Cutaneous Vasomotor Tone Research Articles

Body Temperature, Cutaneous Heat Loss, and Skin Blood Flow During Epidural Anaesthesia for Emergency Cesarean Section

(Anaesthesia. 2018;73:1500–15006) During the peripartum period, hypothermia and hyperthermia are both associated with adverse outcomes. Neuraxial anesthesia hinders a patient’s ability to regulate body temperature by interrupting the sympathetic supply to the cutaneous vasculature. It is unclear how body temperature is affected by epidural administration of a concentrated local anesthetic for emergency cesarean section. This study aimed to determine how dosing of a labor epidural to provide anesthesia for cesarean section would affect mean body temperature and cutaneous vasomotor tone, hypothesizing that active cutaneous vasodilation would be blocked and therefore mean body temperature would increase.

Body temperature, cutaneous heat loss and skin blood flow during epidural anaesthesia for emergency caesarean section.

It is not clear how converting epidural analgesia for labour to epidural anaesthesia for emergency caesarean section affects either cutaneous vasomotor tone or mean body temperature. We hypothesised that topping up a labour epidural blocks active cutaneous vasodilation (cutaneous heat loss and skin blood flow decrease), and that as a result mean body temperature increases. Twenty women in established labour had body temperature, cutaneous heat loss and skin blood flow recorded before and after epidural top-up for emergency caesarean section. Changes over time were analysed with repeated measures ANOVA. Mean (SD) mean body temperature was 36.8 (0.5)°C at epidural top-up and 36.9 (0.6)°C at delivery. Between epidural top-up and delivery, the mean (SD) rate of increase in mean body temperature was 0.5 (0.5) °C.h-1 . Following epidural top-up, chest (p < 0.001) and forearm (p = 0.004) heat loss decreased, but head (p = 0.05), thigh (p = 0.79) and calf (p = 1.00) heat loss did not change. The mean (SD) decrease in heat loss was 15 (19) % (p < 0.001). Neither arm (p = 0.06) nor thigh (p = 0.10) skin blood flow changed following epidural top-up. Despite the lack of change in skin blood flow, the most plausible explanation for the reduction in heat loss and the increase in mean body temperature is blockade of active cutaneous vasodilation. It is possible that a similar mechanism is responsible for the hyperthermia associated with labour epidural analgesia.

Perceptual and Cutaneous Vasomotor Reactivity to Sudden Changes in Ambient Temperature in Older Adults

BackgroundChanges in thermal perception often precede measureable changes in skin temperature when entering a hot or cool environment. This is believed to be due to small changes in peripheral thermoreceptor outflow, which are summed in the central nervous system causing changes in thermal perception and changes in cutaneous vasomotor tone. This is termed thermal spatial summation. Thermal perception and cutaneous vasomotor control are often impaired in older adults. However, the effect of aging on thermal spatial summation is unknown. Thus, we tested the hypothesis that thermal spatial summation is attenuated in older adults.MethodsTwelve young (24 ± 3 y, 5 females) and nine older (66 ± 4 y, 6 females) adults passively moved between a hot (40°C, 20% RH) and cool (17°C, 49% RH) room when they felt ‘too cool’ or ‘too warm’ over a 90 min period. Weighted mean skin (6 site) and intestinal temperatures, forearm skin blood flow (laser Doppler), mean arterial pressure (photoplethysmography, MAP), and thermal sensation (7‐point scale: 1=cold, 4=neutral, 7=hot) and discomfort (4‐point scale: 1=comfortable, 4=very uncomfortable) were measured immediately prior to moving and immediately after entering the new environment (25 s later). Skin blood flow was normalized to MAP and are presented as cutaneous vascular conductance (CVC), providing an of index cutaneous vasomotor tone. Data upon leaving the hot room and entering the cool room (H‐C) and vice versa (C‐H) are presented as the change from the prior environment, providing an index of thermal spatial summation. Data were averaged across 4 ± 2 movements from H‐C and from C‐H.ResultsChanges in intestinal temperature at H‐C (Young: 0.0 ± 0.1, Older: 0.0 ± 0.0°C, P=0.31) and C‐H (Young: 0.0 ± 0.1, Older: 0.0 ± 0.1°C, P=0.46) did not differ between young and older adults. Changes in mean skin temperature at H‐C (Young: 0.0 ± 0.1, Older: 0.0 ± 0.1°C, P=0.51) and C‐H (Young: 0.0 ± 0.1, Older: 0.0 ± 1.0°C, P=0.80) also did not differ between groups. At H‐C, decreases in warmth sensation did not differ between groups (Young: −1.6 ± 1.3, Older: −2.1 ± 1.0 a.u., P=0.36). However, older adults demonstrated greater increases in warmth sensation at C‐H (Young: +1.2 ± 0.8, Older: +2.4 ± 1.1 a.u., P=0.01). Improvements in thermal discomfort at H‐C (Young: −0.7 ± 0.5, Older: −1.2 ± 0.6 a.u., P=0.10) and C‐H (Young: −0.8 ± 0.3, Older: −0.6 ± 0.2 a.u., P=0.01) did not differ between groups. Changes in MAP at H‐C (Young: 8 ± 4, Older: 11 ± 5 mmHg, P=0.20) and C‐H (Young: −6 ± 4, Older: −11 ± 13 mmHg, P=0.18) were not different between groups. Changes in CVC at H‐C were attenuated in older adults (Young: −0.24 ± 0.12, Older: −0.13 ± 0.04, P=0.02), but did not differ between groups at C‐H (Young: +0.10 ± 0.07, Older: +0.11 ± 0.10, P=0.88).ConclusionsThermal spatial summation is apparent in older adults. Upon entering a cool environment, the cutaneous vasomotor response is attenuated in older adults. However, the perceptual response upon entering a hot environment is augmented in this population. These findings suggest the effect of aging on thermal spatial summation is dependent on the population of thermoreceptors activated.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Forearm–finger skin temperature gradient as an index of cutaneous perfusion during steady‐state exercise

