Comparison between two rat sympathetic pathways activated in cold defense

In cold defense and fever, activity increases in sympathetic nerves supplying both tail vessels and interscapular brown adipose tissue (iBAT). These mediate cutaneous vasoconstrictor and thermogenic responses, respectively, and both depend upon neurons in the rostral medullary raphé. To examine the commonality of brain circuits driving these two outflows, sympathetic nerve activity (SNA) was recorded simultaneously from sympathetic fibers in the ventral tail artery (tail SNA) and the nerve to iBAT (iBAT SNA) in urethane-anesthetized rats. From a warm baseline, cold-defense responses were evoked by intermittently circulating cold water through a water jacket around the animal's shaved trunk. Repeated episodes of trunk skin cooling decreased core (rectal) temperature. The threshold skin temperature to activate iBAT SNA was 37.3 +/- 0.5 degrees C (n = 7), significantly lower than that to activate tail SNA (40.1 +/- 0.4 degrees C; P < 0.01, n = 7). A fall in core temperature always strongly activated tail SNA (threshold 38.3 +/- 0.2 degrees C, n = 7), but its effect on iBAT SNA was absent (2 of 7 rats) or weak (threshold 36.9 +/- 0.1 degrees C, n = 5). The relative sensitivity to core vs. skin cooling (K-ratio) was significantly greater for tail SNA than for iBAT SNA. Spectral analysis of paired recordings showed significant coherence between tail SNA and iBAT SNA only at 1.0 +/- 0.1 Hz. The coherence was due entirely to the modulation of both signals by the ventilatory cycle because it disappeared when the coherence spectrum was partialized with respect to airway pressure. These findings indicate that independent central pathways drive cutaneous vasoconstrictor and thermogenic sympathetic pathways during cold defense.     

Heat loss responses in rats acclimated to heat loaded intermittently

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antipyresis due to centrally administered vasopressin differentially alters thermoregulatory effectors depending on the ambient temperature

The intracerebroventricular (i.c.v.) administration of arginine vasopressin (AVP), in the febrile rat elicits an antipyresis at cold, warm and neutral ambient temperatures. These experiments were conducted, therefore, to elucidate the thermoregulatory effector mechanisms responsible for this antipyretic effect. At 25 degrees C, AVP-induced antipyresis was mediated by tail skin vasodilation while metabolic rate was unaffected. At 4 degrees C, the antipyresis produced by AVP was approximately double that seen at 25 degrees C. This effect appeared to be mediated exclusively by inhibition of heat production since the metabolic rate decreased markedly following AVP. This antipyresis at 4 degrees C was accompanied by cutaneous vasoconstriction. At 32 degrees C, neither vasomotor tone, metabolic rate nor evaporative heat loss could be shown to contribute to the small antipyretic effect elicited by AVP. We conclude from these data that i.c.v. AVP is producing antipyresis by affecting the febrile body temperature set-point mechanism since the thermoregulatory strategy to lose heat varies at different ambient temperatures and the decrease in body temperature cannot be shown to be due to changes in a single effector mechanism.     

Effects of estrogen on thermoregulatory tail vasomotion and heat-escape behavior in freely moving female rats

Effects of estrogen on thermoregulatory vasomotion and heat-escape behavior were investigated in ovariectomized female rats supplemented with estrogen (replaced estrogen rats) or control saline (low estrogen rats). First, we measured tail temperature of freely moving rats at ambient temperatures (T(a)) between 13 and 31 degrees C. Tail temperature of the low estrogen rats was higher than that of the replaced estrogen rats at T(a) between 19 and 25 degrees C, indicating that the low estrogen rats exhibit more skin vasodilation than the replaced estrogen rats. There was no significant difference in oxygen consumption and core temperature between the two groups. Second, we analyzed heat-escape behaviors in a hot chamber where rats could obtain cold air by moving in and out of a reward area. The low estrogen rats kept T(a) at a lower level than did the replaced estrogen rats. These results imply that the lack of estrogen facilitates heat dissipation both by skin vasodilation and by heat-escape behavior. Ovariectomized rats may mimic climacteric hot flushes not only for autonomic skin vasomotor activity but also for thermoregulatory behavior.     

