Interactions between local and reflex influences on human forearm skin blood flow.

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.     

Angiotensin II-induced hypothermia in rats

Systemic administration of angiotensin II (ANG II) (200 micrograms/kg sc) to the rat induced a hypothermic response that was characterized within 12 min by a reduction in the rate of O2 consumption, vasodilation of the tail, and a 1.3 degrees C fall in colonic temperature. Administration of ANG II in doses ranging from 10 to 200 micrograms/kg resulted in a decrease in colonic and an increase in tail skin temperature. Angiotensin I (ANG I) (200 micrograms/kg sc) induced a similar hypothermic response which was abolished by pretreatment with the ANG I-converting enzyme inhibitor, captopril (35 mg/kg ip). The interaction of ANG II with cholinergic and adrenergic pathways was evaluated to determine possible mechanisms. Treatment with ANG II (200 micrograms/kg sc) and propranolol, a beta-adrenoceptor antagonist (6 mg/kg ip), resulted in a greater depression of colonic temperature (Tco) than was observed with ANG II alone but did not affect the increase in tail skin temperature (Tsk) accompanying administration of ANG II. When ANG II was administered in combination with the beta-adrenergic agonist, isoproterenol (50 micrograms/kg ip), Tco remained at control levels, whereas an enhancement of the ANG II-induced increase in Tsk occurred. Administration of ANG II in combination with atropine sulfate (6 mg/kg ip), a muscarinic receptor antagonist which crosses the blood-brain barrier, significantly reduced the extent of the fall in Tco without affecting the increase in Tsk. The combined treatment of ANG II and the quaternary analogue, atropine methyl nitrate (3.25 mg/kg ip), which does not cross the blood-brain barrier, failed to affect the hypothermic responses to ANG II. These results suggest that the hypothermic responses to ANG II may be mediated through a central cholinergic pathway and possibly influenced by an adrenergic component. The inability of both adrenergic and cholinergic blockers to affect the vasodilatory response of the tail of the rat to administration of ANG II suggests that the mechanisms subserving heat production can be blocked independently of those subserving heat loss.     

Effect of high local temperature on reflex cutaneous vasodilation

We examined the effect of high local forearm skin temperature (Tloc) on reflex cutaneous vasodilator responses to elevated whole-body skin (Tsk) and internal temperatures. One forearm was locally warmed to 42 degrees C while the other was left at ambient conditions to determine if a high Tloc could attenuate or abolish reflex vasodilation. Forearm blood flow (FBF) was monitored in both arms, increases being indicative of increases in skin blood flow (SkBF). In one protocol, Tsk was raised to 39-40 degrees C 30 min after Tloc in one arm had been raised to 42 degrees C. In a second protocol, Tsk and Tloc were elevated simultaneously. In protocol 1, the locally warmed arm showed little or no change in blood flow in response to increasing Tsk and esophageal temperature (average rise = 0.76 +/- 1.18 ml X 100 ml-1 X min-1), whereas FBF in the normothermic arm rose by an average of 8.84 +/- 3.85 ml X 100 ml-1 X min-1. In protocol 2, FBF in the normothermic arm converged with that in the warmed arm in three of four cases but did not surpass it. We conclude that local warming to 42 degrees C for 35-55 min prevents reflex forearm cutaneous vasodilator responses to whole-body heat stress. The data strongly suggest that this attenuation is via reduction or abolition of basal tone in the cutaneous arteriolar smooth muscle and that at a Tloc of 42 degrees C a maximum forearm SkBF has been achieved. Implicit in this conclusion is that local warming has been applied for a duration sufficient to achieve a plateau in FBF.     

Thermoregulatory control of finger blood flow.

Three men exercised on a bicycle ergometer at 30, 50, asd 70 per cent of maximal aerobic power in ambient temperatures of 15, 25, and 35 degrees C with water vapor pressure less than 18 Torr. Exercies was used to vary internal temperature during as experiment, and different ambient temperatures were used to vary skin temperatures independently of internal temperature. Finger temperature was fixed at about 35.7 degrees C. Espohageal temperature (Tes) was measured with a thermocouple at the level of the left atrium, and mean skin temperature (Tsk) was calcualted from a weighted mean of thermocouple temperatures at eight skin sites. Finger blood flow (BF) was measured by electrocapacitance plethysmography. Although some subjects showed small and equivocal vasomotor effects of exercise, our data are well accounted for by an equation of the form BF equal to alTes + a2Tsk + b, independent of exercise intensity. For these subjects, the ratios a1/a2 (5.9, 8.6, 9.4) were similar to the ratios of the corresponding coefficients recently reported for thermaoregulatory sweating (8.6, 10.4) and for forearm blood flow (9.6).     

