Reduced Skin Blood Flow Research Articles

Cutaneous blood flow and peripheral resistance in type II diabetes as compared to intermittent claudication patients

Insulin deficient, type I diabetic patients have reduced skin blood flow reserve. It is not known whether these skin perfusion abnormalities also exist in non-insulin dependent (type II) diabetic patients. An additional open question is whether the reduced skin blood flow is due to increased resistance of the cutaneous microvasculature or to decreased peripheral perfusion pressure due to increased atherosclerosis in the diabetic population. We measured skin blood flow by laser Doppler flowmetry in patients with type II non-insulin treated diabetes. Limb systolic blood pressure was measured distally using a sensitive sonar Doppler device at the finger and toe. The ratio of pressure to flow was computed as an index of peripheral blood flow resistance. To assess the effect of cutaneous blood flow resistance, we elicited maximal vasodilation by increasing local skin temperature directly at the site of the laser Doppler probe. We compared blood flow and pressure in diabetic patients with the values in non-diabetic control patients. As a further control population, we also assessed these same parameters in non-diabetic patients with peripheral vascular disease, which may be expected to decrease large arterial blood flow pressure without directly affecting the microvasculature. There were 68 type II diabetic patients, 18 non-diabetic control subjects, and 25 non-diabetic patients with intermittent claudication. We measured skin blood flow at the dorsal surfaces of the finger and toe, sites with primarily nutritive capillary perfusion, and at the plantar surfaces of the finger and toe, where arteriovenous shunt perfusion predominates. Heat stimulated flow was markedly lower for the diabetic patients at the finger dorsal surface (16.5 ± 1.4 ml/min/100 g vs 29.8 ± 4.4 ml/min/100 g in the non-diabetic group (p < 0.05). The resistance index was 13.2 ± 1.9 in the diabetic patients and 6.8 ± 1.7 in the controls (p < 0.05). At the toe dorsum, basal temperature flow was significantly lower in the diabetic group (0.6 ± 0.1 ml/min/100 g) than in the non diabetic group (1.1 ± 0.2 ml/min/100 gm) with resistance index almost twice as high (379 ± 32) in the diabetic group versus non-diabetic controls (208 ± 36) [p < 0.01 for both comparisons]. With the local application of heat, there was a much larger increase in flow in the non-diabetic subjects than in the diabetic group. The resistance index dropped much more with heat stimulation for the non-diabetic patients (10.8 ± 3.3) than for the diabetic patients (50.6 ± 10.4) [p < 0.01] There was a lesser rise in flow at the toe pulp surface with heat in the diabetic patients (31.3 ± 3.0 ml/min/199 gm) than in the control subjects (45.4 ± 5.9 ml/min/100 gm; p < 0.05) with a higher resistance index (13 ± 4) than in the non-diabetic subjects (4 ± 1) [p < 0.05]. The claudication patients had substantially greater flow at the toe dorsal surface at basal temperature (2.2 ± 0.4 ml/min/100 gm) with significantly lower resistance index (126 ± 24) than the non-diabetic controls (p < 0.05). At 44°C, toe dorsum flow was significantly higher (17.8 ± 3.7 ml/min/100 gm) than in the diabetic patients with lower resistance index (17.0 ± 6.6) [p < 0.05]. Toe pulp flow at basal temperature was significantly higher (10.1 ± 2.0 ml/min/100 gm) than in either the diabetic (3.8 ± 0.6) or non-diabetic control groups (3.5 ± 1.4) [p < 0.05]. Skin blood flow is impaired in diabetes. The reduction is due to increased resistance in the capillary bed rather than to reduced perfusion pressure. The increased resistance was found only in the diabetic patients, not in the non-diabetic patients with peripheral vascular disease. To the contrary, there appeared to be a compensatory decrease in skin flow resistance in the patients with peripheral vascular disease. Thus, there is a small vessel disease which impairs cutaneous perfusion in diabetes, but there is no such effect on skin blood flow in non-diabetic patients with large vessel disease.