Mechanism of action of physical antipyresis in the rat

To study the mechanism of action of physical antipyresis, core temperature was measured in two groups of rats in which heat loss was increased by cold exposure and by cooling an inferior cava heat exchanger, respectively, both before and after infection with Salmonella enteritidis. Cold exposure did not influence core temperature. On the other hand, cooling the heat exchanger caused a fall in core temperature of approximately 0.7 degree C, to 37 degrees C in normothermia and to 38.5 degrees C 24 h after the infection. These lower core temperatures were then regulated against any further increase in heat loss until the thermoregulatory metabolic capacity of the animals was exhausted and a hypothermia developed. It is concluded that in infectious fever the threshold temperature of shivering increases as much as core temperature. Furthermore it is suggested that physical antipyresis, such as sponging with tepid water, induces a moderate but regulated fall in temperature to about the threshold of shivering and that its efficacy may increase with ambient temperature.     

Cryopreservation of isolated hepatocytes: intracellular ice formation under various chemical and physical conditions.

Kinetics of intracellular ice formation (IIF) for isolated rat hepatocytes was studied using a cryomicroscopy system. The effect of the cooling rate on IIF was investigated between 20 and 400 degrees C/min in isotonic solution. At 50 degrees C/min and below, none of the hepatocytes underwent IIF; whereas at 150 degrees C/min and above, IIF was observed throughout the entire hepatocyte population. The temperature at which 50% of hepatocytes showed IIF (50TIIF) was almost constant with an average value of -7.7 degrees C. Different behavior was seen in isothermal subzero holding temperatures in the presence of extracellular ice. 50TIIF from isothermal temperature experiments was approximately -5 degrees C as opposed to -7.7 degrees C for constant cooling rate experiments. These experiments clearly demonstrated both the time and temperature dependence of IIF. On the other hand, in cooling experiments in the absence of extracellular ice, IIF was not observed until approximately -20 degrees C (at which temperature the whole suspension was frozen spontaneously) suggesting the involvement of the external ice in the initiation of IIF. The effect of dimethyl sulfoxide (Me2SO) on IIF was also quantified. 50TIIF decreased from -7.7 degrees C in the absence of Me2SO to -16.8 degrees C in 2.0 M Me2SO for a cooling rate of 400 degrees C/min. However, the cooling rate (between 75 and 400 degrees C/min) did not significantly affect 50TIIF (-8.7 degrees C) in 0.5 M Me2SO. These results suggest that multistep protocols will be required for the cryopreservation of hepatocytes.     

Nitric oxide and attenuated reflex cutaneous vasodilation in aged skin

Thermoregulatory cutaneous vasodilation is diminished in the elderly. The goal of this study was to test the hypothesis that a reduction in nitric oxide (NO)-dependent mechanisms contributes to the attenuated reflex cutaneous vasodilation in older subjects. Seven young (23 +/- 2 yr) and seven older (71 +/- 6 yr) men were instrumented with two microdialysis fibers in the forearm skin. One site served as control (Ringer infusion), and the second site was perfused with 10 mM N(G)-nitro-l-arginine methyl ester to inhibit NO synthase (NOS) throughout the protocol. Water-perfused suits were used to raise core temperature 1.0 degrees C. Red blood cell (RBC) flux was measured with laser-Doppler flowmetry over each microdialysis fiber. Cutaneous vascular conductance (CVC) was calculated as RBC flux per mean arterial pressure, with values expressed as a percentage of maximal vasodilation (infusion of 28 mM sodium nitroprusside). NOS inhibition reduced CVC from 75 +/- 6% maximal CVC (CVC(max)) to 53 +/- 3% CVC(max) in the young subjects and from 64 +/- 5% CVC(max) to 29 +/- 2% CVC(max) in the older subjects with a 1.0 degrees C rise in core temperature. Thus the relative NO-dependent portion of cutaneous active vasodilation (AVD) accounted for approximately 23% of vasodilation in the young subjects and 60% of the vasodilation in the older subjects at this level of hyperthermia (P < 0.001). In summary, NO-mediated pathways contributed more to the total vasodilatory response of the older subjects at high core temperatures. This suggests that attenuated cutaneous vasodilation with age may be due to a reduction in, or decreased vascular responsiveness to, the unknown neurotransmitter(s) mediating AVD.     

Acute head-down tilt decreases the postexercise resting threshold for forearm cutaneous vasodilation.

