance occurs at many levels of heat production throughout the day and night, and at each level there is a related level of rectal temperature. Heat flow can be sensed by the transcutaneous temperature gradient. The controller for heat loss appears to operate like a servomechanism, with feedback from heat loss and possibly feedforward from heat production. Physiological responses defend the body heat content, but heat content varies over a range that is related to heat load. Changes in body heat content drive deep body temperatures.

Body Temperature↗
PubMed2003

Finger dexterity, skin temperature, and blood flow during auxiliary heating in the cold.

The primary purpose of the present study was to compare the effectiveness of two forms of hand heating and to discuss specific trends that relate finger dexterity performance to variables such as finger skin temperature (T(fing)), finger blood flow (Q(fing)), forearm skin temperature (T(fsk)), forearm muscle temperature (Tfmus), mean weighted body skin temperature (Tsk), and change in body heat content (DeltaH(b)). These variables along with rate of body heat storage, toe skin temperature, and change in rectal temperature were measured during direct and indirect hand heating. Direct hand heating involved the use of electrically heated gloves to keep the fingers warm (heated gloves condition), whereas indirect hand heating involved warming the fingers indirectly by actively heating the torso with an electrically heated vest (heated vest condition). Seven men (age 35.6 +/- 5.6 yr) were subjected to each method of hand heating while they sat in a chair for 3 h during exposure to -25 degrees C air. Q(fing) was significantly (P < 0.05) higher during the heated vest condition compared with the heated gloves condition (234 +/- 28 and 33 +/- 4 perfusion units, respectively), despite a similar T(fing) (which ranged between 28 and 35 degrees C during the 3-h exposure). Despite the difference in Q(fing), there was no significant difference in finger dexterity performance. Therefore, finger dexterity can be maintained with direct hand heating despite a low Q(fing). DeltaH(b), Tsk, and T(fmus) reached a low of -472 +/- 18 kJ, 28.5 +/- 0.3 degrees C, and 29.8 +/- 0.5 degrees C, respectively, during the heated gloves condition, but the values were not low enough to affect finger dexterity.

Adult↗
PubMed1999

Single exposure to heat induces stage-specific germ cell apoptosis in rats: role of intratesticular testosterone on stage specificity.

Short term exposure of the testis to heat causes degeneration of germ cells. However, the mechanisms underlying this process are poorly understood. The major objectives of this study were to determine whether the heat-induced loss of germ cells in the adult rat occurs via apoptosis, to document its stage-specific and cell-specific distribution, and to examine whether intratesticular testosterone (T) plays any role in the stage specificity of heat-induced germ cell death. Testes of adult male Sprague-Dawley rats were exposed to 22 C (control) or 43 C for 15 min. Animals were killed on days 1, 2, 9, and 56 after heat exposure. Germ cell apoptosis was characterized by DNA gel electrophoresis and in situ terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling assay. The incidence of germ cell apoptosis [apoptotic index (AI)] was quite low in control rats (AI = 0.04-0.1). Mild hyperthermia within 1 or 2 days resulted in a marked activation (AI = 4.7-5.6) of germ cell apoptosis predominantly at early (I-IV) and late (XII-XIV) stages. Stages V-VI and VII-VIII were relatively protected from heat-induced apoptosis. Spermatocytes, including pachytenes at stages I-IV and IX-XII, diplotene and dividing spermatocytes at stages XIII-XIV, and early (steps 1-4) spermatids, were most susceptible to heat. On day 9, the majority of the tubules were severely damaged and displayed only a few remaining apoptotic germ cells. By day 56, spermatogenesis was completely recovered, and the incidence of germ cell apoptosis was compatible with the control levels. To determine whether intratesticular T plays a role in protecting germ cells at stages VII-VIII against heat-induced cell death, adult rats were exposed to local testicular heating on day 2 or were given a daily sc injection of GnRH antagonist (GnRH-A) for 4 days with and without a single exposure of testes to heat applied on day 2. By day 4, the incidence of increased germ cell apoptosis at stages other than VII-VIII were not different between heat-treated and GnRH-A- plus heat-treated groups, whereas the control group and the group treated with GnRH-A alone showed minimal apoptosis. GnRH-A addition to heat resulted in a further increase in apoptosis (by 3.2-fold) at stages VII-VIII over the values measured in the heat-treated group, and it became comparable to that at all other stages. Collectively, these results provide evidence that 1) heat induces germ cell apoptosis in a stage-specific and cell-specific fashion; and 2) intratesticular T plays a pivotal role in protecting germ cells at stages VII-VIII against heat-induced cell death. However, the possible involvement of various other factors, including growth factors, thermoprotectants, cytokines, and various death-related proteins, in protecting germ cells against heat-induced apoptosis cannot be ruled out.