The purpose of this study was to examine whether the forearm-finger skin temperature gradient (T(forearm-finger)), an index of vasomotor tone during resting conditions, can also be used during steady-state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow (BFF ) was measured with a laser-Doppler flowmeter, and finger skin blood flow (PPG) was recorded from the left index fingertip using a pulse plethysmogram. T(forearm-finger) of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased (P<0.001), and T(forearm-finger) decreased (P<0.001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between T(forearm-finger) and both PPG (r = -0.68; P<0.001) and BFF (r = -0.50; P<0.001). It is concluded that T(forearm-finger) is a valid qualitative index of cutaneous vasomotor tone during steady-state exercise.

Human temperature regulation when given the opportunity to behave

This study aimed to test the primary hypotheses that human thermoregulatory behavior is: (1) initiated before changes in rectal or esophageal temperatures; and (2) accompanied by indiscernible differences in sweating or shivering. This was achieved by placing nine, healthy, males in a situation where they were free to move between a cold (~8 °C) and a hot (~46 °C) environment. Upon behaving [i.e., move from cold to hot (C→H) or from hot to cold (H→C)], skin, rectal, and esophageal temperatures, indices of cutaneous vasomotor tone, metabolism and evaporation, and local and whole-body thermal discomfort were recorded. Rectal temperatures were similar at H→C (37.1 ± 0.2 °C) and C→H (37.1 ± 0.2 °C); yet esophageal temperatures were higher at C→H (36.9 ± 0.2 vs. 36.8 ± 0.2 °C). Skin temperature (C→H, 28.4 ± 0.9 vs. H→C, 35.0 ± 0.6 °C) and vasomotor tone were drastically different upon the decision to behave. Metabolic heat production was lower at H→C (79 ± 10 W/m(2)) than at C→H (101 ± 20 W/m(2)), yet there were no statistical differences in evaporative heat loss (C→H, 23 ± 33 W/m(2) vs. H→C, 52 ± 36 W/m(2)). Whole-body thermal discomfort was similar at C→H and H→C, yet there were inter-segmental differences. These findings indicate that skin temperature, not core temperature, plays a signaling role in the decision to behaviorally thermoregulate. However, this behavior does not occur in the complete absence of autonomic thermoregulatory responses.

