Delayed distribution of active vasodilation and altered vascular conductance in aged skin

2003 ◽  
Vol 94 (3) ◽  
pp. 1045-1053 ◽  
Author(s):  
Jane M. Pierzga ◽  
Adam Frymoyer ◽  
W. Larry Kenney
Keyword(s):  
Older Men ◽  
Venous Occlusion ◽  
Doppler Imaging ◽  
Passive Heating ◽  
Vascular Conductance ◽  
Forearm Skin ◽  
Forearm Vascular Conductance ◽  
Aged Skin ◽  
Early Passive ◽  
Old Men

Reflex vasodilation is attenuated in aged skin during hyperthermia. We used laser-Doppler imaging (LDI) to test the hypothesis that the magnitude of conductance and the spatial distribution of vasodilation are altered with aging. LDI of forearm skin was compared in 12 young (19- to 29-yr-old) and 12 older (64- to 75-yr-old) men during supine passive heating. Additionally, iontophoresis of bretylium tosylate was performed in a subset of subjects to explore the involvement of sympathetic vasoconstriction in limiting skin blood flow. Passive heating with water-perfused suits clamped mean skin temperature at 41.0 ± 0.5°C, causing a ramp increase in esophageal temperature (Tes) to ≤38.5°C. LDI scans were performed at baseline and at every 0.2°C increase in Tes. LDI at bretylium and control sites was identical, suggesting no influence of noradrenergic vasoconstriction. Forearm vascular conductance (venous occlusion plethysmography) was reduced in the older men ( P ≤ 0.001) at every elevated Tes. Mean cutaneous vascular conductance (CVC) of the scanned area was reduced in the older men at 0.2°C ≤ ΔTes ≤ 0.8°C. Early in heating (0.2°C ≤ ΔTes ≤ 0.6°C), older men also responded with a reduced vasodilated area ( P ≤ 0.05), implying a slower recruitment or filling of skin microvessels. The results indicate that the area of vasodilation and CVC within the vasodilated area are reduced in aged skin during early passive heating, but only CVC is reduced at ΔTes = 0.8°C.

scholarly journals Combined heat and mental stress alters neurovascular control in humans

2010 ◽  
Vol 109 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
Jenna C. Klein ◽  
Craig G. Crandall ◽  
R. Matthew Brothers ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mental Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Thermal Conditions ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Vascular Responses ◽  
Time Condition ◽  
Forearm Skin

This study examined the effect of combined heat and mental stress on neurovascular control. We hypothesized that muscle sympathetic nerve activity (MSNA) and forearm vascular responses to mental stress would be augmented during heat stress. Thirteen subjects performed 5 min of mental stress during normothermia (Tcore; 37 ± 0°C) and heat stress (38 ± 0°C). Heart rate, mean arterial pressure (MAP), MSNA, forearm vascular conductance (FVC; venous occlusion plethysmography), and forearm skin vascular conductance (SkVCf; via laser-Doppler) were analyzed. Heat stress increased heart rate, MSNA, SkVCf, and FVC at rest but did not change MAP. Mental stress increased MSNA and MAP during both thermal conditions; however, the increase in MAP during heat stress was blunted, whereas the increase in MSNA was accentuated, compared with normothermia (time × condition; P < 0.05 for both). Mental stress decreased SkVCf during heat stress but not during normothermia (time × condition, P < 0.01). Mental stress elicited similar increases in heart rate and FVC during both conditions. In one subject combined heat and mental stress induced presyncope coupled with atypical blood pressure and cutaneous vascular responses. In conclusion, these findings indicate that mental stress elicits a blunted increase of MAP during heat stress, despite greater increases in total MSNA and cutaneous vasoconstriction. The neurovascular responses to combined heat and mental stress may be clinically relevant to individuals frequently exposed to mentally demanding tasks in hyperthermic environmental conditions (i.e., soldiers, firefighters, and athletes).

scholarly journals Aerobic training and cutaneous vasodilation in young and older men