Local thermal sensation and finger vasoconstriction in the locally heated hand

The effects of local heating on finger blood flow (BF) and local thermal sensation (Sensw) were studied. Finger BFs in both hands were measured simultaneously; one hand was immersed in water the temperature (Tw) of which was raised from 35 degrees C to 43 degrees C by steps of 2 degrees C every 10 min, while the other hand was kept at Tw 35 degrees C. Finger BF in the locally heated hand decreased at Tw 37 to 41 degrees C, while finger BF in the control hand did not alter. Sensw in the heated hand showed a dynamic response, initially increasing concomitantly with an increase in Tw, then gradually returning and adapting to a new level of Sensw. The dynamic response of Sensw was not perceived during mental calculation even when Tw was raised to 40 degrees C, and the reduction in finger blood flow was not observed. These results suggest that finger vasoconstriction caused by local heating closely relates to the dynamic response characteristic of local thermal sensation at Tw above core temperature, and that the perception of local thermal sensation in the central nervous system is involved in the mechanism of this vasoconstrictor response.     

Core threshold temperatures for sweating

To detect shifts in the threshold core temperature (Tc) for sweating caused by particular nonthermal stresses, it is necessary to stabilize or standardize all other environmental and physiological variables which cause such shifts. It is, however, difficult to cause progressive changes in Tc without also causing changes in skin temperature (Tsk). This study compares the technique of body warming by immersion in water at 40 degrees C, and subsequent body cooling in water at 28 degrees C, to determine the core threshold for sweating, with one by which Tc was raised by cycling exercise in air at 20 degrees C, and then lowered by immersion in water at 28 degrees C. The first of these procedures involved considerable shifts in Tsk upon immersion in water at 40 degrees C, and again upon transfer to water at 28 degrees C; the second procedure caused only small changes in Tsk. The onset of sweating at a lower esophageal temperature (Tes) during immersion in water at 40 degrees C (36.9 +/- 0.1 degrees C) than during exercise (37.4 +/- 0.3 degree C) is attributed to the high Tsk since Tes was then unchanged. Likewise, the rapid decline in the sweat rate during immersion at 28 degrees C had the same time course to extinction after the pretreatments. This related more to the Tsk, which was common, than to the levels or rates of change of Tes, which both differed between techniques. Tes fell most rapidly, and thus sweating was extinguished at a lower Tes, following 40 degrees C immersion than following exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of beta-adrenergic blockade on the control of sweating in humans

To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.     

Sympathoadrenal responses to cold and ketamine anesthesia in the rhesus monkey

The effect of cold exposure on the sympathoadrenal system in primates was studied with and without ketamine anesthesia in eight adult rhesus monkeys. Each monkey was placed in a primate chair at a thermoneutral temperature (25 degrees C) for 1 h (control) followed by cold exposure (12 degrees C) for 3 h or placed in a circulating water bath (28 degrees C) to induce a decrease in core temperature (Tre) to 35 and 33 degrees C. Plasma catecholamines were analyzed by high-pressure liquid chromatography with electrochemical detection (60-65% recovery, coefficient of variation = 15%). The 3-h cold exposure was associated with a 175% increase above control levels of norepinephrine (NE) and a 100% increase in epinephrine (E). Decreases were evident in Tre (0.5 degree C), mean skin temperature (Tsk, 5.5 degrees C), and mean body temperature (Tb, 2.0 degrees C). Continuous infusion of ketamine (0.65 mg . kg-1 . min-1) resulted in no change in the plasma levels of NE and E from the control levels. Tre, Tsk, and Tb all showed greater declines with the addition of ketamine infusion to the cold exposure. Water exposure (28 degrees C) under ketamine anesthesia resulted in a drop in Tre to 33 degrees C within 1 h. Plasma levels of NE and E were unchanged from control values at Tre of 35 and 33 degrees C. The data suggest that the administration of ketamine abolished both the thermoregulatory response and the catecholamine response to acute cold exposure.     