Animals↗
PubMed1984

Modification of membrane function, protein synthesis, and heat killing effect in cultured Chinese hamster cells by glycerol and D2O1.

Glycerol and D2O can provide a protective effect to Chinese hamster V79 cells receiving heat treatment. The mechanism for this effect is assumed to be the ability of these agents to stabilize proteins which implies that one of the possible heat-killing mechanisms is the inactivation of a heat-sensitive molecule (protein?). In addition, we observed that heat can alter the membrane permeability rapidly, and glycerol can reduce the initial heat-induced membrane permeability changes (determined by aminoisobutyric acid uptake). Although not as effective as cycloheximide, glycerol and D2O can retard protein synthesis. These two processes can add to the protective effect of stabilizing cellular protein against heat killing. Since glycerol and D2O added during the heat-conditioning period can interfere with the appearance of thermotolerance, the mechanisms for the protective effect of glycerol and D2O are likely to be different from heat-induced thermotolerance. We propose that the heat-sensitive molecule protected by D2O or glycerol may also play a role in the triggering process of the thermotolerance phenomenon. If the conditioning heat treatment is sufficient to affect this molecule but not other cellular targets, thus allowing the cell to survive, thermotolerance may be observed in surviving cells in response to second or continued heat treatment. Depending on the severity of the heat effect, this heat-sensitive molecule may continue to exist after a conditioning heat treatment in medium containing glycerol or D2O, and therefore, the response of the cells to the challenging heat is altered little. This proposed mechanism is capable of explaining several thermotolerance experimental protocols. Since glycerol can also reduce the toxicity of vincristine, microtubule-related protein is probably one of the proteins stabilized by this agent. D2O also probably affects microtubule protein, because the cells heated in medium containing D2O show little topological changes.

Aminoisobutyric Acids↗
PubMed1996

Interventional thermal injury of the arterial wall: unfolding of von Willebrand factor and its increased binding to collagen after 55 degrees C heating.

PURPOSE: Thermal angioplasty alters the thrombogenicity of the arterial wall. In previous studies, platelet adhesion was found to increase after heating human subendothelium to 55 degrees C and decrease after heating to 90 degrees C. In the present electron microscopic study, the mechanism of this temperature-dependent platelet adhesion to the heated arterial wall is elucidated by investigating temperature-dependent conformational changes of von Willebrand factor (vWF) and collagen types I and III and the binding of vWF to heated collagen. METHODS: Purified vWF and/or collagen was applied to electron microscopic grids and heated by floating on a salt-solution of 37 degrees C, 55 degrees C or 90 degrees C for 15 s. After incubation with a polyclonal antibody against vWF and incubation with protein A/gold, the grids were examined by electron microscopy. RESULTS: At 37 degrees C, vWF was coiled. At 55 degrees C, vWF unfolded, whereas heating at 90 degrees C caused a reduction in antigenicity. Collagen fibers heated to 37 degrees C were 60.3 +/- 3.1 nm wide. Heating to 55 degrees C resulted in the unwinding of the fibers, increasing the width to 87.5 +/- 8.2 nm (p < 0.01). Heating to 90 degrees C resulted in denatured fibers with an enlarged width of 85.1 +/- 6.1 nm (p < 0.05). Heating of collagen to 55 degrees C resulted in an increased vWF binding as compared to collagen heated to 37 degrees C or to 90 degrees C. Incubation of collagen with vWF, prior to heating, resulted in a vWF binding after heating to 55 degrees C that was similar to the 37 degrees C binding and a decreased binding after 90 degrees C. CONCLUSIONS: After 55 degrees C heating, the von Willebrand factor molecule unfolds and collagen types I and III exhibit an increased adhesiveness for von Willebrand factor. Heating to 90 degrees C denatures von Willebrand factor and collagen. The conformation changes of von Willebrand factor and its altered binding to collagen type I and III may explain the increased and decreased platelet adhesion to subendothelium after 55 degrees C and 90 degrees C heating, respectively.

