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PubMedDate not supplied

Mannequin-assessed dry-heat exchanges in the incubator-nursed newborn.

For manufacturers of warming devices for newborn infants, knowledge of the partition of the various channels of heat transfer between the neonate and the environment is necessary to regulate them adequately. The goal of this study was to determine the contributions of the different components of dry heat exchange using a thermal mannequin that replicated a full-term neonate. Each mannequin segment could be controlled separately at a selected surface temperature. The mannequin was placed in a reclining position on a mattress in a single-walled incubator (BioMS C2750). Conductive (K), convective (C), and radiative (R) heat exchanges were measured at incubator temperatures (T alpha) of 29 degrees, 32 degrees, and 34 degrees C and at air velocities (Va of 0 to 0.7 m/sec. Conductive heat exchanges varied from 4.5% to 7.9% of total dry heat loss (H). The conductive heat transfer coefficient was 0.21 W/degree C, and the mannequin surface area in contact with the mattress was 10.4% of the total surface area (A). Under natural convection, the convective and radiative heat transfer coefficients were 4.94 and 4.77 W/m2/degree C, respectively. The radiating surface area was 78% of total surface area. Convective heat exchange decreased from 36% to 17%, and radiative heat exchange increased from 60% to 79% of total dry heat loss as incubator temperature increased from 29 degrees to 34 degrees C. When air velocity was raised, convective heat exchange increased, whereas radiative heat exchange decreased. Whatever the incubator temperature, a fivefold increase in convective heat exchange was observed when air velocity increased, whereas radiative heat exchange was unchanged. At an incubator temperature of 34 degrees C and for air velocities between 0.1 and 0.4 m/sec radiative heat exchange is the dominant mode of heat loss. The results suggest that this thermal mannequin is a good tool for assessing dry heat exchange in incubators.

Body Temperature Regulation↗
PubMed2001

Presence of antibody against the inducible Hsp71 in patients with acute heat-induced illness.

Antibodies against heat shock or stress proteins (Hsps) have been reported in a number of diseases in which they may be involved in the pathogenesis of the disease or may be of use for prognosis. Heat-induced diseases, such as heat cramps, heat exhaustion, or heat stroke, are frequent in hot working or living environments. There are still few investigations on the presence and possible significance of autoantibodies against Hsps in heat-induced illnesses. Using an immunoblotting technique with recombinant human Hsps, we analyzed the presence and titers of antibodies against Hsp60, Hsp71, and Hsp90alpha, and Hsp90beta in a group of 42 young male patients who presented with acute heat-induced illness during training. We also examined the presence of antibody against Hsp71 in a second group of 57 patients with acute heat-induced illness and measured the changes in titers of anti-Hsp71 antibodies in 9 patients hospitalized by emergency physicians. In the first group of young persons exercising in a hot environment, the occurrence of antibodies against Hsp71 and Hsp90alpha was significantly higher among individuals with symptoms of heat-induced illness (P < 0.05) than in the matched group of nonaffected exercising individuals. Moreover titers of antibody against Hsp71 were higher in individuals of the severe and mild heat-induced illness groups, the highest titer being found in the most severe cases. The results from the second group of 57 heat-affected patients exposed to extreme heat were similar. Again, patients with the more severe heat-induced symptoms showed a significantly higher incidence of antibodies to Hsp71 than controls and the titer of anti-Hsp71 was higher in the severely affected group. Finally, in a study of 9 patients, it was observed that the titer of anti-Hsp71 decreased during recovery from severe heat symptoms. These results suggest that measurement of antibodies to Hsps may be useful in assessing how individuals are responding to abnormal stress within their living and working environment and may be used as one biomarker to evaluate their susceptibility to heat-induced diseases.

Adolescent↗
PubMed2006

Expression of chloroplast protein synthesis elongation factor, EF-Tu, in two lines of maize with contrasting tolerance to heat stress during early stages of plant development.