Temperature and sweating responses in one-legged and two-legged exercise.

In looking at the thermoregulatory responses resulting from symmetrical or asymmetrical exercise, this paper has focused on the effect of local skin temperature (Tsk,local) on local sweat rates (msw,local) during one-legged (W1) and two-legged (W2) exercise on an ergocycle. Five subjects underwent four 3-h tests at 36 degrees C, each consisting of six 25-min exercise periods alternating with 5-min rest periods. The subjects performed W1 and W2 at 45 and 90 W, respectively, either dehydrated or rehydrated. Body temperatures and total sweat rate were measured as well as four msw,local (on chest and thighs), assessed from sweat capsules under which Tsk,local was maintained at predetermined levels (37.0 degrees C and 35.5 degrees C). The combinations of Tsk,local levels, capsule locations, exercise intensity and hydration level chosen in our protocol led to the following results. The hydration level affected rectal temperature but not total or msw,local. No specific effect of muscle activity was found; msw,local on thighs of resting and working legs were similar. The msw,local were only influenced by exercise intensity, msw,local being more elevated during the higher intensity. No significant effect of Tsk,local on msw,local was found, whatever the experimental condition and/or the location. It was concluded that local thermal effects on msw,local could have been masked by the strong central drive for sweating which has been found to exist in subjects exercising in a warm environment.     

Effect of nerve block on response of forearm blood flow to local temperature

To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27-29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.     

Heat vasodilatation of the rat tail.

The vasomotor response of the tail of the albino rat to total-body heating and cooling was studied by skin-temperature recording and plethysmography with the tail at 25 degrees C air temperature. Tail vasodilation started at core temperatures lightly above 37 degrees C and increased to a core temperature up to about 39 degrees C. During cooling of warm rats, tail vasoconstriction started at significantly higher levels of core temperature than the values at which vasodilation appeared when the rat was warmed.     

Effects of varied air velocity on sweating and evaporative rates during exercise.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Factors producing elevated core temperature in spontaneously hypertensive rats

Core temperature (Tco) of the spontaneously hypertensive rat (SHR) is consistently higher by approximately 1 degree C than that of normotensive controls. To analyze factors producing the elevated Tco, mean skin temperature (Tsk), metabolic heat production (M), respiratory evaporative heat loss (Eres), effective tissue thermal conductance (K), systolic blood pressure (BP), and Tco were determined in eight male SHR and nine male normotensive Wistar-Kyoto (WKY) rats habituated to rest quietly in neck stock restraint while exposed to ambient temperatures (Ta) of 12.5, 17, 23, 28.5, 32, 34, and 35 degrees C. At all temperatures steady-state BP, Tco, and M were higher for SHR's than for WKY's. SHR's could maintain thermal balance up to Ta 32 degrees C, and WKY's up to 34 degrees C. Eres from SHR's was greater than from WKY's at Ta of 12.5, 17, and 28.5 degrees C. K of SHR's was not different from or was higher than K of WKY's, and K for both groups was 2.6 times greater at Ta 32 degrees C than at 17 degrees C. These results indicate that the high Tco of SHR's is due to increased M uncompensated by increased K or Eres.     

Effects of D-4F on vasodilation, oxidative stress, angiostatin, myocardial inflammation, and angiogenic potential in tight-skin mice