Using intradermal electrical stimulation to evaluate neurogenic control of skin blood flow

Intradermal microdialysis and laser Doppler velocimetry were combined to evaluate neurogenic control of vasomotor activity of human skin blood vessels during non-painful intradermal electrical stimulation (E-stim). The laser Doppler flow probe was mounted directly over the microdialysis probe and the stimulating electrodes penetrated the skin 2 mm with the electrode tips separated by ≈ 4 mm. E-stim consisted of a constant current (1.8 ± 0.2 mA) pulses delivered at increasing frequency (0.2, 1, 2, 4, 8, and 32 Hz) in one minute steps. Stimulus- response curves of frequency versus skin blood flow (SkBF) were constructed and the area under the SkBF-time response curve was calculated. During saline perfusion increasing stimulus frequencies cause progressively greater reductions in SkBF with significant declines from baseline observed at frequencies of ≥2 Hz (p<0.05). The peak reduction in SkBF at 32 Hz was represented by an AUC of −2566 ± 854 SkBF·sec. In contrast, following adrenergic blockade (phentolamine (0.05 mg/ml), propranolol (1 mM), and BIBP-3226 (10 μM) SkBF failed to decline below baseline and the AUC at 32 Hz averaged only −342 ± 540 SkBF·sec (p<0.05). These data support the hypothesis that non-painful E-stim protocol provided a significant activation of the local sympathetic vasoconstrictor nerves and may provide a novel approach to investigating active cutaneous vasodilation.

Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans

Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34°C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ~1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.

A STUDY OF THE FEASIBILITY OF L NAME IONTOPHORESIS: EFFECTS OF L NAME CONCENTRATION AND SMOKING: PP.6.224

Introduction: Early detection of endothelial dysfunction, characterized by a reduced bioavailability of NO, is essential as it is a key phenomenon in the genesis of cardiovascular diseases. Heat-induced vasodilatation is mediated mainly by NO, as shown by L Name (L) microdialysis. L Name is a competitive inhibitor of cNOS, produced by the vascular endothelium, and is polarized negatively. The application of a microcurrent on the skin allows polarized molecules, such as sodium nitroprusside and acetylcholine, to penetrate into the dermis. Whether L Name iontophoresis is feasible, and will reduce skin blood flow measured by a laser Doppler imager (LDI) in response to heating, is not known. We also assessed whether this response is dose-dependent. Last, we compared this response between habitual smokers and non smokers. Methods: In a population of 17 healthy male smokers and 17 matched healthy male non-smokers (aged 28 years ± 5 yrs, BMI 22 ± 3 kg/m2), we conducted an iontophoresis of L Name and placebo on the two arms on Day 0. This was repeated with the same dose, and a double dose of L, on Day 4, on both arms. After iontophoresis, the sites were heated to 44°C to induce vasodilation, and scanned to measure blood flow in the microcirculation. We also determined pulse wave velocity in both groups. Smoking was forbidden 12 hours before the experiments. Results: L Name decreased equally blood flow during heating in the non smokers and smokers (p < 0.01, table 1). Both concentrations of 20 and 40 mM of L Name were equally effective. Pulse wave velocity was normal at 9 m/s, and did not differ between groups.Conclusion: L Name iontophoresis is feasible and is able to inhibit vascular endothelial NOS. Higher concentrations of L Name than 20 mM do not provide further vasodilatation. NO-mediated skin blood flow vasodilatation is not altered in healthy young sportive smokers investigated after 12 hours of smoking cessation.

Galvanic Skin Resistance—A Marker for Endothelial Damage in Diabetes

Aging and diabetes are both associated with impaired vascular endothelial function. This causes a reduction in the resting blood flow and the blood flow response to autonomic stressors. Further, skin moisture and the ability to sweat are also reduced with aging and diabetes. The present investigation was undertaken to determine if the extent of damage from aging and diabetes could be accurately assessed by simply examining the electrodermal skin response (galvanic skin resistance) to a thermal stress. Forty-five subjects whose average age was 31.2 +/- 8.3 years (younger group), 62.4 +/- 9.6 years (older group), and 61.8 +/- 11.3 years (diabetes group) were divided into three groups of 15 subjects. Subjects were exposed to environmental temperatures of 15 degrees C, 23 degrees C, or 32 degrees C for 30 min. During this period of time, sweat rate, skin blood flow, the electrodermal skin response, and skin moisture were measured. There were significant impairments in skin moisture, sweat, skin blood flow, and the galvanic skin response at any of the three environmental temperatures in subjects with diabetes compared to older subjects compared to younger subjects (analysis of variance, P < 0.01). Both a reduction in skin blood flow and impaired sweating contributed to the higher galvanic skin resistance seen in subjects with diabetes. The greatest contributor was impaired sweating. The results show that galvanic skin resistance, at any environmental temperature, may be a good means of assessing vascular damage and impaired sweat response in people with diabetes.