The purpose of this study was to evaluate the role of baroreceptor control on the postexercise threshold for forearm cutaneous vasodilation. On four separate days, six subjects (1 woman) were randomly exposed to 65 degrees head-up tilt and to 15 degrees head-down tilt during a No-Exercise and Exercise treatment protocol. Under each condition, a whole body water-perfused suit was used to regulate mean skin temperature (T(sk)) in the following sequence: 1) cooling until the threshold for vasoconstriction was evident; 2) heating ( approximately 7.0 degrees C/h) until vasodilation occurred; and 3) cooling until esophageal temperature (T(es)) and (T(sk)) returned to baseline values. The Exercise treatment consisted of 15 min of cycling exercise at 70% maximal O(2) uptake, followed by 15 min of recovery in the head-up tilt position. The No-Exercise treatment consisted of 30 min resting in the head-up tilt position. After the treatment protocols, subjects were returned to their pretreatment condition, then cooled and warmed again consecutively. The calculated T(es) threshold for cutaneous vasodilation increased 0.24 degrees C postexercise during head-up tilt (P < 0.05), whereas no difference was measured during head-down tilt. In contrast, sequential measurements without exercise demonstrate a time-dependent decrease for head-up tilt (0.17 degrees C) and no difference for head-down tilt. Pretreatment thresholds were significantly lower during head-down tilt compared with head-up tilt. We have shown that manipulating postexercise venous pooling by means of head-down tilt, in an effort to reverse its impact on baroreceptor unloading, resulted in a relative lowering of the resting postexercise elevation in the T(es) for forearm cutaneous vasodilation.     

Viscoelastic and light scattering studies on thermally induced sol to gel phase transition in fish myosin solutions

Viscoelastic (VE) and dynamic light scattering (DLS) analyses of fish (white croaker) myosin solutions were performed at myosin concentrations of 30 mg/mL for VE and 0.1 mg/mL for DLS at 0.6M KCl and pH 7.0 to clarify thermally induced gelation. The hydrodynamic radius R(h) considerably decreased around 30-35 degrees C. The shear modulus G was constant below 25 degrees C and increased by incubating the sample at 30 degrees C. G further increased as the temperature of the incubated sample decreased. The curves of G vs T for different time courses showed a sharp peak around 35 degrees C and a moderate peak around 60 degrees C in the heating process, while a stepwise increase in G was observed around 30 degrees C in the cooling process when the temperature was elevated to not more than 60 degrees C. No distinct stepwise change was observed once the temperature of the sample exceeded 60 degrees C. The absolute value of G strongly depended on the maximum elevated temperature and the incubation time at that temperature. The corresponding behavior of the viscosity eta was observed for each time course. Based on these results, the mechanism of thermally induced gelation of myosin solutions is discussed in view of S-S bridge formation in the head and tail portions and unwinding/rewinding of coiled-coil alpha-helices in the tail portion.     

Hypohydration effect on finger skin temperature and blood flow during cold-water finger immersion.

This study was conducted to determine whether hypohydration (Hy) alters blood flow, skin temperature, or cold-induced vasodilation (CIVD) during peripheral cooling. Fourteen subjects sat in a thermoneutral environment (27 degrees C) during 15-min warm-water (42 degrees C) and 30-min cold-water (4 degrees C) finger immersion (FI) while euhydrated (Eu) and, again, during Hy. Hy (-4% body weight) was induced before FI by exercise-heat exposure (38 degrees C, 30% relative humidity) with no fluid replacement, whereas during Eu, fluid intake maintained body weight. Finger pad blood flow [as measured by laser-Doppler flux (LDF)] and nail bed (T(nb)), pad (T(pad)), and core (T(c)) temperatures were measured. LDF decreased similarly during Eu and Hy (32 +/- 10 and 33 +/- 13% of peak during warm-water immersion). Mean T(nb) and T(pad) were similar between Eu (7.1 +/- 1.0 and 11.5 +/- 1.6 degrees C) and Hy (7.4 +/- 1.3 and 12.6 +/- 2.1 degrees C). CIVD parameters (e.g., nadir, onset time, apex) were similar between trials, except T(pad) nadir was higher during Hy (10.4 +/- 3.8 degrees C) than during Eu (7.9 +/- 1.6 degrees C), which was attributed to higher T(c) in six subjects during Hy (37.5 +/- 0.2 degrees C), compared with during Eu (37.1 +/- 0.1 degrees C). The results of this study provide no evidence that Hy alters finger blood flow, skin temperature, or CIVD during peripheral cooling.     