1999 ◽  
Vol 86 (5) ◽  
pp. 1676-1686 ◽  
Author(s):  
Carla M. Thomas ◽  
Jane M. Pierzga ◽  
W. Larry Kenney
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Aerobic Training ◽  
Older Men ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Response To Exercise ◽  
Cutaneous Vascular Conductance

To determine the effect and underlying mechanisms of exercise training and the influence of age on the skin blood flow (SkBF) response to exercise in a hot environment, 22 young (Y; 18–30 yr) and 21 older (O; 61–78 yr) men were assigned to 16 wk of aerobic (A; YA, n = 8; OA, n = 11), resistance (R; YR, n = 7; OR, n = 3), or no training (C; YC, n = 7; OC, n = 7). Before and after treatment, subjects exercised at 60% of maximum oxygen consumption (V˙o 2 max) on a cycle ergometer for 60 min at 36°C. Cutaneous vascular conductance, defined as SkBF divided by mean arterial pressure, was monitored at control (vasoconstriction intact) and bretylium-treated (vasoconstriction blocked) sites on the forearm using laser-Doppler flowmetry. Forearm vascular conductance was calculated as forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure. Esophageal and skin temperatures were recorded. Only aerobic training (functionally defined a priori as a 5% or greater increase inV˙o 2 max) produced a decrease in the mean body temperature threshold for increasing forearm vascular conductance (36.89 ± 0.08 to 36.63 ± 0.08°C, P < 0.003) and cutaneous vascular conductance (36.91 ± 0.08 to 36.65 ± 0.08°C, P < 0.004). Similar thresholds between control and bretylium-treated sites indicated that the decrease was mediated through the active vasodilator system. This shift was more pronounced in the older men who presented greater training-induced increases in V˙o 2 maxthan did the young men (22 and 9%, respectively). In summary, older men improved their SkBF response to exercise-heat stress through the effect of aerobic training on the cutaneous vasodilator system.

scholarly journals Comparison of the vasodilatory effects of sodium nitroprusside vs. nitroglycerin

2017 ◽  
Vol 123 (2) ◽  
pp. 402-406 ◽  
Author(s):  
Sushant M. Ranadive ◽  
Andy R. Eugene ◽  
Gabrielle Dillon ◽  
Wayne T. Nicholson ◽  
Michael J. Joyner
Keyword(s):  
Sodium Nitroprusside ◽  
Doppler Ultrasound ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Similar Concentration ◽  
Vascular Conductance ◽  
Significant Difference ◽  
Forearm Vascular Conductance ◽  
Higher Doses ◽  
Healthy Participants

The vasodilatory mechanism of Nntroglycerin (NTG) is similar to sodium nitroprusside (SNP) in regard to action on guanosine 3′5′-monophosphate (cyclic GMP) via nitric oxide. However, it is unknown whether NTG can achieve the same magnitude of vasodilation in the forearm as SNP. Therefore, the purpose of the study was to evaluate the differences in forearm blood flow (FBF) and forearm vascular conductance (FVC) during escalating infusions of NTG vs. SNP at similar concentration doses and rates. We measured FBF using venous occlusion plethysmography (VOP) and Doppler ultrasound in eight young, healthy participants (mean age = 28 ± 2 yr) during four forearm volume (FAV)-specific doses (0.25, 0.5, 1, and 2 µg·100 ml FAV−1·min−1) of SNP and NTG infused via a brachial artery catheter. There was a significant difference in FVC of SNP vs. NTG only at the higher doses, as measured by VOP (14.9 ± 1.4 and 18.3 ± 1.5 vs. 11.6 ± 1.2 and 12.5 ± 1.2 ml/dl FAV−1·min−1·100 mmHg−1). FVC as measured by Doppler ultrasound unadjusted for FAV was significantly different at the lowest and the higher two doses of SNP compared with NTG (202.1 ± 25.8, 329.4 ± 46.7, and 408 ± 63.5 vs. 142.9 ± 22.4, 217.2 ± 18.8, and 247.5 ± 18.2 ml·min−1·100 mmHg−1). SNP induces significantly higher vasodilatory actions compared with NTG. However, NTG is comparable in eliciting equivalent vasodilator effects to SNP during low concentration doses when measured by VOP. Importantly, for forearm pharmacology studies, NTG can elicit marked endothelium-independent forearm vasodilation. NEW & NOTEWORTHY We compared the vasodilatory capacities of NTG vs. SNP at similar concentration doses and rates into the forearm. Based on the results of the study, it may be feasible to use intra-arterial NTG as a measure of endothelial-independent vasodilator in research studies. However, NTG dosing may need to be higher if used as an endothelial-independent vasodilator due to significant differences in the vasodilatory effects during higher doses of SNP compared with NTG.