Analysis of Variance↗
PubMedDate not supplied

Heat from an implanted power source is mainly dissipated by blood perfusion.

Heat dissipation and its effects on tissue and blood interfaces are common problems associated with the development and increased use of artificial hearts, because all of the implantable actuators for artificial hearts generate waste heat due to inefficiencies of energy conversion. To determine the mechanisms of heat dissipation from artificial hearts, heated disks producing constant heat fluxes of 0.08 watts/cm2 were implanted adjacent to the left lung and the latissimus dorsi muscle in calves for 2 weeks, 4 weeks, and 7 weeks. At the end of each experiment, a series of acute studies was performed in which blood perfusion to the heated tissue was decreased or stopped to observe the contribution of blood perfusion to heat dissipation. The cooling effect of ventilation was also examined to determine its relative contribution to heat dissipation in lung tissue by decreasing the minute ventilation volume. The importance of blood perfusion for heat dissipation was demonstrated by the temperature rise after cessation of blood perfusion to the heated tissue. The contribution of ventilation to heat dissipation in the heated lung tissue was minimal. Contribution of total blood perfusion to heat dissipation was increased with time in the muscle tissue, which has relatively low resting blood perfusion, but not in the lung tissue, which has relatively high blood perfusion. In the heated muscle tissue, the in vivo adaptive response to chronic heat was functionally shown by the increased perfusion. In conclusion, blood perfusion was the main mechanism of heat dissipation from tissues that were adjacent to an implanted power source.

Adaptation, Physiological↗
PubMed1994

Heat shock response in the liver: expression and regulation of the hsp70 gene family and early response genes after in vivo hyperthermia.

Heat shock response in cultured cells has been studied extensively; however few data are available on heat shock response in an intact organ of a living animal. In this study we analyzed the kinetics of expression of the heat shock protein 70 gene family (heat shock protein 70, heat shock cognate protein 73 and glucose-regulated protein 78) in the liver of the thermally stressed rat. New synthesis of heat shock protein 70 and heat shock cognate protein 73 was shown in liver slices pulse labeled in vitro with 35S-methionine. Accumulation of heat shock protein 70 and heat shock cognate protein 73 proteins was shown in total cellular extracts. 32P-labeled complementary DNA probes encoding heat shock protein 70, heat shock cognate protein 73 and glucose-regulated protein 78 were used to show that the levels of the corresponding messenger RNAs increase as a fraction of total RNA and in polysomes at different extents and with different kinetics. The induction of heat shock protein 70 and heat shock cognate protein 73 messenger RNAs reflected the increase in the synthesis of the corresponding proteins. Run-on transcription analysis indicated that the expression of heat shock protein 70 and heat shock cognate protein 73 genes was mainly regulated at the transcriptional level. On the contrary, both transcriptional and posttranscriptional regulatory mechanisms can explain the induction of the glucose-regulated protein 78 gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Protective role of heat stress in burn trauma.