Systemic sclerosis (scleroderma, SSc) is an autoimmune, connective tissue disorder that is characterized by impaired vascular function, increased oxidative stress, inflammation of internal organs, and impaired angiogenesis. Tight skin mice (Tsk(-/+)) have a defect in fibrillin-1, resulting in replication of many of the myocardial and vascular features seen in humans with SSc. D-4F is an apolipoprotein A-I (apoA-I) mimetic that improves vascular function in diverse diseases such as hypercholesterolemia, influenza, and sickle cell disease. Tsk(-/+) mice were treated with either phosphate-buffered saline (PBS) or D-4F (1 mg.kg(-1).day(-1) for 6-8 wk). Acetylcholine and flow-induced vasodilation were examined in facialis arteries. Proinflammatory HDL (p-HDL) in murine and human plasma samples was determined by the cell-free assay. Angiostatin levels in murine and human plasma samples were determined by Western blot analysis. Hearts were examined for changes in angiostatin and autoantibodies against oxidized phosphotidylcholine (ox-PC). Angiogenic potential in thin sections of murine hearts was assessed by an in vitro vascular endothelial growth factor (VEGF)-induced endothelial cell (EC) tube formation assay. D-4F improved endothelium-, endothelial nitric oxide synthase-dependent, and flow-mediated vasodilation in Tsk(-/+) mice. Tsk(-/+) mice had higher plasma p-HDL and angiostatin levels than C57BL/6 mice, as did SSc patients compared with healthy control subjects. Tsk(-/+) mice also had higher triglycerides than C57BL/6 mice. D-4F reduced p-HDL, angiostatin, and triglycerides in the plasma of Tsk(-/+) mice. Tsk(-/+) hearts contained notably higher levels of angiostatin and autoantibodies against ox-PC than those of control hearts. D-4F ablated angiostatin in Tsk(-/+) hearts and reduced autoantibodies against ox-PC by >50% when compared with hearts from untreated Tsk(-/+) mice. Angiogenic potential in Tsk(-/+) hearts was increased only when the Tsk(-/+) mice were treated with D-4F (1 mg.kg(-1).day(-1), 6-8 wk), and cultured sections of hearts from the D-4F-treated Tsk(-/+) mice were incubated with D-4F (10 microg/ml, 5-7 days). Failure to treat the thin sections of hearts and Tsk(-/+) mice with D-4F resulted in loss of VEGF-induced EC tube formation. D-4F improves vascular function, decreases myocardial inflammation, and restores angiogenic potential in the hearts of Tsk(-/+) mice. As SSc patients have increased plasma p-HDL and angiostatin levels similar to the Tsk(-/+) mice, D-4F may be effective at treating vascular complications in patients with SSc.     

Metabolic and vasomotor insulative responses occurring on immersion in cold water

Twenty male volunteers (17-28 yr of age) exhibiting a range of body weights (60 kg less than or equal to Wt less than or equal to 95 kg) and body fat (7% less than or equal to BF less than or equal to 23%) underwent total immersion while at rest in water between 36 and 20 degrees C. The metabolic heat production measured as a function of time and water temperature was converted to explicit linear functions of core (Tre) and mean skin (Tsk) temperature for each individual immersion. The metabolic functions defined planes of thermogenic activity that showed a fourfold steeper slope with respect to changes in Tsk for small lean subjects than for large fatter subjects. Small lean males also exhibited steeper slopes with respect to changes in Tre than heavier phenotypes. The time course of Tsk and Tre was simulated for each individual immersion with the aid of a time-dependent system of differential heat balance equations coupling different body compartments to the water bath. This formulation permitted the evaluation of internal and external conductances as a function of water temperature. Maximal internal insulation, indicating full vasoconstriction, was achieved at higher bath temperatures in small lean subjects than large fatter subjects. A decline in insulation is seen above a critical metabolic level (approximately 150 W) in small to average size subjects.     

Muscle blood flow is not reduced in humans during moderate exercise and heat stress

The effect of heat stress on circulation in an exercising leg was determined using one-legged knee extension and two-legged bicycle exercise, both seated and upright. Subjects exercised for three successive 25-min periods wearing a water-perfused suit: control [CT, mean skin temperature (Tsk) = 35 degrees C], hot (H, Tsk = 38 degrees C), and cold (C, Tsk = 31 degrees C). During the heating period, esophageal temperature increased to a maximum of 37.91, 39.35, and 39.05 degrees C in the three types of exercise, respectively. There were no significant changes in pulmonary O2 uptake (VO2) throughout the entire exercise period with either one or two legs. Leg blood flow (LBF), measured in the femoral vein of one leg by thermodilution, remained unchanged between CT, H, and C periods. Venous plasma lactate concentration gradually declined over time, and no trend for an increased lactate release during the heating period was found. Similarly, femoral arteriovenous O2 difference and leg VO2 remained unchanged between the three exercise periods. Although cardiac output (acetylene rebreathing) was not significantly higher during H, there was a tendency for an increase of 1 and 2 l/min in one- and two-legged exercise, respectively, which could account for part of the increase in total skin blood flow during heating (gauged by changes in forearm blood flow). Because LBF was not reduced during exercise and heat stress in these experiments, the additional increase in skin blood flow must have been met by redistribution of blood away from vascular beds other than active skeletal muscle.     