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Normotensive Subjects ◽  
Cutaneous Vascular Conductance

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.

Maximal skin vascular conductance in subjects aged 5-85 yr

1995 ◽  
Vol 79 (1) ◽  
pp. 297-301 ◽  
Author(s):  
H. L. Martin ◽  
J. L. Loomis ◽  
W. L. Kenney
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Activity Level ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Resting Blood Pressure ◽  
Forearm Skin ◽  
Linear Fit ◽  
Minimal Resistance

This study examined maximal forearm skin vascular conductance (FVCmax) as a function of age in 74 healthy male and female subjects ranging in age from 5 to 85 yr. The skin temperature of the left forearm was uniformly clamped at 42 degrees C by spraying a fine mist of water over the surface. Forearm blood flow (FBF) was measured by venous occlusion plethysmography (Hg-in-Silastic strain gauge). After 60 min of heating, a reactive hyperemia maneuver was performed to verify that forearm skin blood flow was maximal by using laser Doppler flowmetry to isolate the skin component of FBF. The maximal FBF of each subject was then divided by mean arterial pressure to yield FVCmax (in ml.100 ml-1.min-1.100 mmHg-1), i.e., minimal resistance. The model that best fits the data was curvilinear, as described by FVCmax = 13.1 + 86.9 (age-0.75) (r2 = 0.52, P < 0.001). The exclusion of subjects younger than 18 yr of age simplified the model to a linear fit with a slope of -0.16 conductance units/yr for adults. Interindividual variability remained constant across the entire age span. Once the age effect was considered, there were no significant effects of gender, adiposity, resting blood pressure, physical activity level, or body surface area on FVCmax.

scholarly journals Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm

1996 ◽  
Vol 81 (4) ◽  
pp. 1807-1814 ◽  
Author(s):  
Keith A. Engelke ◽  
John R. Halliwill ◽  
David N. Proctor ◽  
Niki M. Dietz ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Peak Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
No Synthase ◽  
Vascular Conductance ◽  
Human Forearm ◽  
Before And After ◽  
Forearm Vascular Conductance ◽  
Modest Effect

Engelke, Keith A., John R. Halliwill, David N. Proctor, Niki M. Dietz, and Michael J. Joyner. Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm. J. Appl. Physiol. 81(4): 1807–1814, 1996.—We investigated the separate and combined contributions of nitric oxide (NO) and vasodilating prostaglandins as mediators of reactive hyperemia in the human forearm. Forearm blood flow (FBF) was measured with venous occlusion plethysmography after 5 min of ischemia. In one protocol ( n = 12), measurements were made before and after intra-arterial administration of the NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) to one forearm. In a separate protocol ( n = 7), measurements were made before and after systemic administration of the cyclooxygenase inhibitor ibuprofen and again afterl-NMMA.l-NMMA reduced baseline FBF at rest (2.7 ± 0.4 to 1.6 ± 0.2 ml ⋅ 100 ml−1 ⋅ min−1; P < 0.05) and had a modest effect on peak forearm vascular conductance and flow (forearm vascular conductance = 31.1 ± 3.1 vs. 25.7 ± 2.5 ml ⋅ min−1 ⋅ 100 ml forearm−1 ⋅ 100 mmHg of perfusion pressure−1 ⋅ min−1, P < 0.05; FBF = 26.6 ± 2.9 vs. 22.8 ± 2.6 ml ⋅ 100 ml−1 ⋅ min−1, P = 0.055). Total excess flow above baseline during reactive hyperemia was unaffected byl-NMMA (14.3 ± 3.0 vs. 13.1 ± 2.3 ml/100 ml; P < 0.05). Ibuprofen did not change FBF at rest, reduced peak FBF from 27.6 ± 1.9 to 20.3 ± 2.7 ml ⋅ 100 ml−1 ⋅ min−1( P < 0.05), but had no effect on total excess flow above baseline. Infusion ofl-NMMA after ibuprofen reduced FBF at rest by 40%, had no effect on peak flow, but reduced total excess flow above baseline from 12.0 ± 2.5 to 7.6 ± 1.3 ml/100 ml ( P < 0.05). These data demonstrate that NO synthase inhibition has a modest effect on peak vasodilation during reactive hyperemia but plays a minimal role later. Prostaglandins appear to be important determinants of peak flow. The effects of NO synthase inhibition during reactive hyperemia may also be potentiated by concurrent cyclooxygenase inhibition.