Partially irreversible cold-induced lipid phase transitions in mammalian sperm plasma membrane domains: freeze-fracture study

In an effort to investigate the nature of the cellular injury caused when mammalian spermatozoa are cooled prior to cryopreservation, the occurrence of thermal phase transitions amongs the lipid components of the sperm plasma membrane was investigated by the use of freeze-fracture electron microscopy. The mechanisms by which glycerol and egg yolk exert protective effects during semen cooling and freezing were also examined. Ram and blackbuck spermatozoa, maintained at 30 degrees C prior to fixation at this temperature, exhibited randomly distributed intramembranous particles over the acrosomal, postacrosomal, and flagellar regions of the plasma membrane. In contrast, spermatozoa fixed at 5 degrees C after slow cooling to this temperature exhibited particle clustering over the postacrosomal region of the head as well as over the tail. These effects were not influenced by the presence of egg yolk or glycerol during the cooling procedure, although these substances protected the spermatozoa against loss of motility. Particle clustering over the sperm tail, induced by the slow cooling process, was found to be only partially reversible. The extensive areas of particle-free lipid, noted to result from the cooling procedure, were absent if the spermatozoa were rewarmed to 30 degrees C; however, the original distribution of particles was not restored and numerous small particle-free domains persisted. It is proposed that this type of irreversible change within the sperm plasma membrane may contribute to the loss of motility and fertility suffered by spermatozoa after cooling and freezing. Furthermore, it is suggested that protective substances such as egg yolk may exert their effects by countering these deleterious changes, rather than by preventing their occurrence.     

Effects of raised body temperature on reasoning, memory, and mood

Volunteers' body core temperatures were raised to 38.80-39.05 degrees C within a few minutes by immersion in water at 41 degrees C. Tests were then made with the subjects insulated and cooling slowly. Control immersions were made in water at 37 degrees C when core temperatures remained at 36.60-37.40 degrees C. Neither memory registration nor recall of memories registered an hour earlier, nor immediate ability to recall digit spans forward or backward was affected by the increase in core temperature. The increase in temperature did not have any significant effect on accuracy of performance of verbal logic problems or of two-digit subtractions. However, the increase in core temperature was associated with a significant increase in the speed of performance of the tests, by 11 and 10%, respectively. The warm immersions also induced a significant decrease in alertness and an increase in irritability as assessed subjectively by the volunteers; control immersions had no such effects.     

Studies on the cryopreservation of eggs of Angiostrongylus cantonensis

The possibility of cryopreserving the eggs of Angiostrongylus cantonensis collected from the uterus of female worms was investigated. Eggs were cultured in NCTC 109 medium containing 50% rat serum, and various growth stages, from one-cell eggs to embryonated eggs, were used in this study. As a cryoprotective agent, dimethylsulphoxide (Me2SO) was added to the medium at a final concentration of 1 M. Eggs suspended in 0.2 ml of the medium at 37 degrees C were cooled to 0 degrees C at a rate of 1 degree C min-1, then an equal volume of 2M-Me2SO solution was added. After equilibration for 15 min, the freezing procedures were started. In the freezing procedures, the effectiveness of (i) a seeding process, (ii) different cooling and warming rates and (iii) the relationship between the growth stages of the eggs and their tolerance to freezing at -20 degrees C were investigated. It was found the highest level of survival could be obtained with 32-cell eggs cooled at a rate of 0.3 degrees C min-1 or more slowly with seeding at -4 degrees C and warming at a rate of 5 degrees C min-1. Survival was influenced more by cooling rate than by warming rate. Using these optimum conditions, the survival of eggs was then investigated following cooling to various temperatures. While more than 50% of eggs were found to survive cooling to -30 degrees C, extremely low survival was noted from lower temperatures.     

Neuropeptide Y and Y1-receptor agonists increase blood flow through arteriovenous anastomoses in rat tail

The purpose of this study was to characterize neuropeptide Y(NPY)-induced vasodilation in the rat tail. Sterile surgical techniquewas used (with pentobarbital sodium anesthesia) to equip rats with ajugular catheter and a blind-ended thermocouple reentrant tube next tothe carotid artery. Tail skin and core temperature were measured withthermocouples during experiments. Tail skin blood flow was monitoredwith a laser Doppler flowmeter, and tail total blood flow and volumewere measured with plethysmography. After baseline data were collected,saline, NPY (16, 32, 64, and 128 µg/kg),[Leu³¹Pro³⁴]NPY (63.25 µg/kg),or NPY[13-36] (44.7 µg/kg) was administered intravenously. Tail total blood flow, volume, and tail skin temperature increased, whereas tail skin blood flow and core temperature decreased in response to both NPY- and theY₁-receptor agonist[Leu³¹Pro³⁴]NPY but not inresponse to saline or NPY[13-36]. Studies conducted with the use of color microspheres demonstrated that arteriovenous anastomoses are involved in this NPY-induced vasodilation.