OBJECTIVE: This study was designed to determine whether cutaneous burn injury up-regulated expression of myocardial heat shock protein (HSP)70 and to determine a potential cardioprotective role of inducible HSP70 (iHSP70) in postburn myocardial contractile function. DESIGN: Experimental study. SETTING: Research laboratory. SUBJECTS: Adult Hartley guinea pigs. INTERVENTIONS: The first set of studies determined whether heat stress (increasing body temperature to 42 degrees C for 20 mins) in adult Hartley guinea pigs would increase expression of myocardial iHSP70. MEASUREMENTS AND MAIN RESULTS: Our model of heat stress increased expression of inducible HSP in the myocardium (Western blot), and this response persisted 1, 2, 4, and 24 hrs after the initial heat stress. We then determined whether burn trauma over 40% total body surface area (TBSA) increased myocardial expression of iHSP70. Time-matched sham and burned guinea pigs were killed 1, 2, 4, 12, 18, or 24 hrs postburn, and hearts were used either to examine myocardial iHSP70 expression by Western blot or to determine myocardial contractile function (Langendorff). Burn trauma produced a two-fold increase in myocardial iHSP70 that was evident as early as 1 hr postburn and persisted 24 hrs postburn; increased iHSP70 expression occurred despite only a modest and transient increase in body temperature after burn trauma. We then determined whether heat shock stress before burn trauma provided a protective or detrimental effect on cardiac function. Body temperature was increased to 42 degrees C for 20 mins, animals were allowed to recover, and body temperature returned to baseline; burn trauma was then produced (40% TBSA) either 1, 2, 4, or 24 hrs after the initial heat stress. Myocardial contraction and relaxation deficits were evident after burn trauma alone; however, heat stress 1 hr before burn trauma improved left ventricular developed pressure and positive or negative maximum change in pressure in time and shifted left ventricular function curves upward and leftward from those calculated for burn in the absence of heat stress, indicating improved ventricular performance. Increasing the time between the initial heat stress and burn injury decreased the cardioprotective effects of heat stress. Thus, organ protection was evident only when the time period between the initial heat stress and the second insult was brief (1 hr). CONCLUSIONS: Our finding that the amount of myocardial iHSP70 remained constantly elevated after heat stress while the cardio-protective effect afforded by a prior heat stress declined with time suggested that the initial heat stress evoked several compensatory/adaptive mechanisms that may include modulation of autonomic nervous system responses, changes in metabolic function, modulation of pro/anti-inflammatory cytokine responses, and heat stress-related alterations in antioxidant capacity.

Animals↗
PubMed2006

Glutamine: the first clinically relevant pharmacological regulator of heat shock protein expression?

PURPOSE OF REVIEW: It is well known that enhanced heat shock protein expression protects organisms against morbidity and mortality following experimental injury/illness. Presently, chemical/gene therapy based laboratory methods of enhancing heat shock protein expression are impractical for clinical application. Our laboratory has shown glutamine enhances heat shock protein expression following models of experimental illness/injury. The purpose of this review is to examine recent data supporting the use of glutamine as a clinically relevant enhancer of heat shock protein expression. RECENT FINDINGS: Recent studies indicate glutamine induces heat shock protein-70, HO-1 (heat shock protein-32), and heat shock protein-27 in models of illness/injury. Enhanced expression of heat shock proteins correlates with improved outcome in these models. Further, in-vitro data reveal glutamine enhances DNA binding of heat shock factor-1 (heat shock protein transcription factor) to its promoter. Finally, recently published pilot data show that glutamine enhances serum heat shock protein-70 expression in critically ill patients and this enhanced expression correlates with improved outcome. SUMMARY: Currently, extensive data support glutamine as a gene level regulator of heat shock protein expression. Glutamine depletion, following critical illness/injury, is likely to lead to a state in which organisms are unable to induce heat shock proteins appropriately. Further, pharmacologic supplementation of glutamine potentiates the heat shock protein response prior to and following a stress. Pharmacologic trials utilizing glutamine to enhance heat shock proteins in humans are indicated.

Animals↗
PubMed1987

Effect of cycloheximide or puromycin on induction of thermotolerance by sodium arsenite in Chinese hamster ovary cells: involvement of heat shock proteins.

After sodium arsenite (100 microM) treatment, the synthesis of three major heat shock protein families (HSPs; Mr = 110,000, 87,000, and 70,000), as studied with one-dimensional gels, was enhanced twofold relative to that of unheated cells. The increase of unique HSPs, if studied with two-dimensional gels, would probably be much greater. In parallel, thermotolerance was observed as a 100,000-fold increase in survival from 10(-6) to 10(-1) after 4 hr at 43 degrees C, and as a thermotolerance ratio (TTR) of 2-3 at 10(-3) isosurvival for heating at 45.5 degrees C. Cycloheximide (CHM: 10 micrograms/ml) or puromycin (PUR: 100 micrograms/ml), which inhibited total protein synthesis and HSP synthesis by 95%, completely suppressed the development of thermotolerance when either drug was added after sodium arsenite treatment and removed prior to the subsequent heat treatment. Therefore, thermotolerance induced by arsenite treatment correlated with an increase in newly synthesized HSPs. However, with or without arsenite treatment, CHM or PUR added 2-6 hr before heating and left on during heating caused a 10,000-100,000-fold enhancement of survival when cells were heated at 43 degrees C for 4 hr, even though very little synthesis of heat shock proteins occurred. Moreover, these cells manifesting resistance to heating at 43 degrees C after CHM treatment were much different than those manifesting resistance to 43 degrees C after arsenite treatment. Arsenite-treated cells showed a great deal of thermotolerance (TTR of about 10) when they were heated at 45 degrees C after 5 hr of heating at 43 degrees C, compared with less thermotolerance (TTR of about 2) for the CHM-treated cells heated at 45 degrees C after 5 hr of heating at 43 degrees C. Therefore, there are two different phenomena. The first is thermotolerance after arsenite treatment (observed at 43 degrees C or 45.5 degrees C) that apparently requires synthesis of HSPs. The second is resistance to heat after CHM or PUR treatment before and during heating (observed at 43 degrees C with little resistance at 45.5 degrees C) that apparently does not require synthesis of HSPs. This phenomenon not requiring the synthesis of HSPs also was observed by the large increase in thermotolerance to 45 degrees C caused by heating at 43 degrees C, with or without CHM, after cells were incubated for 6 hr following arsenite pretreatment. For both phenomena, a model based on synthesis and redistribution of HSPs is presented.