Maize chloroplast protein synthesis elongation factor, EF-Tu, has been implicated in heat tolerance, and previous studies have shown that under heat stress this protein accumulates in 14-d-, 17-d-, and 21-d-old plants of maize genotypes with increased tolerance to stress. In the present study, we investigated the expression of EF-Tu genes in heat tolerant, ZPBL 1304, and heat sensitive, ZPL 389, maize lines during early stages of their development (5-21-d-old plants) under both control and heat stress conditions. We also investigated the expression of EF-Tu in mature plants of these lines under field conditions and assessed heat tolerance in young seedlings at different stages of their development. The expression of EF-Tu was studied by determining the relative levels of EF-Tu protein and the steady state levels of EF-Tu mRNA. Chloroplast EF-Tu showed differential expression during early stages of plant development, and the heat tolerant and the heat sensitive line differed in the expression of EF-Tu under heat stress. In ZPBL 1304, plants of all ages (except 5-d-old shoots) showed heat-induced accumulation of both EF-Tu transcript and EF-Tu protein. In contrast, in ZPL 389, only plants up to 14d of age displayed increased accumulation of EF-Tu under heat stress. The increase in the relative level of EF-Tu in ZPL 389 was not preceded by an increase in the steady state level of EF-Tu mRNA. Under heat stress, the relative levels of EF-Tu correlated positively with plant heat tolerance. The results are consistent with the hypothesis that maize EF-Tu plays a role in heat tolerance and suggest that under heat stress conditions, the regulation of expression of EF-Tu may be different in the heat tolerant and heat sensitive maize lines.

Chloroplasts↗
PubMed1992

Activation of potassium channels: relationship to the heat shock response.

We examined the possibility that whole cell currents are involved and possibly trigger the response of mammalian cells to heat shock. Heat-sensitive cells from a radiation-induced fibrosarcoma (RIF-1) and heat-resistant variants (TR-4, TR-5) were heated at 45 degrees C for 3-30 min. We observed induction of voltage-dependent currents after heating in the heat-resistant cells. These currents decayed to nonmeasurable levels over a period of 6 h. In RIF-1 cells, however, voltage-dependent currents were detectable during heating only; these currents then decayed rapidly. Tetraethylammonium (TEA) cations blocked the currents; changing the concentration of extracellular K+ modified the current-voltage (I-V) relationship. These currents, therefore, resulted from the activation of voltage-dependent K+ channels. Addition of TEA during heating sensitized TR-4 cells to heat but had no effect on the heat response of the RIF-1 cells. Continuous exposure of the RIF-1 cells to 2% (vol/vol) dimethyl sulfoxide (DMSO) for 7 days induced the expression of additional functional, voltage-dependent K+ channels; these gave rise to currents that were measurable after heating. In parallel, these cells became heat resistant. Addition of TEA to DMSO-treated cells blocked channels and returned the heat response almost to the pre-DMSO levels. Our data show a correlation between heat resistance and expression of K+ channels. Because resistance to heat very likely relates to the heat shock response, our data suggest that activation of channels may be a very early event in initiation of the heat shock response.

Animals↗
PubMed1975

The heat production associated with the passage of a single impulse in pike olfactory nerve fibres.

1. A study has been made of the temperature changes associated with the passage of a single impulse in the non-myelinated fibres of the pike olfactory nerve. 2. The initial heat occurs in two phases: a burst of positive heat, followed by an evolution of negative heat. The positive and negative heats, and the net initial heat, are temperature-dependent. 3. At 0 degrees C the measured positive initial heat is 44.2 mucal/g.impulse; and the corresponding negative initial heat is 48.9 mucal/g.impulse. There is thus a net initial heat that is negative, of about 4.7 mucal/g.impulse. 4. The positive heat has a positive temperature coefficient, being increased by a factor of 1.86 when the temperature is rasied from 0 degrees C to 10 degrees C. 5. The negative initial heat also increases when the temperature is raised, but less than the positive initial heat. As a result, the net initial heat tends to become positive at higher temperatures. 6. Because of temporal dispersion of the action potential over the face of the thermopile, the observed temperature changes are smaller than those that occur at a single point in the nerve close to the stimulating cathode. The value of the positive heat at 0 degrees C corrected for temporal dispersion is estimated to be about 62 mucal/g.impulse: the corresponding value for the negative heat is about 67 mucal/g.impulse. 7. All records were analysed in terms of only two phases of initial heat (one positive, one negative). No analysis required four phases; but it is unclear whether this finding reflects a true absence of four phases, or merely the inability of the recording equipment to resolve them. 8. The positive heat seems to be derived from two sources. First, there is a dissipation of the free energy stored in the membrane capacity. Secondly, there is an evolution of heat corresponding with a decrease in entropy of the membrane dielectric with depolarization.