     

Investigating the warming and cooling rates of human cadavers by development of a gel-filled model to validate core temperature

Tissue Services (within NHS Blood and Transplant) plans to bring deceased donors to its state of the art retrieval suite at its new centre in Speke, Liverpool in air-conditioned transport at circa 20 degrees C but without dedicated active cooling. The aim of this study was to determine how quickly a refrigerated body would warm at different ambient temperatures using a gel-filled model. Two models of a human body were prepared consisting of neoprene wetsuits filled with approximately 7 or 18 l of a viscous solution, which once set has similar properties to ballistics gel. This gel consisted of 47.5% distilled water, 47.5% glycerol and 5% agar. Final "dummy" weights were 7.4 and 18.6 kg respectively, representing "virtual" weights of approximately 40 kg and 70 kg. A K-class thermocouple probe was then inserted into a "rectal" position within each model and the models were cooled to a series of different core temperatures: 5 degrees C, 10 degrees C and 15 degrees C and then were placed in an orbital incubator set at 20 degrees C or 30 degrees C ambient temperature. The rate of temperature increase, in the dummy, was measured, until the model's core temperature was close to the ambient temperature. This was done in triplicate for each size model and ambient temperature. Data indicate that increase in core temperature depends on the size of the model and the initial core temperature. For an equivalent donor weight of 70 kg and background temperature of 20 degrees C, core temperature rises from 5 degrees C to 9.2 degrees C; 10 degrees C to 13.3 degrees C and 15 degrees C to 15.5 degrees C after 2 h. The final core temperatures after 2 h are likely to retard bacterial growth, movement or contamination during transport. Cooling rate data indicated that a 70 kg donor equivalent cooled from 37 degrees C to 15 degrees C within 6 h in a cold room at 4 degrees C. This work has shown that a body can be transported without refrigeration and not cause further tissue deterioration as a result.     

Effects of temperature upon capacitation of guinea pig spermatozoa

Spermatogenesis in many mammalian species requires a temperature a few degrees below body core temperature. Upon ascent through the male tract and deposition in the female tract, the temperature of spermatozoa is increased to body core temperature. This report investigates the effects of temperatures above or below normal body core temperature, which is also the usual temperature of in vitro gamete incubations and fertilization, upon sperm acrosome reacting ability and fertility. Epididymal guinea pig spermatozoa were preincubated in a Ca2+-free medium at temperatures of 15 degrees C, 25 degrees C, 37 degrees C, or 44 degrees C for increasing periods of time. At 15 degrees C or 25 degrees C, no or very few spermatozoa acquired the ability to acrosome react upon exposure to Ca2+ even after 18 hr of culture or warming up to 37 degrees C. A known stimulator of acrosome-reacting ability, lysophosphatidylcholine, was ineffective in promoting acrosome-reacting ability in spermatozoa incubated at 15 degrees C or 25 degrees C. At 37 degrees C the percentage of acrosome reaction increased steadily over time, reaching about 65% after 18 hr. At 44 degrees C the time course of acquisition of acrosome-reacting ability was greatly accelerated with a percentage at 2 hr comparable to that achieved at 37 degrees C only after 18 hr of preincubation. This effect of incubation at 44 degrees C could be reversed by cooling the spermatozoa to 37 degrees C before they were exposed to Ca2+. Spermatozoa induced to undergo the acrosome reaction after preincubation at 44 degrees C were fully capable of fertilizing intact guinea pig eggs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative analysis of the structure and thermal stability of sea urchin peristome and rat tail tendon collagen

We have purified collagen from two distinct sources; the vertebrate, rat tail tendon and an invertebrate, sea urchin adult tissue, the peristome. The collagenous nature of the purification products was confirmed by amino acid compositional analysis. Both preparations had high contents of glycine and proline residues and hydroxyproline was also present. The total pyrrolidine (proline+hydroxyproline) content decreased from 17.9 mole% in rat tail collagen to 12.9 mole% in peristome collagen. Distinctly different circular dichroic spectra were measured for these collagens. Analyses of spectra, measured as a function of temperature, revealed distinct thermal denaturation profiles. The melting temperature for rat tail collagen was 38.5 degrees C, while the corresponding value for peristome collagen was significantly lower at 27 degrees C. A similar thermal denaturation profile was obtained for rat tail collagen in digestion experiments using a 41-kDa gelatinase activity, isolated from sea urchin eggs. These results identify structural differences between a typical, vertebrate type I fibrillar collagen and an echinoderm collagen which serves as a constituent of a mutable connective tissue. These differences may relate to the functional roles played by collagen in these distinctly different tissues.     