Differential involvement of .ALPHA.1-adrenoceptors in vasoconstrictor responses to cooling in mouse plantar arteries in vitro and in vivo

Cooling-induced reduction of skin blood flow results from a reflex increase in sympathetic output and an enhanced vasoconstrictor activity of skin vessels. The latter has been proposed to be mediated by increased reactivity of alpha(2C)-adrenoceptors during cooling in studies with isolated cutaneous vessels in vitro. We have previously shown in studies with tetrodotoxin-treated mice in vivo that reduction of plantar skin blood flow (PSBF) induced by local cooling results primarily from increased reactivity of alpha(2C)-adrenoceptors. In addition, we showed that part of the cooling-induced response was also mediated by alpha(1)-adrenoceptors. However, the mechanisms involved in the cooling-induced responses mediated by alpha(1)-adrenoceptors have not been elucidated. The present study is an investigation seeking to clarify the mechanisms involving alpha(1)-adrenoceptors. Medial plantar arteries were isolated from male ddY mice and changes in vessel diameter were measured in vitro using pressurized arteriography. In vivo measurements of PSBF were performed on artificially ventilated tetrodotoxin treated mice, anaesthetized with pentobarbital sodium, using laser Doppler flowmetry, with the probe positioned above the medial plantar artery. In the in vitro studies with isolated plantar arteries, cooling from 37 to 28 degrees C did not affect the constrictor potency of phenylephrine, an alpha(1)-adrenoceptor agonist, and the threshold concentration to evoke constriction was rather higher at 28 degrees C than it was at 37 degrees C. The cooling also suppressed the constrictor efficacy of UK14,304, an alpha(2)-adrenoceptor agonist. In contrast, cooling the air temperature around the foot from 25 to 10 degrees C in vivo decreased PSBF, which was significantly inhibited by phentolamine, an alpha-adrenoceptor antagonist, although MK-912, an alpha(2C)-adrenoceptor antagonist, had no effect on it. These results suggest that although alpha(1)-adrenoceptors are involved in cooling-induced reduction of PSBF in mice, the response is unlikely to result from an enhancement of alpha(1)-adrenoceptor-mediated vasoconstriction of plantar arteries during cooling.

Preliminary Measurement of Intraoperative Sympathetic Nerve Activity Using Microneurography and Laser Doppler Flowmetry During Surgical Resection of Suprasellar Tumors

Intraoperative microneurography (enabling direct measurement of sympathetic outflow) and laser Doppler flowmetry were used to measure skin sympathetic nerve activity (SSNA) and skin blood flow (SBF) as indicators of hypothalamic damage during resection of 12 suprasellar tumors, 6 craniopharyngiomas, 4 meningiomas, 1 pituitary adenoma, and 1 germ cell tumor. SSNA was measured from a tungsten microelectrode inserted into the peroneal nerve, and SBF was measured from the foot innervated by the peroneal nerve. SBF reduction was induced by nociceptive procedures and non-nociceptive procedures before tumor exposure, on exposed tumors, and directly on the hypothalamus. SSNA could be reliably recorded in only 4 patients because of technical difficulties. In these patients, SSNA bursts appeared, followed by SBF reduction. The number of SSNA bursts was 37% to 100% of the number of SBF reduction events. Various surgical procedures involving painful stimuli or mechanical stress on the hypothalamus induced SSNA bursts and SBF reduction. The present findings suggest that SSNA and SBF can be used to detect sympathetic nerve activity, as an indicator of hypothalamic function, during neurosurgical procedures.