The influence of internal and skin temperatures on active cutaneous vasodilation under different levels of exercise and ambient temperatures in humans

To clarify the influence of internal and skin temperature on the active cutaneous vasodilation during exercise, the body temperature thresholds for the onset of active vasodilation during light or moderate exercise under different ambient temperature conditions were compared. Seven male subjects performed 30 min of a cycling exercise at 20 % or 50 % of peak oxygen uptake in a room maintained at 20, 24, or 28 °C. Esophageal (Tes) and mean skin temperature (Tsk) as measured by a thermocouple, deep thigh temperature (Tdt) by the zero-heat-flow (ZHF) method, and forearm skin blood flow by laser-Doppler flowmetry (LDF) were monitored. The mean arterial pressure (MAP) was also monitored non-invasively, and the cutaneous vascular conductance (CVC) was calculated as the LDF/MAP. Throughout the experiment, the Tsk at ambient temperatures of 20, 24, and 28 °C were approximately 30, 32, and 34 °C, respectively, for both 20 % and 50 % exercise. During 50 % exercise, the Tes or Tdt thresholds for the onset of the increase in CVC were observed to be similar among the 20, 24, and 28 °C ambient conditions. During 20 % exercise, the increase in Tes and Tdt was significantly lower than those found at 50 %, and the onset of the increase in CVC was only observed at 28 °C. These results suggest that the onset of active vasodilation was affected more strongly by the internal or exercising tissue temperatures than by the skin temperatures during exercise performed at a moderate load in comparison to a light load under Tsk variations ranging from 30 °C to 34 °C. Therefore, the modification by skin temperature of the central control on cutaneous vasomotor tone during exercise may differ between different exercise loads.

Effects of motion sickness on thermoregulatory responses in a thermoneutral air environment

Motion sickness (MS) has been identified as a non-thermal factor that can moderate autonomic thermoregulatory responses. It has been shown that MS exaggerates core cooling during immersion in cold (15 °C) and luke-warm (28 °C) water by attenuating cold-induced vasoconstriction. The aim of the present study was to investigate whether MS affects thermal balance in a thermoneutral air environment. Eleven subjects were exposed to rotation in two conditions, control (CN) and MS. In the CN condition subjects refrained from head movements, whereas in the MS condition they performed a sequence of maximal head movements (left, right, up, down) at 15-s intervals until they were very nauseous. Sweating rate, rectal temperature (T(re)), the difference in temperature between the right forearm and tip of the second finger (T(ff)) as an index of cutaneous vasomotor tone, perceived MS, thermal comfort and temperature perception were recorded before and during rotation, and during 90-min post-rotation. During the post-rotation period, T(re) dropped and sweating rate increased in the MS but not in the CN condition. The T(ff) response suggests that MS-induced peripheral vasodilatation which, together with the sweating resulted in increased heat loss. During rotation, subjects perceived temperature to be uncomfortably high, suggesting that MS may also affect thermoregulatory behaviour. It thus appears that also in a thermoneutral air environment MS may substantially affect thermal balance.

Atypical Antipsychotics Cause an Acute Increase in Cutaneous Hand Blood Flow in Patients with Schizophrenia and Schizoaffective Disorder

Clinical studies suggest resting thermoregulatory cutaneous vasomotor tone could be increased in schizophrenia, resulting in reduced hand blood flow. In animal models, atypical antipsychotics including clozapine potently inhibit sympathetic neural outflow to the thermoregulatory cutaneous vascular beds. We have now determined whether antipsychotic medication administration is associated with an acute increase in hand blood flow in patients with schizophrenia and schizoaffective disorder, and whether this increase correlates with clinical status. Hand temperature was measured with an infrared camera in 12 patients with chronic schizophrenia or schizoaffective disorder 30 min prior to, then 30 and 60 min following medication. Clinical status was assessed via the Brief Psychiatric Rating Scale (BPRS). Results were compared using regression and repeated measures analysis of variance. A robust and significant increase in hand temperature (p < 0.001) was observed following antipsychotic administration. The mean increase after 60 min was 4.1 ± 2.4°C. This increase was significantly associated with colder hand temperature prior to medication (p < 0.05; suggestive of increased resting vasoconstriction) and with more severe psychiatric symptoms (p < 0.05). Atypical antipsychotics were associated with increased hand blood flow, consistent with inhibition of thermoregulatory sympathetic outflow to the cutaneous vascular bed in patients with schizophrenia and schizoaffective disorder. This increase correlated with symptom severity. Hand temperature increase following antipsychotic medication may therefore be a simple and informative physiological marker of disease activity and potential response in patients with schizophreniform disorders. Given that antipsychotics also inhibit sympathetic outflow to brown adipose tissue, which normally converts energy to heat, future studies should examine whether antipsychotic-induced hand temperature increase is associated with antipsychotic-induced weight gain.