Comparative thermoregulatory response to passive heat loading by exposure to radiofrequency radiation

1. Colonic and tail skin temperature of the unrestrained Fischer rat were measured immediately after a 90 min exposure to 600 MHz radiofrequency radiation in a waveguide-type system. Ambient temperature (Ta) was maintained at either 20, 28 or 35 degrees C. The specific absorption rate (SAR) in dimensions of W/kg was controlled at a constant level through a feedback control circuit. 2. The SAR needed to elevate colonic and tail skin temperature decreased with increasing Ta. For example, a 0.5 degrees C elevation in colonic temperature occurred at SARs of 4.3, 0.9 and 0.5 W/kg when Ta was maintained at 20, 28 and 35 degrees C, respectively. 3. Data from the present study were combined with data from earlier studies to assess the impact of varying Ta on the thermogenic effect of RF radiation in different species. In species ranging in mass from 0.02 to 3.2 kg, a double logarithmic plot of body mass versus SAR needed to elevate colonic temperature by 0.5 degrees C was linear and inverse with a high goodness of fit (r2 = -0.94). 4. The highly correlated allometric relationship shows that, as body mass decreases, the relative impact of Ta on the thermogenic effect of RF radiation increases.     

Influence of body temperature on histamine-induced bronchoconstriction in guinea pigs

The effects of body temperature on histamine-induced bronchoconstriction were investigated in anesthetized, paralyzed, and mechanically ventilated guinea pigs. Four groups of guinea pigs were studied with constant body temperatures of 40, 38, 35, and 32 degrees C, respectively. Histamine was infused for 5 min at a rate of 50 ng.kg-1.s-1. Body cooling from 40 to 32 degrees C augmented the bronchomotor responses to histamine, which eventually rose almost fourfold. The enhancement of histamine-induced bronchoconstriction induced by body cooling was not suppressed by pretreating guinea pigs with 5 mg/kg hexamethonium or 5 mg/kg hexamethonium plus 3 mg/kg atropine; neither was the enhancement of histamine-induced bronchoconstriction suppressed in pithed guinea pigs, demonstrating that the autonomic nervous system is not involved in potentiating bronchoconstriction at low body temperatures. These results suggest that, at low body temperatures, increased airway responsiveness to histamine may be because of some direct effect of temperature on bronchial airway smooth muscle.     

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.     

Control of local heat gain by vasomotor response of the hand

Finger blood flow (BF) was measured by venous occlusion plethysmography using mercury-in-Silastic strain gauges during immersion of one hand in hot water (raised by steps of 2 degrees C every 10 min from 35 to 43 degrees C), the other being a control (kept immersed in water at 35 degrees C). The measurements were made in three different thermal states on separate days: 1) cool-25 degrees C, 40% rh, esophageal temperature (Tes) = 36.64 +/- 0.10 degrees C; 2) warm-35 degrees C, 40% rh, Tes = 36.71 +/- 0.11 degrees C; and 3) hot-35 degrees C, 80% rh with the legs immersed in water at 42 degrees C, Tes = 37.26 +/- 0.11 degrees C. When water temperature was raised at 42 degrees C, Tes = 37.26 +/- 0.11 When water temperature was raised to 39-41 degrees C in the warm state, finger BF in the hand heated locally (BFw) decreased. When water temperature was raised to 43 degrees C, however, BFw returned to the control value. In the hot state, Tes rose steadily, reaching 37.90 +/- 0.12 degrees C at the end of the 50-min sessions. BF in the control finger also increased gradually during the session. BFw showed a tendency to decrease when water temperature was raised to 39 degrees C, but the change was not greater than that observed in the warm state. In the cool state, no such reduction in BFw was observed when water temperature was raised to 39-41 degrees C. On the contrary, BFw increased at water temperatures of 41-43 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)