Action Potentials↗
PubMed1991

Effect of heat acclimation on diurnal changes in body temperature and locomotor activity in rats.

1. The present study was performed to examine the effects of heat exposure hours hours at a fixed time once a day on diurnal variations of deep body temperature, heat balance and locomotor activity in rats. 2. The heat-exposed group (HE) was subjected to an ambient temperature of 33.5 degrees C for about 5 h in the last half of the dark phase daily for at least 10 consecutive days, while the control rats were constantly kept at 24 degrees C. 3. After the completion of the heat exposure schedule, hypothalamic temperature (Thy), heat loss, heat production and locomotor activity of HE rats significantly decreased for 3-4 h during the period of previous heat exposure time and formed a characteristic trough in the dark phase, which was never observed in the control rats or in the HE rats before the start of the heat exposure schedule. 4. The troughs of Thy, heat loss and heat production in the dark phase were persistent for at least 2 days after the end of the heat exposure schedule. The reductions of locomotor activity in this period were, however, observed only on the first day after stopping the heat exposure schedule. 5. These results suggest that the time memory for heat exposure was formed in heat-acclimated rats and was persistent for at least 2 days after the removal of heat exposure. It is also concluded that the reduction in metabolic heat production contributed to the fall of Thy during the period of heat exposure.

Acclimatization↗
PubMed1995

Evidence for two different heat transduction mechanisms in nociceptive primary afferents innervating monkey skin.

1. Mechano- and heat-sensitive A fibre nociceptors (AMHs) and C fibre nociceptors (CMHs) in hairy skin (forty-six AMHs and twenty-one CMHs) and in glabrous skin (fifty-nine AMHs and ten CMHs) of anaesthetized monkeys were tested with a 30 s, 53 degrees C heat stimulus, delivered by a laser thermal stimulator (0.1 s rise time, 7.5 mm diameter). 2. Two types of heat response were observed in hairy skin AMHs. Type I AMHs had a peak discharge towards the end of the stimulus, response latencies to heat of up to several seconds, a median heat threshold greater than 53 degrees C, and a mean conduction velocity of 25 m s-1 (n = 33). Type II AMHs had a peak discharge within 1-3 s, a mean response latency of 120 ms, a median heat threshold of 46 degrees C, and a mean conduction velocity of 15 m s-1 (n = 13). Type I AMH fibres were sensitized to heat, whereas heat responses of type II AMHs were suppressed following the intense heat stimulus. 3. In glabrous skin, only type I AMHs were found. The absence of type II AMHs is consistent with the absence of first pain to heat in glabrous skin. 4. C fibre nociceptors in hairy skin had a peak discharge near stimulus onset, a mean response latency of 100 ms and a median heat threshold of 41 degrees C. Heat responses of CMHs in glabrous skin were not significantly different from those in hairy skin. 5. Only type II AMHs had response latencies that were short enough to explain first pain to heat. Heat thresholds of type II AMHs were significantly higher than those of CMHs. 6. These results suggest two different heat transduction mechanisms in nociceptive afferents. For one, heat energy is quickly transduced into action potentials, and the peak discharge is reached soon after stimulus onset. For the other, the transduction of heat is distinctly slower, and the peak discharge occurs near the end of the stimulus. Chemically mediated sensitization may be involved in the second transduction mechanism.

Animals↗
PubMed2001

Optimization of power deposition and a heating strategy for external ultrasound thermal therapy.

