scholarly journals Effects of atropine and l-NAME on cutaneous blood flow during body heating in humans

2000 ◽  
Vol 88 (2) ◽  
pp. 467-472 ◽  
Author(s):  
Shubha Shastry ◽  
Christopher T. Minson ◽  
Shurea A. Wilson ◽  
Niki M. Dietz ◽  
Michael J. Joyner

We sought to investigate further the roles of sweating, ACh spillover, and nitric oxide (NO) in the neurally mediated cutaneous vasodilation during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured with a laser-Doppler flowmeter. After a rise in core temperature (1.0 ± 0.1°C) and the establishment of cutaneous vasodilation, atropine and subsequently the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) were given to the forearm via a brachial artery catheter. After atropine infusion, cutaneous vascular conductance (CVC) remained constant in five of six subjects, whereasl-NAME administration blunted the rise in CVC in three of six subjects. A subsequent set of studies using intradermal microdialysis probes to selectively deliver drugs into forearm skin confirmed that atropine did not affect CVC. However, perfusion ofl-NAME resulted in a significant decrease in CVC (37 ± 4%, P < 0.05). The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.

1998 ◽  
Vol 85 (3) ◽  
pp. 830-834 ◽  
Author(s):  
Shubha Shastry ◽  
Niki M. Dietz ◽  
John R. Halliwill ◽  
Ann S. Reed ◽  
Michael J. Joyner

We sought to examine further the potential role of nitric oxide (NO) in the neurally mediated cutaneous vasodilation in nonacral skin during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured by using laser-Doppler flowmeters placed on both forearms. The NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) was given selectively to one forearm via a brachial artery catheter after marked cutaneous vasodilation had been established. During body heating, oral temperature increased by 1.1 ± 0.1°C while heart rate increased by 30 ± 6 beats/min. Mean arterial pressure stayed constant at 84 ± 2 mmHg. In the experimental forearm, cutaneous vascular conductance (CVC; laser-Doppler) decreased to 86 ± 5% of the peak response to heating ( P < 0.05 vs. pre-l-NMMA values) afterl-NMMA infusion. In some subjects, l-NMMA caused CVC to fall by ∼30%; in others, it had little impact on the cutaneous circulation. CVC in the control arm showed a similar increase with heating, then stayed constant whilel-NMMA was given to the contralateral side. These results demonstrate that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans. They also indicate that NO is not the only factor responsible for the dilation.


1984 ◽  
Vol 246 (3) ◽  
pp. R321-R324 ◽  
Author(s):  
L. A. Stephenson ◽  
C. B. Wenger ◽  
B. H. O'Donovan ◽  
E. R. Nadel

To characterize the changes in the control of the heat loss responses associated with the circadian variation in body temperature, we studied five men during 20 min of exercise in 25 degrees C on 6 separate days. Experiments were conducted at six times, equally spaced over the 24-h day. Esophageal temperature (Tes) and chest sweat rate (msw) were measured continuously, and forearm blood flow (FBF) was measured one to two times per minute. The thresholds for sweating and forearm vasodilation were significantly higher at 1600 and 2000 than at 2400 and 0400, averaging 0.57 and 0.65 degrees C higher, respectively, at 1600 than at 0400. Resting Tes and the Tes thresholds for cutaneous vasodilation and sweating during exercise all showed a similar circadian rhythm. The level at which core temperature is regulated therefore varies over the 24-h day with the zenith occurring around 1600 and the nadir at 0400. However, whereas the slope of the msw-to-Tes relation did not change over the 24-h day, the slope of the FBF-to-Tes relation tended to increase between 0400 and 2400, implying that the circadian rhythm may be more complex than just a shift in the central reference temperature.


2016 ◽  
Vol 310 (11) ◽  
pp. R1081-R1087 ◽  
Author(s):  
Naoto Fujii ◽  
Robert D. Meade ◽  
Christopher T. Minson ◽  
Vienna E. Brunt ◽  
Pierre Boulay ◽  
...  

Nitric oxide (NO) increases cutaneous blood flow; however, the underpinning mechanism(s) remains to be elucidated. We hypothesized that the cutaneous blood flow response during intradermal administration of sodium nitroprusside (SNP, a NO donor) is regulated by calcium-activated potassium (KCa) channels and cyclooxygenase (COX) in young adults. We also hypothesized that these contributions are diminished in older adults given that aging can downregulate KCa channels and reduce COX-derived vasodilator prostanoids. In 10 young (23 ± 5 yr) and 10 older (54 ± 4 yr) adults, cutaneous vascular conductance (CVC) was measured at four forearm skin sites infused with 1) Ringer (Control), 2) 50 mM tetraethylammonium (TEA), a nonspecific KCa channel blocker, 3) 10 mM ketorolac, a nonspecific COX inhibitor, or 4) 50 mM TEA + 10 mM ketorolac via intradermal microdialysis. All skin sites were coinfused with incremental doses of SNP (0.005, 0.05, 0.5, 5, and 50 mM each for 25 min). During SNP administration, CVC was similar at the ketorolac site (0.005–50 mM, all P > 0.05) relative to Control, but lower at the TEA and TEA + ketorolac sites (0.005–0.05 mM, all P < 0.05) in young adults. In older adults, ketorolac increased CVC relative to Control during 0.005–0.05 mM SNP administration (all P < 0.05), but this increase was not observed when TEA was coadministered (all P > 0.05). Furthermore, TEA alone did not modulate CVC during any concentration of SNP administration in older adults (all P > 0.05). We show that during low-dose NO administration (e.g., 0.005–0.05 mM), KCa channels contribute to cutaneous blood flow regulation in young adults; however, in older adults, COX inhibition increases cutaneous blood flow through a KCa channel-dependent mechanism.


