Effects of chronic sympathectomy on locally mediated cutaneous vasodilation in humans

2002 ◽  
Vol 92 (2) ◽  
pp. 685-690 ◽  
Author(s):  
Nisha Charkoudian ◽  
John H. Eisenach ◽  
John L. D. Atkinson ◽  
Robert D. Fealey ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Human Skin ◽  
Lower Body Negative Pressure ◽  
Local Heating ◽  
Sympathetic Innervation ◽  
Sensory Nerve ◽  
Laser Doppler ◽  
Sympathetic Denervation ◽  
Vascular Conductance ◽  
Local Warming

In human skin, the vasodilator response to local heating includes a sensory nerve-dependent peak followed by a nadir and then a slower, nitric oxide-mediated, endothelium-dependent vasodilation. To investigate whether chronic sympathectomy diminishes this endothelium-dependent vasodilation, we studied individuals who had previously undergone surgical T2 sympathectomy ( n = 9) and a group of healthy controls ( n = 8). We assessed the cutaneous vascular response (laser-Doppler) to 30 min of local warming to 42.5°C on the ventral forearm (no sympathetic innervation) and the lower legs (sympathetic nerves intact). Lower body negative pressure (LBNP) was measured to confirm sympathetic denervation. During local warming in sympathectomized individuals, vascular conductance reached an initial peak at both sites [achieving 1.73 ± 0.22 laser-Doppler units (LDU)/mmHg in the forearm and 1.92 ± 0.21 LDU/mmHg in the leg]. It then decreased to a nadir in the innervated leg [to 1.77 ± 0.23 LDU/mmHg ( P < 0.05)] but not in the sympathectomized arm (1.69 ± 0.21 LDU/mmHg; P > 0.10). The maximal vasodilation seen during the slower phase was not different between limbs or between groups. Furthermore, LBNP caused a 44% reduction in forearm vascular conductance (FVC) in control subjects, but FVC did not decrease significantly in sympathectomized individuals, confirming sympathetic denervation. These data indicate that endothelial function in human skin is largely preserved after sympathectomy. The altered pattern of the response suggests that the nitric oxide-dependent portion may be accelerated in sympathectomized limbs.

Reflex control of the cutaneous circulation during passive body core heating in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Body Core ◽  
Doppler Techniques ◽  
The Impact

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

The acute impact of local cooling versus local heating on human skin microcirculation using laser Doppler flowmetry and tissue spectrophotometry

Burns ◽  
2020 ◽  
Vol 46 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Dominik Bender ◽  
Stephanie Tweer ◽  
Frank Werdin ◽  
Jens Rothenberger ◽  
Adrien Daigeler ◽  
...  
Keyword(s):  
Human Skin ◽  
Laser Doppler Flowmetry ◽  
Local Heating ◽  
Laser Doppler ◽  
Local Cooling ◽  
Skin Microcirculation ◽  
Doppler Flowmetry

scholarly journals Geldanamycin attenuates NO-mediated dilation in human skin

2002 ◽  
Vol 282 (1) ◽  
pp. H232-H236 ◽  
Author(s):  
Shubha Shastry ◽  
Michael J. Joyner
Keyword(s):  
Human Skin ◽  
Potential Role ◽  
Local Heating ◽  
Specific Inhibitor ◽  
Heat Shock Protein 90 ◽  
No Synthase ◽  
Vascular Conductance ◽  
Endothelial Nitric Oxide ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Blood

The binding of heat shock protein 90 (HSP90) to endothelial nitric oxide (NO) synthase (eNOS) can enhance eNOS activation. Studies have shown that the HSP90-specific inhibitor geldanamycin (GA) can cause attenuation of NO-mediated processes. Twenty subjects participated in one of two protocols. In each protocol, one forearm of each subject was instrumented with two intradermal microdialysis probes for drug delivery. Laser Doppler flowmeters were used to measure cutaneous blood flow. Skin sites were either treated with the endothelial agonist acetylcholine or locally heated to 42°C, a maneuver that evokes NO-mediated dilation. Interventions were performed with and without GA. In the presence of GA, maximal cutaneous vascular conductance (CVC) to ACh was 20 ± 3% lower than with ACh alone ( P < 0.001). During local heating, maximal CVC in the presence of GA was 22 ± 6% lower than during heating alone ( P < 0.01). The results show that GA can attenuate NO-mediated dilation in human skin, suggesting a potential role for HSP90 in activation of eNOS in the microcirculation.