Ambient Temperature Affects Glabrous Skin Vasculature and Sweating Responses to Mental Task in Humans

We compared responses in heart rate (HR), mean blood pressure (MAP), sweating rate (SR), sweating expulsion (SwE), and skin vascular conductance (VC) to mental task among different ambient temperature (Ta) conditions, i.e., 12, 16, 20, and 24 degrees C. Seven subjects (27+/-5 yrs, 64+/-14 kg) underwent a 2-min color word conflict test (CWT) after 2 mins of baseline data acquisition following a 20-min resting period. All subjects wore long sleeve shirts and long pants. The skin blood flow was measured with a laser Doppler probe on the left index finger pulp to calculate skin VC, and the SR and sweating expulsion (SwE) were measured with a ventilated capsule on the left thenar. CWT significantly increased the HR and MAP, while there was no significant effect of Ta on the magnitudes of these responses. CWT significantly decreased the skin VC when the Ta was 24 degrees C, whereas it significantly increased the skin VC when the Ta was 12 or 16 degrees C. CWT significantly increased SR and SwE in all Ta conditions, and the SwE was greater in warmer conditions. These findings suggest that different ambient temperatures induce different responses in finger skin vasculature to mental task, implying the independent response of cutaneous vasomotor tone and sweat glands in glabrous skin to mental task.

Mechanisms of acetylcholine‐mediated vasodilatation in young and aged human skin

Thermoregulatory cutaneous vasodilatation (VD) is attenuated in aged skin. While acetylcholine (ACh) plays a role in thermally mediated VD, the precise mechanisms through which ACh-mediated VD acts and whether those downstream mechanisms change with ageing are unclear. We tested the hypotheses that both nitric oxide (NO)- and prostanoid-mediated pathways contribute to exogenous ACh-mediated VD, and that both are attenuated with advanced age. Twelve young (Y: 23 +/- 1 years) and 10 older (O: 69 +/- 1 years) subjects underwent infusions of 137.5 mum ACh at four intradermal microdialysis sites: control (C, Ringer solution), NO synthase inhibited (NOS-I, 10 mm l-NAME), cyclooxygenase inhibited (COX-I, 10 mm ketorolac) and NOS-I + COX-I. Red blood cell flux was monitored using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated (laser-Doppler flux/mean arterial pressure) and normalized to maximal CVC (%CVC(max)) (28 mm sodium nitroprusside + local heating to 43 degrees C). Baseline %CVC(max) was increased in the O at COX-I sites (COX-I 16 +/- 1, NOS-I + COX-I 16 +/- 2 versus C 10 +/- 1%CVC(max); P < 0.001) but not in the young, suggesting an age-related shift toward COX vasoconstrictors contributing to basal cutaneous vasomotor tone. There was no difference in peak %CVC(max) during ACh infusion between age groups, and the response was unchanged by NOS-I (O: NOS-I 35 +/- 5 versus C 38 +/- 5%CVC(max); P = 0.84) (Y: NOS-I 41 +/- 4 versus C 39 +/- 4%CVC(max); P = 0.67). COX-I and NOS-I + COX-I attenuated the peak CVC response to ACh in both groups (COX-I O: 29 +/- 3, Y: 22 +/- 2%CVC(max) versus C; P < 0.001 both groups; NOS-I + COX-I O: 32 +/- 3 versus Y: 29 +/- 2%CVC(max); versus C; P < 0.001 both groups). ACh mediates cutaneous VD through prostanoid and non-NO-, non-prostanoid-dependent pathways. Further, older subjects have a diminished prostanoid contribution to ACh-mediated VD.

Role of cardiopulmonary baroreflexes during dynamic exercise.

To examine the role of cardiopulmonary (CP) mechanoreceptors in the regulation of arterial blood pressure during dynamic exercise in humans, we measured mean arterial pressure (MAP), cardiac output (Q), and forearm blood flow (FBF) during mild cycle ergometer exercise (77 W) in 14 volunteers in the supine position with and without lower-body negative pressure (LBNP). During exercise, MAP averaged 103 +/- 2 mmHg and was not altered by LBNP (-10, -20, or -40 mmHg). Steady-state Q during exercise was reduced from 10.2 +/- 0.5 to 9.2 +/- 0.5 l/min (P less than 0.05) by application of -10 mmHg LBNP, whereas heart rate (97 +/- 3 beats/min) was unchanged. MAP was maintained during -10 mmHg LBNP by an increase in total systemic vascular resistance (TSVR) from 10.3 +/- 0.5 to 11.4 +/- 0.6 U and forearm vascular resistance (FVR) from 17.5 +/- 1.9 to 23.3 +/- 2.6 U. The absence of a reflex tachycardia or reduction in arterial pulse pressure during -10 mmHg LBNP supports the hypothesis that the increase in TSVR and FVR results primarily from the unloading of CP mechanoreceptors. Because CP mechanoreceptor unloading during exercise stimulates reflex circulatory adjustments that act to defend the elevated MAP, we conclude that the elevation in MAP during exercise is regulated and not merely the consequence of differential changes in Q and TSVR. In addition, a major portion of the reduction in FBF in our experimental conditions occurs in the cutaneous circulation. As such, these data support the hypothesis that CP baroreflex control of cutaneous vasomotor tone is preserved during mild dynamic exercise.