Upright LBPP application attenuates elevated postexercise resting thresholds for cutaneous vasodilation and sweating.

We evaluated postexercise venous pooling as a factor leading to previously reported increases in the postexercise esophageal temperature threshold for cutaneous vasodilation (ThVD) and sweating (ThSW). Six subjects were randomly exposed to lower body positive pressure (LBPP) and to no LBPP after an exercise and no-exercise treatment protocol. The exercise treatment consisted of 15 min of upright cycling at 65% of peak oxygen consumption, and the no-exercise treatment consisted of 15 min upright seated rest. Immediately after either treatment, subjects donned a liquid-conditioned suit used to regulate mean skin temperature and then were positioned within an upright LBPP chamber. The suit was first perfused with 20 degrees C water to control and stabilize skin and core temperature before whole body heating. Subsequently the skin was heated ( approximately 4.0 degrees C/h) until cutaneous vasodilation and sweating occurred. Forearm skin blood flow and arterial blood pressure were measured noninvasively and were used to calculate cutaneous vascular conductance during whole body heating. Sweat rate response was estimated from a 5.0-cm2 ventilated capsule placed on the upper back. Postexercise ThVD and ThSW were both significantly elevated (0.27 +/- 0.04 degrees C and 0.25 +/- 0.04 degrees C, respectively) compared with the no-exercise trial without LBPP (P < 0.05). However, the postexercise increases in both ThVD and ThSW were reversed with the application of LBPP. Our results support the hypothesis that the postexercise warm thermal responses of cutaneous vasodilation and sweating are attenuated by baroreceptor modulation via lower body venous pooling.     

Attenuated thermoregulatory sweating and cutaneous vasodilation after 14-day bed rest in humans.

We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental room was air-conditioned (27 degrees C, 30-40% relative humidity). We measured skin blood flow (chest and forearm), skin temperatures (chest, upper arm, forearm, thigh, and calf), and tympanic temperature. We also measured sweat rate by the ventilated capsule method in which the skin area for measurement was drained by dry air conditioned at 27 degrees C under similar skin temperatures in both trials. We calculated cutaneous vascular conductance (CVC) from the ratio of skin blood flow to mean blood pressure. From tympanic temperature-sweat rate and -CVC relationships, we assessed the threshold temperature and sensitivity as the slope response of variables to a given change in tympanic temperature. HDBR increased the threshold temperature for sweating by 0.31 degrees C at the chest and 0.32 degrees C at the forearm, whereas it reduced sensitivity by 40% at the chest and 31% at the forearm. HDBR increased the threshold temperature for cutaneous vasodilation, whereas it decreased sensitivity. HDBR reduced plasma volume by 11%, whereas it did not change plasma osmolarity. The increase in the threshold temperature for sweating correlated with that for cutaneous vasodilation. In conclusion, HDBR attenuated thermoregulatory sweating and cutaneous vasodilation by increasing the threshold temperature and decreasing sensitivity. HDBR increased the threshold temperature for sweating and cutaneous vasodilation by similar magnitudes, whereas it decreased their sensitivity by different magnitudes.     

Are non-thermal factors important in the cutaneous vascular response to exercise? A proponent's view.

Direct forearm blood flow measurements showed that the threshold for vasodilation is shifted to a higher core temperature and that the slope describing the relationship between skin blood flow and core temperature is reduced during submaximum exercise in comparison with supine resting conditions. These changes in skin blood flow characteristics have been shown to be proportionately related to work load in at least one study, but not in others. With heavy exercise, indirect evidence was obtained for the elicitation of vasoconstriction after body core temperature had attained a level of 39 degrees C; this caused a dramatic rise of T core to above 40 degrees C. In other studies, such terminal vasoconstriction was not observed; the subjects stopped exercising (75 percent VO2 max), independently of its duration, when rectal temperature had reached about 39 degrees C. Such inconsistent results in regard to the importance of extrathermal control of skin blood flow may be traced to variations in the motivational and emotional state; moreover, a phenomenon described as "short-term adaptation" may be responsible for some discrepant results. In conclusion, there is evidence for the concept that blood pressure control by peripheral vasoconstriction may have, under certain circumstances, preference over the demands of temperature regulation.