Differences in skin sympathetic involvements between two chronic autonomic disorders: Multiple system atrophy and pure autonomic failure

Objective Certain stimuli evoke increased sweat secretion (sympathetic sweat response; SSwR) and reduced skin blood flow (skin vasomotor reflex; SkVR) in the palm/sole. We evaluated SSwR and SkVR in patients with multiple system atrophy (MSA) and pure autonomic failure (PAF). Methods SSwR and SkVR on the palm in response to deep inspiration and mental arithmetic were recorded in 11 MSA patients, 11 PAF patients, and 11 healthy controls. In addition, the head-up tilt test was performed, and the coefficient of variation of R–R intervals (CV R–R) was obtained. Results SSwR amplitudes were significantly lower in the MSA and PAF patients than the controls. SkVR amplitudes in the PAF patients were significantly lower than the controls, but preserved in the MSA patients. In head-up tilt tests, all MSA and PAF patients showed orthostatic hypotension, with similar severity. CV R–R was low in the MSA and PAF patients, but a significant difference was found only between the PAF and control groups. Conclusion In the MSA patients, SkVR was preserved, but SSwR was diminished. In the PAF patients, both SkVR and SSwR were attenuated. The combination of SkVR and SSwR tests may differentiate MSA and PAF.

Sweating Responsiveness to Reduced Skin Blood Flow During Passive Heat Stress

PURPOSE: Test the hypothesis that reduced SkBF, independent of local temperature, attenuates sweating during whole-body passive heat stress. METHODS: Nine subjects underwent a passive heat stress (i.e., Δ internal temperature ~0.6 °C). Sweat rate and SkBF were continuously measured over two intradermal microdialysis probes. One site received Ringer's solution (CONTROL), while an adjacent site received norepinephrine (NE) to reduce SkBF throughout the heat stress. Sweat rate was normalized to peak responses obtained via local administration of methacholine after the heat stress. SkBF was expressed as cutaneous vascular conductance (CVC; SkBF/mean arterial pressure) and normalized to maximum CVC obtained via administration of sodium nitroprusside. RESULTS: Heat stress increased internal temperature (0.6 ± 0.1 °C, P<0.001) and mean body temperature (Tb) (1.1 ± 0.1 °C, P<0.001). The onset of sweating for CONTROL and NE sites occurred at a similar Δ Tb (0.67 ± 0.1 °C and 0.68 ± 0.2 °C; respectively, P=0.36), while at this time CVC was lower at the NE site (25.7 ± 5.4 %max CVC and 8.1 ± 1.5 %max CVC; P<0.01). At the end of the heat stress, CVC remained lower at the NE site (CONTROL: 62.6 ± 5.8 %max CVC; NE: 12.3 ± 1.5 %max CVC (P<0.001). Likewise sweat rate was also lower at the NE site when expressed as absolute sweat rate (0.7 ± 0.2 mg·cm−2·min−1 versus 0.44 ± 0.2 mg·cm−2·min−1; P=0.03), or relative sweat rate (60.1 ± 8.1%max versus 36.9 ± 7.3%max; P=0.004). During methacholine administration, CVC (CONTROL: 89.6 ± 33.3 %max CVC; NE: 93.1 ± 27.2 %max CVC; P=0.36) and sweat rate (CONTROL: 1.1±0.1 mg·cm−2·min−1; NE: 1.0±0.2 mg·cm−2·min−1; P=0.38) were not different. CONCLUSIONS: These results indicate that reduced SkBF affects the magnitude but not the onset of sweating during passive whole-body heating. This finding suggests that at least a component of the reduction in sweat rate during local cooling could be related to reduced SkBF. Supported by NIH Grant HL61388 and HL84072

Measurements of sweat response and skin vasomotor reflex for assessment of autonomic dysfunction in patients with diabetes