The purpose of this paper is to examine the thermal dose distribution, to configure the optimal absorbed power deposition, and to design an appropriate heating strategy for ultrasound thermal therapy. This work employs simulation programs, which are based on the transient bio-heat transfer equation and an ideal absorbed power deposition or an ideal temperature elevation within a cube of tissue, to study the optimal absorbed power deposition. Meanwhile, a simplified model of a scanned ultrasound transducer power deposition (a cone with convergent/divergent shape) is used to investigate the heating strategy for a large tumor with a sequence of heating pulses. The distribution of thermal dose equivalence defined by Sapareto and Dewey is used to evaluate the heating result for a set of given parameters. The parameters considered are the absorbed power density, heating duration, temperature elevation, blood perfusion, and the size of heating cube. The results demonstrate that the peak temperature is the key factor determining the thermal dose for this short-duration heating. Heat conduction has a very strong influence on the responses of temperature and thermal dose for a small heating cube and the boundary portion of a large heating cube. Hence, for obtaining the same therapeutic result, a higher power density is required for these two conditions to compensate the great temperature difference between the heating cube and the surrounding tissue. The influence of blood perfusion on the thermal dose is negligible on the boundary portion of the heating cube, while in the central portion it may become a crucial factor as a lower power density is used in this portion to save the delivered energy. When using external ultrasound heating method to treat a large tumor, the size of heating unit, the sequence of heating pulses, and the cooling-time interval between the consecutive heating pulses are the important factors to be determined to have an appropriate treatment within a reasonable overall treatment time.

Hot Temperature↗
PubMed1998

Effect of heating delay on conversion and strength of a post-cured resin composite.

Physical property enhancement in light-cured resin composites from post-cure heating is attributed to free radicals created during initial photocuring, the number of which decreases following initial light-curing. Clinically, it is important to know when the number of remaining free radicals is too low to provide for additional conversion of monomer in post-cure-heated specimens. The hypothesis tested is that the potential for additional conversion in post-cure-heated resin composite restorations is dependent upon the time after initial light-curing at which the specimen is exposed to heat treatment. This research examined the effect of delay in post-cure heating after initial photo-activation on strength and monomer conversion of a commercial resin composite material. Discs (10 x 1 mm) of Herculite XRV (Kerr/Sybron, Orange, CA) were photocured at standardized conditions. One group was left unheated, and another was subjected to post-cure heating (Brilliant DI-500, Coltène AG, Altstätten, Switzerland) at the following times after being light-cured: 5 and 30 min, and 6, 24, 48, 72, 96, and 120 hrs. After the appropriate delay time, unheated and heated specimens (n = 10) were tested for biaxial flexural strength at a constant stressing rate. Recovered, fractured strength specimens (n = 10) were analyzed for cure by means of IR spectroscopy. Post-cure heating increased strength over that of the unheated specimens only for the shortest delay times: 5 or 30 min. Thereafter, strength values were statistically equivalent (p < 0.05). Delay in heating did not significantly enhance strength of post-cure-heated specimens, but delay in time did improve strength of the unheated groups. The greatest monomer conversion was obtained when post-cure heating was applied within 6 hrs following light-curing. The difference in cure between unheated and heated specimens remained significant up to 96 hrs of delay. Flexural strength of post-cure-heated specimens remained unchanged with time delay for heating specimens. Maximal monomer conversion of post-cured specimens is obtained only within 6 hrs of light-curing. The potential for additional conversion arising from post-cure heat treatment is dependent upon the time following initial curing at which heat is applied following initial light-curing. However, delay in heat application has no influence on flexural strength.

Analysis of Variance↗
PubMedDate not supplied

Effect of fractionated heating on the blood flow in normal tissues.

The changes in blood flow in the skin and muscle of rat by single, two or six heatings, were measured with the radioactive microsphere method. The blood flow rose continuously during the 2 h heatings at temperatures up to 43.0 degrees C and 44.0 degrees C in the skin and muscle, respectively. When heated at higher temperatures, the blood flow increased and then decreased. When heated twice at 43.5 degrees C for 1 h each, the magnitude of the increase in blood flow by the second heating varied depending on the time interval between the two heatings; e.g., the second heating on the 14th day after the first heating induced an increase in blood flow much greater than that by the first heating. When the heating at 43.5 degrees C for 1 h was repeated at intervals of five days, the second and third heatings were as effective as the first heating in increasing the skin blood flow. In the muscle, the second and third heatings were 2-3-fold more effective than the first heating in raising the blood flow. The heat-induced increase in blood flow in the skin and muscle gradually diminished from the fourth heating. The tissue temperature varied considerably during heating with a water bath at a constant temperature, due probably to the changes in blood flow.