Animals↗
PubMed1989

Inhibition of heat shock (stress) protein induction by deuterium oxide and glycerol: additional support for the abnormal protein hypothesis of induction.

The patterns of radioactively labeled proteins from cultured chicken embryo cells stressed in the presence of either D2O or glycerol were analyzed by using one-dimensional polyacrylamide gel electrophoresis. These hyperthermic protectors blocked the induction of stress proteins during a 1-hour heat shock at 44 degrees C. The inhibitory effect of glycerol but not D2O on the induction of heat shock proteins could be overcome by increased temperature. By using transcriptional run-on assays of isolated nuclei and cDNA probes to detect hsp70- and hsp88-specific RNA transcripts, it was shown that the D2O and glycerol blocks occurred at or before transcriptional activation of the hsp70 and hsp88 genes. After heat-stressed cells were returned to 37 degrees C and the protectors were removed, heat shock proteins were inducible by a second heating. This result and the fact that the chemical stressor sodium arsenite induced stress proteins in glycerol medium indicated that the treatments did not irreversibly inhibit the induction pathways and that the stress response could be triggered even in the presence of glycerol by a stressor other than heat. In principle then, cells incurring thermal damage during a 1-hour heat shock at 44 degrees C in D2O or glycerol medium should be competent to respond by inducing heat shock proteins during a subsequent recovery period at 37 degrees C in normal medium. We found that heat shock proteins were not induced in recovering cells, suggesting that glycerol and D2O protected heat-sensitive targets from thermal damage. Evidence that the heat-sensitive target(s) is likely to be a protein(s) is summarized. During heat shocks of up to 3 hours duration, neither D2O nor glycerol significantly altered hsp23 gene activity, a constitutively expressed chicken heat shock gene whose RNA transcripts and protein products are induced by stabilization (increased half-life). During a 2-hour heat shock, glycerol treatment blocked the heat-induced stabilization of hsp23 RNA and proteins; however, D2O treatment only blocked RNA transcript stabilization, effectively uncoupling the hsp23 protein stabilization pathway from hsp23 RNA stabilization and transcriptional activation of hsp70 and hsp88 genes.

Animals↗
PubMed1996

Responses of heat stressed chickens to exogenous reverse triiodothyronine (rT3).