1978 ◽  
Vol 235 (3) ◽  
pp. R160-R167 ◽  
Author(s):  
E. N. Smith ◽  
S. Robertson ◽  
D. G. Davies

Nine alligators, Alligator mississippiensis, were injected with 133Xe and the clearance half times measured in response to heating and cooling. Mean half times for thermostable, heating, and cooling conditions were 12.2, 8.6, and 28.3 min, respectively, indicating cutaneous vasodilation in response to local heating and reduced blood flow during cooling. Alterations of cutaneous blood flow occurred before changes in body temperature or heart rate. Warming portions of the animal while shading the injection site resulted in reduced blood flow when heat loss occurred. Skin thickness (S in cm) was related to body mass (M in kg) as S = 0.08 M0.38. Cutaneous blood flow per unit area was found to increase with increasing body mass from approximately 0.0025 to 0.025 ml blood-cm-2 of skin-min-1 during warming and from 0.0018 to 0.0045 during cooling for the 0.18--8.6 kg animals, respectively.


2003 ◽  
Vol 94 (5) ◽  
pp. 1829-1835 ◽  
Author(s):  
Narihiko Kondo ◽  
Shuji Yanagimoto ◽  
Takeshi Nishiyasu ◽  
Craig G. Crandall

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects ( n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35°C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 ± 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 ± 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.


2007 ◽  
Vol 102 (5) ◽  
pp. 1856-1861 ◽  
Author(s):  
Kenichi Kimura ◽  
David A. Low ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Craig G. Crandall

The aim of this study was to evaluate cutaneous vasodilation and sweating responses to exogenous administration of acetylcholine (ACh) and methacholine (MCh), which have different sensitivities to endogenous cholinesterase. Four intradermal microdialysis probes were placed in dorsal forearm skin: two sites were perfused with ACh (1 × 10−7–1 M) and the other two with the same molar concentrations of MCh. Sweat rate (SR) and cutaneous blood flow were simultaneously assessed directly over each microdialysis membrane. Dose-response curves were constructed, and the effective concentration of the drug resulting in 50% of the maximal response (EC50) was identified. For SR and cutaneous vascular conductance (CVC), there were no significant differences in EC50 between sites receiving the same drug: −1.52 ± 0.18 and −1.19 ± 0.09 log-molar concentration of ACh at distal and proximal sites, respectively, and −2.35 ± 0.24 and −2.42 ± 0.23 log-molar concentration of MCh at distal and proximal sites, respectively, for SR ( P > 0.05) and −3.87 ± 0.32 and −3.97 ± 0.27 log-molar concentration of ACh at distal and proximal sites, respectively, and −4.78 ± 0.17 and −4.46 ± 0.16 log-molar concentration of MCh at distal and proximal sites, respectively, for CVC ( P > 0.05). However, the EC50 for CVC and SR was significantly lower at the MCh than at the ACh sites. A second procedure was performed to confirm that differences in responses between ACh and MCh could be attributed to different cholinesterase sensitivities. Similarly, four microdialysis membranes were placed in dorsal forearm skin: two sites were perfused with ACh and other two with MCh. However, one of each of the ACh and MCh sites was also perfused with 10 μM neostigmine (an acetylcholinesterase inhibitor). Neostigmine at the ACh site induced a leftward shift (i.e., lower EC50) of the SR and CVC dose-response curves compared with the site treated with ACh alone, resulting in no difference in the EC50 for SR and CVC between the ACh + neostigmine and the MCh site. These results suggest that elevations in SR and CVC occur earlier with MCh than with ACh treatment because of differences in cholinesterase susceptibility between these drugs.


1977 ◽  
Vol 43 (5) ◽  
pp. 770-777 ◽  
Author(s):  
T. M. Gilbert ◽  
C. M. Blatteis

The cutaneous blood flow (mbl), rate of oxygen consumption (Vo2), rectal (Tre) and cutaneous (Tsk) temperatures, and shivering activity were measured in unanthetized male rats during a 2-h exposure to 26, 33, or 5 degrees C 2 wk after selective bilateral hypothalamic microknife cuts. Animals with preoptic-anterior hypothalamic (PO/AH) junction cuts 1.5 or 3.0 mm lateral to the midline, as well as parasagittal cuts which separated connections between the PO/AH and medial forebrain bundle exhibited a higher mbl at 26 degrees C than did sham-operated rats. At 5 degrees C the extended (3.0 mm) PO/AH cuts as well as the parasagittal cuts prevented cutaneous vasoconstriction but had no effect on shivering activity; hence Tre was not maintained. None of the cuts demonstrably impaired thermoregulation in the 33 degrees C environment. These results suggest that different sites in the hypothalamus may separately control cold-induced skin vasoconstriction and shivering activity, as well as heat-induced skin vasodilation. It would seem therefore that the integrity of the PO/AH is indispensable in rats for cold-induced cutaneous vasoconstriction but not for cold thermogenesis, and also not for heat-induced cutaneous vasodilation.


1992 ◽  
Vol 34 (4) ◽  
pp. 426-432 ◽  
Author(s):  
Toshimitsu Takayanagi ◽  
Masafumi Fukuda ◽  
Yoshiro Tsuji ◽  
Makoto Nakazawa

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