Animals↗
PubMed1986

Relationship between heat sensitivity and polyamine levels after treatment with alpha-difluoromethylornithine (DFMO).

Alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase, was used to study the effect of polyamine depletion on delayed heat sensitization in Chinese hamster ovary cells (CHO). The cells were treated with 1 or 10 mM DFMO for 8 or 48 h and then given a single heat treatment (43 degrees C, 90 min) at intervals up to 150 h after DFMO addition. Cellular survival, DNA polymerase activity, and polyamine levels were measured. Delayed heat sensitization for cell lethality began 50-55 h (about two cell divisions) after addition of 10 or 1 mM of DFMO for 8 or 48 h, respectively; i.e., cell survival of heated control cells was about 10(-1), but decreased to 10(-4)-10(-5) in heated DFMO-treated cells by 100 h. During this same interval, delayed heat sensitization also was observed for loss of DNA polymerase beta activity (from 20% in cells heated without DFMO treatment to 7% in heated DFMO-treated cells), but none was observed for DNA polymerase alpha activity. Delayed heat sensitization disappeared at 120-130 h after DFMO addition, with survival of heated DFMO-treated cells returning to that for heated control cells. The onset of delayed heat sensitization occurred 30-40 h after intracellular levels of putrescine and spermidine were depleted by more than 95%; however, spermine levels were not lowered, and in some cases even increased. Levels of putrescine and spermidine increased 5-10 h before delayed heat sensitization disappeared. While putrescine reached 25% of control, spermidine exceeded control levels during this time. Furthermore, delayed heat sensitization could be reversed by adding 10(-3) M putrescine or 5 X 10(-5) M spermidine 85-95 h after DFMO addition; in both cases spermidine increased 5-10 h before the decrease in heat sensitization. Finally, neither delayed heat sensitization nor depletion of spermidine was observed in nondividing plateau-phase cells treated with DFMO, although putrescine was depleted. These results lead to the hypothesis that DFMO-induced heat sensitization which occurs after inhibition of the synthesis of putrescine is secondary to the depletion of spermidine in some critical compartment of the cell or to a biochemical alteration. This depletion or biochemical alteration apparently occurs as the cells divide about two times after the intracellular levels of soluble spermidine have been depleted.

Cell Division↗
PubMed2004

Insulin potentiates expression of myocardial heat shock protein 70.

OBJECTIVE: Since insulin stimulates nitric oxide (NO) production and an increase in NO following heat shock is required for myocardial heat shock protein 70 (Hsp70) synthesis, we hypothesized that insulin would enhance myocardial Hsp70 synthesis by augmenting NO signaling. We examined whether a physiologic dose of insulin increased myocardial Hsp70 in unstressed and heat shock treated rats. METHODS: Adult male Sprague-Dawley rats were assigned to groups: (1) control, (2) insulin injected (200 microU/gm body weight), (3) heat shock treated (core body temperature 42 degrees C for 15 min), (4) heat shock and insulin treated, (5) L-nitroarginine methyl ester (L-NAME) and heat shock and insulin treated, (6) sodium nitroprusside (SNP) and heat shock and insulin treated. Six hours later, myocardial Hsp70 content and localization was analyzed. RESULTS: Hsp70 was increased in heat shock treated hearts (120.6+/-16.8 ng/mg protein, P < 0.001) vs. control (12.9+/-2.0 ng/mg protein), or insulin treated hearts (15.5+/-0.83 ng/mg protein). In addition, Hsp70 was increased in the heat shock and insulin treated hearts (164.4+/-7.53 ng/mg protein) compared to control, insulin only (P = 0.001) or heat shock only treated hearts (P = 0.01). L-NAME did not abolish the insulin induced increase in Hsp70 in heat shocked hearts (195.2+/-13.4 ng/mg protein, P = 0.21) and SNP did not further enhance Hsp70 in the insulin and heat shocked group (188.9+/-8.2 ng/mg protein, P = 0.71). Western analysis and confocal microscopy revealed a lowlevel expression of myocardial Hsp70 in response to insulin. Hsp70 was localized primarily in blood vessels after insulin or heat shock treatments. CONCLUSIONS: Insulin caused a low-level expression of myocardial Hsp70 and potentiated Hsp70 synthesis in response to heat shock. The ability of insulin to potentiate Hsp70 after heat shock is independent of NO signaling as it was not altered by either LNAME or SNP pretreatment. Blood vessels appear to be the primary site of Hsp70 after insulin or heat shock treatment.