Aims Some physical or arousal stimuli induce a rise in sweat secretion (sympathetic sweat response or SSwR) and a reduction in skin blood flow (skin vasomotor reflex or SkVR) to the palm. We recorded SSwRs and SkVRs in diabetic patients and assessed the usefulness of these parameters for evaluating autonomic dysfunction in diabetes. Methods We studied 42 diabetic patients (58±12 years) and 42 normal control subjects (59±11 years). Focal sweat secretion and skin blood flow were measured on the palm by a sudorometer and a Doppler flowmeter, respectively. SSwRs and SkVRs to deep inspiration, mental arithmetic, and isotonic exercise were recorded. SSwR amplitude was measured from baseline to peak, and SkVR amplitude (reduction rate) was calculated as: (blood flow reduction/basal blood flow)×100%. We also conducted head-up tilt tests and R–R interval variation tests (coefficient of variation of R–R intervals or CV R–R). Results The SSwR or SkVR amplitudes in the diabetic group were significantly lower than those in the control group for any stimulus. CV R–R in the diabetic group was significantly less than that in the control group. The diabetic group showed a significantly greater reduction in systolic blood pressure during head-up tilt compared with the control group. In the diabetic group, there were significant correlations in SSwR or SkVR amplitudes versus blood pressure falls during the head-up tilt test, and CV R–R values. Conclusion We believe that SSwR and SkVR are useful indexes for the evaluation of autonomic involvement in diabetic patients.

Skin Blood Flow and Its Oscillatory Components in Patients with Acute Myocardial Infarction

Background/Aims: Laser Doppler flowmetry (LDF) was used to determine the influence of acute myocardial infarction (AMI) and of successful reperfusion treatment on basal skin blood flow and its oscillatory components. Methods: Skin LDF was performed on all extremities in 58 patients 4–9 days after AMI (Killip class I), and in 71 healthy age- and sex-matched controls. Wavelet analysis was applied to evaluate oscillatory components within the interval 0.005–2 Hz. Results: AMI patients had reduced mean flow (p < 0.01) and oscillatory components (p < 0.04) in all extremities. Reperfused (n = 40), compared to nonreperfused (n = 18), patients had higher mean flow and total spectral amplitude at all recording points. The difference was statistically significant only in legs (group median LDF in the left leg was 9.68 AU for reperfused and 5.71 AU for nonreperfused patients, p < 0.04, and 11.47 and 4.24 AU in the right leg, p < 0.01). Reperfused patients had significantly higher total spectral amplitude in both legs (p < 0.04). Conclusions: In AMI patients, reduced skin blood flow and its oscillatory components may reflect ongoing neurohumoral activation despite absence of clinically apparent heart failure. The reduction of blood flow and its oscillatory components was larger in nonreperfused AMI patients, although they had a comparable left ventricular function.

Role of α2C‐adrenoceptors in the reduction of skin blood flow induced by local cooling in mice

The reduction of skin blood flow induced by local cooling results from a reflex increase in sympathetic output and an enhanced vasoconstrictor activity of cutaneous vessels. The present study investigated the latter local response in vivo in tetrodotoxin-treated mice, in which the sympathetic nerve tone was abolished. Male ddY mice, anaesthetized with pentobarbitone, were treated with tetrodotoxin and artificially ventilated. The plantar skin blood flow (PSBF) was measured by laser Doppler flowmetry. Cooling the air temperature around the left foot from 25 to 10 degrees C decreased the PSBF of the left foot. Bunazosin, an alpha (1)-adrenoceptor antagonist, RS79948, an alpha (2)-adrenoceptor antagonist, and MK-912, an alpha (2C)-adrenoceptor antagonist, all significantly inhibited the cooling-induced reduction of PSBF; the inhibition by bunazosin was relatively small compared with that by RS79948 and MK-912. The response was not affected by guanethidine or bretylium, but was diminished in adrenalectomized mice. An intra-arterial injection of clonidine, an alpha (2)-adrenoceptor agonist, to the left iliac artery of adrenalectomized mice caused a transient decrease in PSBF, which was significantly augmented at 10 degrees C. MK-912 suppressed only the augmented portion at 10 degrees C. Y-27632, H-1152 and fasudil, Rho kinase inhibitors, also inhibited the cooling-induced reduction of PSBF. RS79948 caused no further reduction of the cooling-induced response after the inhibition by Y-27632. Local cooling-induced reduction of skin blood flow in mice primarily results from increased reactivity of alpha (2C)-adrenoceptors to circulating catecholamines, in which the Rho/Rho kinase pathway is involved.