Does local heating-induced nitric oxide production attenuate vasoconstrictor responsiveness to lower body negative pressure in human skin?

2007 ◽  
Vol 102 (5) ◽  
pp. 1839-1843 ◽  
Author(s):  
David A. Low ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David M. Keller ◽  
Craig G. Crandall
Keyword(s):  
Nitric Oxide ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Local Heating ◽  
Ringer Solution ◽  
No Production ◽  
Lower Body ◽  
Forearm Skin ◽  
Per Se ◽  
Cutaneous Vascular Conductance

We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of NG-nitro-l-arginine (l-NAME) and two with Ringer solution (control), and all sites were locally heated to 34°C. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an l-NAME site) were then heated to 39°C, while the other two sites were heated to 42°C. At the l-NAME sites, skin blood flow was elevated using 0.75–2 mg/ml of adenosine in the perfusate solution (Adn + l-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34°C, cutaneous vascular conductance (CVC) decreased (Δ) similarly at both control and l-NAME sites during LBNP (Δ7.9 ± 3.0 and Δ3.4 ± 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + l-NAME sites at 39°C (control Δ11.4 ± 2.5 vs. Adn + l-NAME Δ7.9 ± 2.0% maximum; P > 0.05) and 42°C (control Δ1.9 ± 2.7 vs. Adn + l-NAME Δ 4.2 ± 2.7% maximum; P > 0.05). However, the decrease in CVC at 42°C, regardless of site, was smaller than at 39°C ( P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms.

scholarly journals Nitric oxide and cutaneous active vasodilation during heat stress in humans

1998 ◽  
Vol 85 (3) ◽  
pp. 824-829 ◽  
Author(s):  
D. L. Kellogg ◽  
C. G. Crandall ◽  
Y. Liu ◽  
N. Charkoudian ◽  
J. M. Johnson
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Laser Doppler Flowmetry ◽  
Sweat Rate ◽  
Ringer Solution ◽  
No Synthase ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vascular Conductance

Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions,l-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38–38.5°C, internal temperature rose from 36.66 ± 0.10 to 37.34 ± 0.06°C ( P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 ± 2 to 44 ± 5% of maximum, but only rose from 13 ± 2 to 30 ± 5% of maximum at l-NAME-treated sites ( P < 0.05 between sites) during heat stress. l-NAME had no effect on sweat rate ( P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.

scholarly journals Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin

2006 ◽  
Vol 572 (3) ◽  
pp. 811-820 ◽  
Author(s):  
Belinda L. Houghton ◽  
Jessica R. Meendering ◽  
Brett J. Wong ◽  
Christopher T. Minson
Keyword(s):  
Nitric Oxide ◽  
Human Skin ◽  
Local Heating ◽  
Reflex Response ◽  
Temperature Threshold ◽  
Axon Reflex

scholarly journals Ten days of repeated local forearm heating does not affect cutaneous vascular function

2017 ◽  
Vol 123 (2) ◽  
pp. 310-316 ◽  
Author(s):  
Michael A. Francisco ◽  
Vienna E. Brunt ◽  
Krista Nicole Jensen ◽  
Santiago Lorenzo ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Young Adults ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Function ◽  
Forearm Blood Flow ◽  
Local Heating ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Doppler Flowmetry