Animals↗
PubMed1998

Factors affecting the heat resistance of Escherichia coli O157:H7.

Escherichia coli O157:H7 has been reported as being not particularly heat resistant. However, several factors which might increase its heat resistance have been investigated in this study using five strains. Increase in growth temperature to 40 degrees C, as found in the cow gut, heat-shock at sub-lethal temperatures of 42, 45, 48 and 50 degrees C, and variable heating rate (1 degree C min-1 to 23 degrees C min-1) had no dramatic effect on heat resistance. Growth phase had a marked impact on heat resistance; late stationary phase cells were more heat-resistant than were log phase cells. The difference in heat resistance between the two phases of growth became more pronounced when cells were resuspended in fresh nutrient broth; heat resistance of late stationary phase cells increased dramatically whereas no such effect was observed with log phase cells. The addition of polyphosphates to the heating medium did not increase heat resistance. A reduction in water activity of the heating medium from 0.995 to levels between 0.980 and 0.960 also resulted in a marked increase in heat resistance. This effect was more pronounced under conditions of extremely low water activity created by resuspending late stationary phase cells in sunflower oil. Survivors were detected even after a heat treatment at 60 degrees C for 1 h or 70 degrees C for 5 min. It can be confirmed that this serotype has no unusual heat resistance and that the heating environment markedly affects resistance.

Animals↗
PubMed1996

Differential effects of exercise and heat stress on liver HSP70 accumulation with aging.

Previous reports have suggested that the heat shock response to passive heating may be blunted by aging. However, during exertional heating, factors in addition to elevated temperature may amplify the degree of stress compared with hyperthermia alone. The purpose of this study was to compare the pattern of accumulation of the highly inducible 72-kDa heat shock protein (HSP72) in liver tissue of mature (12-mo-old) and senescent (24-mo-old) male Fischer 344 rats after either passive or exertional heat stress. A euthermic control group was exposed to an ambient temperature (Ta) of 25 degrees C for 4.5 h. A passive heating (heat) group was exposed to an Ta of 42 degrees C until colonic temperature (Tco) reached 41 degrees C. An exertional heating (exercise) group performed intermittent moderate-intensity treadmill exercise (similar absolute intensities for the two age groups) at an Ta of 32 degrees C until Tco reached 41 degrees C. Heating rates were similar in the heat and exercise groups (approximately 0.08 degrees C/min). Rats in both the heat and exercise groups were maintained at a Tco of 41 degrees C for an additional 30 min and subsequently returned to an Ta of 25 degrees C for 3 h. Liver HSP72 accumulation was increased in mature rats after both the heat (+192% vs. control) and exercise (+292%) protocols. In contrast, the senescent rats demonstrated no significant increase in inducible HSP70 with heating but a large increase with exercise (+232%; P < 0.01 compared with control and heat groups). These data suggest that the blunted heat shock protein response to heating observed with aging is not a result of the inability to produce inducible HSP72 because older rats had an robust response to exertional hyperthermia.

Aging↗
PubMed1999

Heat-induced modulation of lamin B content in two different cell lines.