The raphe magnus/pallidus regulates sweat secretion and skin vasodilation of the cat forepaw pad: A preliminary electrical stimulation study

In the human palm/sole, mental or physical stimuli induce an increase in sweat secretion and a decrease in skin blood flow (SkBF). However, the central pathways of these responses remain unclear. We measured sweat secretion and SkBF in the cat footpad by electrically stimulating the raphe. Stimulation of the rostral raphe magnus/pallidus elicited a reduction in SkBF without affecting sweat secretion. Stimulation of the mid to caudal raphe magnus/pallidus elicited an increase in both sweat secretion and SkBF. The raphe magnus/pallidus may play a crucial role in skin vasomotor and sudomotor responses in the cat footpad.

Vibration causes ischemia‐reperfusion injury in the rat‐tail artery

Hand-arm vibration syndrome is a vasospastic disease affecting workers using hand held powered-tools. In a rat-tail vibration model, 4 hr of 60 Hz vibration caused free radical production (nitration) in the ventral artery. To test if ischemia-reperfusion causes free radical production, tails of male Sprague-Dawley rats were vibrated 4 hr at 60 Hz, 49 m/s2acceleration. Blood perfusion to the tail skin was monitored with laser Doppler after 5 min, 1, 2 and 4 hr of vibration. Perfusion was significantly reduced to 62% by 5 min, 94% at 2 and 4 hr, and significantly increased to 122% at 3 hr of exposure. In other rats, tails were vibrated 5 min, 1, 2 or 4 hr at 60 Hz, 49 m/s2, and ventral arteries were processed for light microscopy. Compared to control, 100% of 5 min, 50% of 1 hr, 75% of 2 hr and 57% of 4 hr vibrated animals had smaller arterial lumens with morphological signs of endothelial and smooth muscle cell vacuolation damage. The vibration-induced transient reduction in skin blood flow, the morphological signs of vasoconstriction and the temporal pattern of vasoconstriction and dilation indicate that vibration immediately induces vasoconstriction which is followed by cycles of relaxation and constriction. This temporal pattern is consistent with ischemia reperfusion generating free radicals-induced nitration in the artery. Support: Medical College of Wisconsin, NIOSH grant R01 OH003493

Ice-Water Hand Immersion Causes a Reflex Decrease in Skin Temperature in the Contralateral Hand

Cutaneous receptors stimulated by ice-water immersion of one hand will increase sympathetic nerve activity to the palm skin in the nonimmersed contralateral hand and reduce blood flow, reflecting on a decrease in skin surface temperature under a constant ambient environment. To test the hypothesis that gender might affect the contralateral vasoconstrictor response, we analyzed the spatiotemporal pattern of palm skin surface temperature during ice-water immersion for 10 min using thermography in eight males and eight females. As soon as the left hand was immersed in ice-water, palm skin temperature in the nonimmersed right hand quickly decreased in all subjects, particularly in the periphery of the digits and palm. The reduction in skin temperature was short-lasting in 63% of males and 38% of females, but it lasted throughout immersion in the remaining subjects. The average decrease in palm skin temperature was not significantly different between males and females, though it tended to be greater in males. The mean arterial blood pressure significantly increased and heart rate decreased during immersion in males, whereas no substantial cardiovascular changes were observed in females. Cold sensation was well coincident with the appearance of a reduction in the palm skin temperature. In consideration of all these results, we suggest that cutaneous cold stimuli increased skin sympathetic nerve activity in the nonimmersed hand and reduced skin blood flow. We also contend that gender difference in the contralateral vasoconstrictor response was denied because the time course and magnitude of the decrease in palm skin temperature were not different between males and females.

Thermoregulatory Function During the Marathon

Marathon races are performed over a broad range of environmental conditions. Hyperthermia is a primary challenge for runners in temperate and warm weather, but hypothermia can be a concern during cool-wet or cold conditions. Body temperature during the marathon is a balance between metabolic heat production and exchange with the environment described by the heat balance equation. During exercise, core temperature is proportional to the metabolic rate and largely independent of a wide range of environmental conditions. In temperate or cool conditions, a large skin-to-ambient temperature gradient facilitates radiant and convective heat loss, and reduces skin blood flow requirements, which may explain the tolerance for high core temperature observed during marathons in cool conditions. However, in warmer environments, skin temperatures and sweating rates increase. In addition, greater skin blood flow is required for heat loss, magnifying thermoregulatory and circulatory strain. The combined challenge of exercise and environment associated with marathon running can substantially challenge the human thermoregulatory system.