Heat stress is accompanied by a decrease in basal metabolic rate and plasma thyroid hormones. Unlike 3,5,3'-triiodothyronine (T3) and thyroxine (T4), 3,3',5'-triiodothyronine (rT3) displays hypometabolic properties and antagonizes the hypermetabolic effect of T3. This study analyses the role of rT3 in heat (38-39 degrees C) stressed immature chickens. Two experiments which differed in frequency of rT3 injections (one or two times a day), duration of heat stress (72 or 48 h) and blood sampling were performed. The dose was 14 micrograms rT3/100 gb.wt./injection (s.c.). It has been shown that rT3 treatment aggravates heat stress symptoms (enhances circulating corticosterone, catecholamines and free fatty acids) and increases mortality. The critical survival time of the rT3 treated and heated birds was at first 24 h of stress. No more chickens died during the next days of the experiment despite the continuation of rT3 injection, suggesting that rT3 might disturb the adaptation to heat. Reverse T3 in heat stressed chickens led to the highest reduction in food consumption (69.9%) and body weight gain (14.0% compared to initial weight). The opposite effect in water consumption (216.9%) was observed. In a neutral environment, rT3 significantly suppressed body temperature 6 h after injection (40.4; control; 41.1 degrees C), confirming its hypometabolic properties. However, at the same time rT3 significantly enhanced body temperature in heat stress (43.03 versus heated control 42.56 degrees C). In addition, in rT3 treated birds decreased plasma triglycerides (TG; 24.3%) and increased plasma free fatty acids (FFA; neutral temperature; 26.4% heat stress: 57%) were demonstrated. A correlation between corticosterone and FFA (r = 0.52) shows that some of the FFA may originate from lipolysis since hormones of the pituitary-adrenocortical axis accelerate lipolysis. The remaining part of the increased FFA appears to be due to suppressed utilization of FFA as a consequence of hypometabolic properties of rT3. Low and negative relation between TG and FFA (r = -0.26; P < 0.05) may support such an assumption. The two times higher peak of corticosterone in the rT3 and the overheated group, as compared to the heated control, occurred at 6 h of heat stress and indicates that rT3 increases the unfavourable effect of high temperature. This was also confirmed by elevated plasma adrenaline and noradrenaline in rT3-injected and heated chickens (55.5 and 120%, respectively). However, a single and two times higher peak of adrenaline at 24 h of heat stress was observed in saline treated birds, but not in rT3 supplemented animals, suggesting that this difference might explain one of the factors responsible for high mortality. In conclusion, the results obtained demonstrate that physiological doses of rT3, a hypometabolic hormone, enhance the unfavourable effect of heat stress in chickens.

Animals↗
PubMed2004

Development of a high-performance boiling heat exchanger by improved liquid supply to narrow channels.

A two-phase flow loop is a promising method for application to thermal management systems for large-scale space platforms handling large amounts of energy. Boiling heat transfer reduces the size and weight of cold plates. The transportation of latent heat reduces the mass flow rate of working fluid and pump power. To develop compact heat exchangers for the removal of waste heat from electronic devices with high heat generation density, experiments on a method to increase the critical heat flux for a narrow heated channel between parallel heated and unheated plates were conducted. Fine grooves are machined on the heating surface in a transverse direction to the flow and liquid is supplied underneath flattened bubbles by the capillary pressure difference from auxiliary liquid channels separated by porous metal plates from the main heated channel. The critical heat flux values for the present heated channel structure are more than twice those for a flat surface at gap sizes 2 mm and 0.7 mm. The validity of the present structure with auxiliary liquid channels is confirmed by experiments in which the liquid supply to the grooves is interrupted. The increment in the critical heat flux compared to those for a flat surface takes a maximum value at a certain flow rate of liquid supply to the heated channel. The increment is expected to become larger when the length of the heated channel is increased and/or the gravity level is reduced.

Cold Temperature↗
PubMed2003

Exertional heat illness in Air Force basic military trainees.

OBJECTIVE: Exertional heat illnesses (heat stroke, heat exhaustion, and heat cramps) are a serious problem in military operations. Air Force basic military training at Lackland Air Force Base is a prime example of where exertional heat illnesses can occur. This project was conducted to evaluate the problem o exertional heat illnesses during basic military training a Lackland Air Force Base. METHODS: Data were obtained from the Ambulatory Data System, the Air Force Reportable Event Surveillance System, and a published report in the December 1999 issue of Military Medicine (Drehner, Neuhauser, Neuhauser, and Blackwood). RESULTS: In 1999, there were 51 cases of heat illness (not necessarily exertional) among basic trainees at Lackland Air Force Base, for a rate of 1.3 per 1,000 trainees. Many of the cases (21) had the nonspecific diagnosis of "heat effect," 4 were diagnosed as heat syncope, 22 as heat exhaustion, and 5 as heat stroke. From 1956 to 1999, there were seven deaths among trainees at Lackland Air Force Base due to heat stroke. CONCLUSION: After reviewing Air Force basic military training, it is apparent that the heat stress incident rates are low. Heat injury rates are low despite being located in an area that has extremely hot temperatures. However, there are some areas, such as tracking and reporting heat illness that need improvement.

Adaptation, Physiological↗