Previous work in our laboratory indicates that the nuclear matrix protein lamin B is a "prompt" heat shock protein, which increases significantly when human U-1 melanoma and HeLa cells are exposed to 45.5 degrees C for 5-40 min. Using Western blotting, we found that the lamin B content in U-1 and HeLa cells increased to a greater extent during post-heat incubation at 37 degrees C than during the heat dose itself. When HeLa cells were heated at 45.5 degrees C for 30 min, and then incubated at 37 degrees C for up to 7 h, lamin B content was increased significantly (1.69-fold maximum increase at 3 h) compared to unincubated heated cells. Also, thermotolerant HeLa cells showed a greater increase (up to 1.72-fold) in lamin B content during subsequent heating compared to nontolerant cells. The increase in lamin B content in thermotolerant cells, or when heated cells were incubated at 37 degrees C, was also observed in U-1 cells. HeLa cells heated in the presence of glycerol (a heat protector) showed a 1.21-1.72-fold increase in lamin B content compared to cells heated for 10-30 min without glycerol. In contrast, lamin B content decreased 1.23-1.85-fold when cells were heated for 10-30 min in the presence of procaine (a heat sensitizer) compared to cells heated without procaine. These data suggest that lamin B may play an important role in the heat shock response, and that modulation of lamin B content by heat sensitizers or protectors may play a role in regulation of heat sensitivity.

Anesthetics, Local↗
PubMed2000

Heat stress attenuates skeletal muscle atrophy in hindlimb-unweighted rats.

This study tested the hypothesis that elevation of heat stress proteins by whole body hyperthermia is associated with a decrease in skeletal muscle atrophy induced by reduced contractile activity (i.e. , hindlimb unweighting). Female adult rats (6 mo old) were assigned to one of four experimental groups (n = 10/group): 1) sedentary control (Con), 2) heat stress (Heat), 3) hindlimb unweighting (HLU), or 4) heat stress before hindlimb unweighting (Heat+HLU). Animals in the Heat and Heat+HLU groups were exposed to 60 min of hyperthermia (colonic temperature approximately 41.6 degrees C). Six hours after heat stress, both the HLU and Heat+HLU groups were subjected to hindlimb unweighting for 8 days. After hindlimb unweighting, the animals were anesthetized, and the soleus muscles were removed, weighed, and analyzed for protein content and the relative levels of heat shock protein 72 (HSP72). Compared with control and HLU animals, the relative content of HSP72 in the soleus muscle was significantly elevated (P < 0.05) in both the Heat and Heat+HLU animals. Although hindlimb unweighting resulted in muscle atrophy in both the HLU and Heat+HLU animals, the loss of muscle weight and protein content was significantly less (P < 0.05) in the Heat+HLU animals. These data demonstrate that heat stress before hindlimb unweighting can reduce the rate of disuse muscle atrophy. We postulate that HSP70 and/or other stress proteins play a role in the control of muscle atrophy induced by reduced contractile activity.

Animals↗
PubMed1991

Sensitization to hyperthermia induced in a normal tissue by step-down heating.

The effect of step-down heating was investigated in the skin of the CDF1 mouse foot. Step-down heating was induced with a 44.7 degrees C/10 min pretreatment followed by a test treatment at a lower temperature for variable time. Step-up heating, that is, a test treatment followed by a 44.7 degrees C/10 min treatment, and single heating were used as controls. The normal tissue reaction was scored at five levels of damage (from slight redness and oedema to loss of a toe or greater reaction), and the heating time to induce each level in 50% of the animals, RD50, was used as the endpoint. The effect of step-down heating was quantified by the step-down ratio, calculated as the ratio of test heating times to obtain the endpoint. A significant reduction of the RD50 was seen at all score levels when the 44.7 degrees C/10 min was given in a step-down heating schedule, and the effect increased with decreasing test treatment temperature. In contrast, the heat sensitivity was only marginally influenced by step-up heating. An analysis of the time-temperature relationship demonstrated a log-linear relationship between temperature and RD50 for single heating in the range 42.2-44.7 degrees C and for step-down heating in the range 41.7-44.7 degrees C. The curve for step-down heating showed a lesser slope indicating a decrease of the activation energy. The kinetics of the SDH effect were investigated by inserting an interval between a primary 44.7 degrees C/10 min treatment and a test treatment performed at 42.2 degrees C. The effect of step-down heating was maximal with no interval between the priming treatment and the test treatment. As the interval was increased to 1.5 hr the step-down sensitization disappeared, and with even longer intervals thermotolerance developed. From a clinical point of view, the present data indicate that step-down heating may increase the extent of both reversible and irreversible heat damage in the normal tissue.