The aim of the present study was to determine whether 10 days of repeated local heating could induce peripheral adaptations in the cutaneous vasculature and to investigate potential mechanisms of adaptation. We also assessed maximal forearm blood flow to determine whether repeated local heating affects maximal dilator capacity. Before and after 10 days of heat training consisting of 1-h exposures of the forearm to 42°C water or 32°C water (control) in the contralateral arm (randomized and counterbalanced), we assessed hyperemia to rapid local heating of the skin ( n = 14 recreationally active young subjects). In addition, sequential doses of acetylcholine (ACh, 1 and 10 mM) were infused in a subset of subjects ( n = 7) via microdialysis to study potential nonthermal microvascular adaptations following 10 days of repeated forearm heat training. Skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as laser-Doppler red blood cell flux divided by mean arterial pressure. Maximal cutaneous vasodilation was achieved by heating the arm in a water-spray device for 45 min and assessed using venous occlusion plethysmography. Forearm vascular conductance (FVC) was calculated as forearm blood flow divided by mean arterial pressure. Repeated forearm heating did not increase plateau percent maximal CVC (CVCmax) responses to local heating (89 ± 3 vs. 89 ± 2% CVCmax, P = 0.19), 1 mM ACh (43 ± 9 vs. 53 ± 7% CVCmax, P = 0.76), or 10 mM ACh (61 ± 9 vs. 85 ± 7% CVCmax, P = 0.37, by 2-way repeated-measures ANOVA). There was a main effect of time at 10 mM ACh ( P = 0.03). Maximal FVC remained unchanged (0.12 ± 0.02 vs. 0.14 ± 0.02 FVC, P = 0.30). No differences were observed in the control arm. Ten days of repeated forearm heating in recreationally active young adults did not improve the microvascular responsiveness to ACh or local heating. NEW & NOTEWORTHY We show for the first time that 10 days of repeated forearm heating is not sufficient to improve cutaneous vascular responsiveness in recreationally active young adults. In addition, this is the first study to investigate cutaneous cholinergic sensitivity and forearm blood flow following repeated local heat exposure. Our data add to the limited studies regarding repeated local heating of the cutaneous vasculature.

Does Local Heating Induced Nitric Oxide Production Attenuate Cutaneous Vasoconstrictor Responsiveness in Human Skin?

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S198
Author(s):  
David A. Low ◽  
Manabu Shibasaki ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Nitric Oxide ◽  
Human Skin ◽  
Local Heating ◽  
Nitric Oxide Production ◽  
Oxide Production

Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skin

2005 ◽  
Vol 98 (2) ◽  
pp. 629-632 ◽  
Author(s):  
D. L. Kellogg ◽  
J. L. Zhao ◽  
U. Coey ◽  
J. V. Green
Keyword(s):  
Nitric Oxide ◽  
Human Skin ◽  
Control Site ◽  
Relative Increase ◽  
No Synthase ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Endothelial Nitric Oxide ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Blood

Acetylcholine (ACh) can effect vasodilation by several mechanisms, including activation of endothelial nitric oxide (NO) synthase and prostaglandin (PG) production. In human skin, exogenous ACh increases both skin blood flow (SkBF) and bioavailable NO levels, but the relative increase is much greater in SkBF than NO. This led us to speculate ACh may dilate cutaneous blood vessels through PGs, as well as NO. To test this hypothesis, we performed a study in 11 healthy people. We measured SkBF by laser-Doppler flowmetry (LDF) at four skin sites instrumented for intradermal microdialysis. One site was treated with ketorolac (Keto), a nonselective cyclooxygenase antagonist. A second site was treated with NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NO synthase. A third site was treated with a combination of Keto and l-NAME. The fourth site was an untreated control site. After the three treated sites received the different inhibiting agents, ACh was administered to all four sites by intradermal microdialysis. Finally, sodium nitroprusside (SNP) was administered to all four sites. Mean arterial pressure (MAP) was monitored by Finapres, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). For data analysis, CVC values for each site were normalized to their respective maxima as effected by SNP. The results showed that both Keto and l-NAME each attenuated the vasodilation induced by exogenous ACh (ACh control = 79 ± 4% maximal CVC, Keto = 55 ± 7% maximal CVC, l-NAME = 46 ± 6% maximal CVC; P < 0.05, ACh vs. Keto or l-NAME). The combination of the two agents produced an even greater attenuation of ACh-induced vasodilation (31 ± 5% maximal CVC; P < 0.05 vs. all other sites). We conclude that a portion of the vasodilation effected by exogenous ACh in skin is due to NO; however, a significant portion is also mediated by PGs.

Sign in / Sign up

Export Citation Format

Share Document