Local regulation of skin blood flow during cooling involving presynaptic P2 purinoceptors in rats

1. This study investigated a local effect of cooling on the plantar skin blood flow (PSBF) of tetrodotoxin-treated rats by laser-Doppler flowmetry. 2. When the air temperature around the left foot was locally cooled from 25 to 10 degrees C, the PSBF of the left foot decreased. 3. The response was inhibited by the alpha-adrenoceptor antagonist phentolamine, the alpha1-adrenoceptor antagonist bunazosin, the alpha2-adrenoceptor antagonist RS79948, and bretylium and guanethidine that inhibit noradrenaline release from sympathetic nerves. Adrenalectomy of the rats did not affect the cooling-induced response. 4. The P2 purinoceptor antagonists suramin and PPADS also significantly suppressed the cooling-induced reduction of PSBF. However, the inhibitory effect of PPADS on the cooling-induced response was abolished after the treatment with phentolamine. Intra-arterial injections of ATPgammaS, a stable P2 purinoceptor agonist, at 25 degrees C caused a transient decrease in PSBF in a dose-dependent manner, which was significantly inhibited by phentolamine and guanethidine. 5. These results suggest a novel mechanism for local cooling-induced reduction of skin blood flow in vivo; moderate cooling of the skin induces the release of ATP, which stimulates presynaptic P2 purinoceptors on sympathetic nerve terminals and facilitates the release of noradrenaline, thereby causing contractions of skin blood vessels via the activation of alpha1-and alpha2-adrenoceptors.

Intermittent Exercise Reduces Skin Blood Flow and Increases Heat Storage in the Heat

Intermittent Exercise Reduces Skin Blood Flow and Increases Heat Storage in the Heat

Enhanced sweating during exercise at 3200m is caused by increased esophageal temperature due to reduced skin blood flow by hypoxia

Enhanced sweating during exercise at 3200m is caused by increased esophageal temperature due to reduced skin blood flow by hypoxia

Relative roles of local and reflex components in cutaneous vasoconstriction during skin cooling in humans

The reduction in skin blood flow (SkBF) with cold exposure is partly due to the reflex vasoconstrictor response from whole body cooling (WBC) and partly to the direct effects of local cooling (LC). Although these have been examined independently, little is known regarding their roles when acting together, as occurs in environmental cooling. We tested the hypothesis that the vasoconstrictor response to combined LC and WBC would be additive, i.e., would equal the sum of their independent effects. We further hypothesized that LC would attenuate the reflex vasoconstrictor response to WBC. We studied 16 (7 women, 9 men) young (30.5+/-2 yr) healthy volunteers. LC and WBC were accomplished with metal Peltier cooler-heater probe holders and water-perfused suits, respectively. Forearm SkBF was monitored by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Subjects underwent 15 min of LC alone or 15 min of WBC with and without simultaneous LC, either at equal levels (34-31 degrees C) or as equipotent stimuli (34-28 degrees C LC; 34-31 degrees C WBC). The fall in CVC with combined WBC and LC was greater (P<0.05) than for either alone (57.0+/-5% combined vs. 39.2+/-6% WBC; 34.4+/-4% LC) with equipotent cooling, but it was only significantly greater than for LC alone with equal levels of cooling (51.3+/-8% combined vs. 29.5+/-4% LC). The sum of the independent effects of WBC and LC was greater than their combined effects (74.9+/-4 vs. 51.3+/-8% equal and 73.6+/-7 vs. 57.0+/-5% equipotent; P<0.05). The fall in CVC with WBC at LC sites was reduced compared with control sites (17.6+/-2 vs. 42.4+/-8%; P<0.05). Hence, LC contributes importantly to the reduction in SkBF with body cooling, but also suppresses the reflex response, resulting in a nonadditive effect of these two components.