Age alters the cardiovascular response to direct passive heating

1998 ◽  
Vol 84 (4) ◽  
pp. 1323-1332 ◽  
Author(s):  
Christopher T. Minson ◽  
Stacey L. Wladkowski ◽  
Anthony F. Cardell ◽  
James A. Pawelczyk ◽  
W. Larry Kenney
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Thermal Tolerance ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Young Men ◽  
Older Men ◽  
Venous Occlusion ◽  
Passive Heating ◽  
Total Blood

During direct passive heating in young men, a dramatic increase in skin blood flow is achieved by a rise in cardiac output (Q˙c) and redistribution of flow from the splanchnic and renal vascular beds. To examine the effect of age on these responses, seven young (Y; 23 ± 1 yr) and seven older (O; 70 ± 3 yr) men were passively heated with water-perfused suits to their individual limit of thermal tolerance. Measurements included heart rate (HR),Q˙c (by acetylene rebreathing), central venous pressure (via peripherally inserted central catheter), blood pressures (by brachial auscultation), skin blood flow (from increases in forearm blood flow by venous occlusion plethysmography), splanchnic blood flow (by indocyanine green clearance), renal blood flow (by p-aminohippurate clearance), and esophageal and mean skin temperatures.Q˙c was significantly lower in the older than in the young men (11.1 ± 0.7 and 7.4 ± 0.2 l/min in Y and O, respectively, at the limit of thermal tolerance; P < 0.05), despite similar increases in esophageal and mean skin temperatures and time to reach the limit of thermal tolerance. A lower stroke volume (99 ± 7 and 68 ± 4 ml/beat in Y and O, respectively, P < 0.05), most likely due to an attenuated increase in inotropic function during heating, was the primary factor for the lowerQ˙c observed in the older men. Increases in HR were similar in the young and older men; however, when expressed as a percentage of maximal HR, the older men relied on a greater proportion of their chronotropic reserve to obtain the same HR response (62 ± 3 and 75 ± 4% maximal HR in Y and O, respectively, P < 0.05). Furthermore, the older men redistributed less blood flow from the combined splanchnic and renal circulations at the limit of thermal tolerance (960 ± 80 and 720 ± 100 ml/min in Y and O, respectively, P < 0.05). As a result of these combined attenuated responses, the older men had a significantly lower increase in total blood flow directed to the skin.