Effect of bombesin on thermoregulation of the rabbit.

Injections of bombesin (BOM, 125, 250 and 500 ng) into the preoptic/anterior hypothalamus caused dose-related decreases of threshold temperatures for metabolic cold defence, cutaneous vasomotor tone and respiratory rate, combined with a reduced sensitivity of these thermoregulatory effectors in response to core temperature changes induced at thermoneutral or warm ambient conditions. Intracisternal (i.c.) injections of BOM (250 ng) produced qualitatively identical thermoregulatory effector changes in response to core temperature changes. Injections of BOM into the posterior hypothalamus did not affect body temperature control. Increased locomotor behavior, licking and grooming was elicited, however, from all injection sites. The results explain the prevailing hypothermic effect of BOM as the consequence of the concerted decrease in threshold temperatures and "gains" of all autonomic thermoregulatory effectors and suggest the activation of warm inputs, relative to cold inputs, at the hypothalamic level as the underlying mechanism. Direct or indirect inhibition of the intrinsic hypothalamic system involving thyrotropin-releasing hormone (TRH) and consequent deactivation of central noradrenergic pathways known to generate the entire autonomic pattern of cold defence might be involved in the neuro-humoral changes resulting in hypothermic effects of centrally applicated BOM.

Renal and cutaneous vasomotor and respiratory rate adjustments to peripheral cold and warm stimuli and to bacterial endotoxin in conscious rabbits

In conscious rabbits peripheral cold stimuli decreased respiratory rate and increased cutaneous vasomotor tone while simultaneously renal sympathetic nervous discharge decreased. Peripheral warm stimuli produced the reverse pattern of autonomic effector activity. Injection of a bacterial endotoxin at warm ambient temperature elicited a biphasic fever response. Within the first 60 min cutaneous vasomotor tone increased, simultaneously renal sympathetic activity decreased. Thereafter, ear skin vessels dilated and renal sympathetic activity increased by about 100%. Respiratory rate remained depressed during both fever phases. Renal blood flow was investigated in a second series of experiments and showed a negative correlation with the changes of renal constrictor activity during peripheral thermal stimulation but only in the first phase of fever. The results show that renal innervation is involved in the typical thermoregulatory autonomic activity pattern by which temperature homeostasis is preserved. The vasomotor patterns of cold and heat stress developing during fever are compatible with the concept of a changed set-point of the body thermostat. The depressed respiratory rate and the lack of the renal vascular response to the increased nervous activity during the second fever phase and their reversal to normal after acetylsalicylate (ASA) indicate the participation of prostaglandins modifying peripheral and central neurotransmitter mechanisms.

Local and regional variations in cutaneous vasomotor tone of the human trunk.

1. These studies have been concerned with regional or segmental variations in vasomotor activity in “normal” individuals. 2. The methods used included the segment-to-segment measurement of the temperature, red responses, and light absorption of the paravertebral skin. 3. The observations show that the cutaneous vasomotor activity on the trunk is not uniform, as appears to be commonly assumed. Topographical patterns of temperature, red responses and light absorption of the skin were found. 4. Local or segmental deviations from these average or “normal” topographical patterns were found in most individuals. 5. Local deviations in all three types of observations were usually found at the same segmental levels in a given individual. 6. The topographical patterns of vascular activity appear to be functional rather than anatomic and are analogous to similar patterns in sudomotor activity. 7. The topographical patterns of cutaneous vasomotor manifestations appear, therefore, to reflect normal regional variations in sympathetic activity. 8. The local deviations of vasomotor activity from the “normal” patterns appear to be related to local deviations in sympathetic activity.