Acclimatization↗
PubMedDate not supplied

The effect of uniform heating on the biomechanical properties of the intervertebral disc in a porcine model.

BACKGROUND CONTEXT: The use of minimally invasive lumbar intradiscal heating techniques, including intradiscal electro-thermal therapy (IDET), endoscopic radio-frequency annuloplasty, nucleoplasty and laser discectomy, for chronic lumbar discogenic pain and contained disc herniation has recently gained popularity. The purported therapeutic mechanisms of these interventions include subtotal nuclectomy, annular nociceptor ablation, and stabilization of the annular fibers. Basic science data elucidating the biomechanical and histomorphologic alterations of heat treatments on disc remain sparse. PURPOSE: The purpose of this study is to examine the effects of uniform heating on biomechanical properties and histomorphology of intervertebral disc tissues using a porcine model. STUDY DESIGN/SETTING: In a laboratory setting, porcine functional spinal units consisting of vertebra-nucleus pulposus-vertebra core and porcine hamstring tendons were harvested. Studies were performed on these tissue samples by uniformly heating the specimens in a constant temperature water bath. Ten porcine lumbar disc core and twenty-five porcine hamstring tendons were utilized as the subjects for this study. The effects of uniform heat treatments on disc core and hamstring tendon were measured for shrinkage, stiffness, and load to failure strength. Histomorphological study was also carried on the same specimen. METHODS: The porcine vertebra-nucleus pulposus-vertebra segments were cored to a uniform 1-cm diameter. The hamstring tendons were cut to uniform 1.2-inch lengths. The tendon specimens were divided into groups of five each and heated in constant temperature water baths of 60 degrees C, 65 degrees C, 70 degrees C, or 75 degrees C for 10 min. Unheated specimens served as controls. The disc core specimens were divided in two group of five each, and tested at room temperature or after immersion in a 70 degrees C bath. The shrinkage was monitored during immersion in the water bath. Biomechanical testing to failure was carried out using mechanical loading on an MTS servohydraulic testing machine operating under stroke control. Strength and stiffness of the tissue was determined. Histomorphology was studied by staining the specimen with hematoxylin and eosin (H&E), and examined under 200 times magnification. Non-heated controls were used for comparisons. RESULTS: The porcine hamstring tendons had no measurable shrinkage in specimens heated up to 65 degrees C. At temperatures above 65 degrees C, the shrinkage was concluded within 2 min of immersion and 70 degrees C appeared to be the optimal temperature, as temperatures higher than this did not demonstrate incremental effects. The disc core samples were heated to 70 degrees C (optimum temperature), and there appeared to be gross contraction of the disc core circumference to visual inspection, but no measurable lengthwise shrinkage could be appreciated. Histologically, the specimens demonstrated progressive loss of individual collagen fiber outline as the temperature increased. In the tendons, at 75 degrees C all of the fibers appear to be fused together, and the voids between individual collagen fibers were no longer present. Biomechanical testing revealed that the tendons undergo a substantial reduction in stiffness after heating. The mean tendon stiffness for the unheated specimens was 19,356 psi, while the corresponding value for the heated tendons was 1023 psi. These were significantly different using the paired t-test at p=0.0043. For the disc core samples, there was no significant difference in either stiffness (p=0.182) or failure strength (p=0.998) after heating. All failures occurred in mid-substance of the specimen. CONCLUSIONS: The application of uniform heating to nucleus pulposus disc core caused visible contraction of its circumference but not lengthwise shrinkage. The same heating shrinks the hamstring tendon and reduces its stiffness. Ultimate failure strength of the disc core specimen remains unchanged. The failure data was not obtainable for the tendon due to premature slippage from the fixation apparatus before failure. The results of this study fail to support a biomechanical justification for the application of uniform heat treatment to the whole intervertebral disc. Heating annulus fibrosus and nucleus pulposus separately to specific temperatures may have potential clinical benefits.

Animals↗