β-Receptor agonist activity of phenylephrine in the human forearm

2001 ◽  
Vol 90 (5) ◽  
pp. 1855-1859 ◽  
Author(s):  
Klaus D. Torp ◽  
Michael E. Tschakovsky ◽  
John R. Halliwill ◽  
Christopher T. Minson ◽  
Michael J. Joyner
Keyword(s):  
Receptor Agonist ◽  
Blocking Drug ◽  
Agonist Activity ◽  
Vascular Conductance ◽  
Vasodilator Activity ◽  
Human Forearm ◽  
Forearm Vascular Conductance ◽  
Β Receptor ◽  
Phenylephrine Infusion ◽  
Adrenergic Blocking

Phenylephrine is generally regarded as a “pure” α1-agonist. However, after treatment of the forearm with the α-adrenergic-blocking drug phentolamine, brachial artery infusion of phenylephrine can cause transient forearm vasodilation. To determine whether this response was β-receptor mediated, phenylephrine, phentolamine, and propranolol were infused into the brachial arteries of six healthy volunteers. Forearm vascular conductance (FVC) was also calculated and expressed as arbitrary units (units). Infusion of phenylephrine by itself (0.5 μg · dl forearm volume−1 · min−1) caused a sustained decrease ( P < 0.05) in FVC from 3.5 ± 0.7 to 0.9 ± 0.2 units ( P < 0.05). Infusion of the α-blocker phentolamine increased ( P < 0.05) baseline FVC to 5.7 ± 1.3 units. Subsequent infusion of phenylephrine after α-blockade caused FVC to increase ( P < 0.05) for ∼1 min from 5.7 ± 1.3 to a peak of 13.1 ± 1.8 units. Propranolol had no effect on baseline flow, and subsequent phenylephrine infusion after α- and β-blockade caused a small, but significant, sustained decrease in FVC from 5.1 ± 1.0 to 3.6 ± 0.8 units. There were no systemic effects from the infusions, and saline infusion at the same rate (1–2 ml/min) had no forearm vasoconstrictor or dilator effects. These data indicate that in humans phenylephrine can exert transient β2-vasodilator activity when its predominant α-constrictor effects are blocked.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

scholarly journals Skin microvascular reactivity correlates to clinical microangiopathy in type 1 diabetes: A pilot study

2020 ◽  
Vol 17 (3) ◽  
pp. 147916412092830
Author(s):  
Sara Tehrani ◽  
Karin Bergen ◽  
Louisa Azizi ◽  
Gun Jörneskog
Keyword(s):  
Type 1 Diabetes ◽  
Sodium Nitroprusside ◽  
Repeated Measures ◽  
Doppler Imaging ◽  
Healthy Controls ◽  
Microvascular Reactivity ◽  
Repeated Measures Analysis ◽  
Peak Flux ◽  
Forearm Skin

Aim: The aim of this study was to investigate the correlation between skin microvascular reactivity and clinical microangiopathy in patients with type 1 diabetes. Methods: We included 61 patients with type 1 diabetes, that is, 31 patients with and 30 without clinical microangiopathy, and 31 healthy controls. A microangiopathy scoring system was introduced for comparison of data between patients with microangiopathy. Responses to iontophoresis of acetylcholine and sodium nitroprusside were assessed by laser Doppler imaging. Results: Patients with microangiopathy had reduced acetylcholine- and sodium nitroprusside-mediated flux in forearm skin microcirculation compared to healthy controls ( p = 0.03 and p < 0.001, respectively, repeated measures analysis of variance), whereas no significant differences were found between patients without microangiopathy and controls. Skin reactivity was reduced in patients with microangiopathy compared to patients without microangiopathy: 1.43 ± 0.38 versus 1.59 ± 0.39 arbitrary units for acetylcholine-mediated peak flux and 1.44 ± 0.46 versus 1.74 ± 0.34 arbitrary units for sodium nitroprusside-mediated peak flux ( p < 0.05 for both). A tendency of gradual decrease in acetylcholine and sodium nitroprusside responses was found in patients with increasing microangiopathy scores. Conclusion: We conclude that skin microvascular reactivity is associated with clinical microangiopathy in patients with type 1 diabetes. Impaired skin microvascular function in type 1 diabetes seems to be multifactorial and involves both endothelial-dependent and endothelial-independent pathways. We introduce a novel microangiopathy score that could easily be used in a clinical setting for comparison of patients with various degrees of microangiopathy.

Sign in / Sign up

Export Citation Format

Share Document