Evidence map›Paper›PMID 18469149›Full record

Trial reportAmerican journal of physiology. Heart and circulatory physiology2008

Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo.

Dean L Kellogg, Joan L Zhao, Yubo Wu

Abstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. ETAmerican journal of physiology. Heart and circulatory physiology · 2021
    Trial
  3. Trial
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  6. Intensive vasodilatation in the sciatic pain area after dry needling.BMC complementary and alternative medicine · 2015
    Trial
  7. Trial
  8. Trial
  9. Trial
  10. Article
  11. Article
  12. Oral contraceptive pill phase alters mechanisms contributing to cutaneous microvascular function in response to local heating.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Dean L KelloggDivision of Geriatrics and Gerontology, Univ. of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. kelloggd@uthscsa.edu
Joan L Zhao
Yubo Wu

Funding

MECHANISMS OF CUTANEOUS ACTIVE VASODILATIONR01HL065599 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KELLOGG, DEAN L · 2000 to 2008
$2.0M
NHLBI NIH HHS HL-065599
6 · The paper itself

Abstract

Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (T(loc)) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist N(G)-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased T(loc) and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF [laser-Doppler flowmetry (LDF)] and blood pressure [mean arterial pressure (MAP)] were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF / MAP). In protocol 1, T(loc) was controlled with LDF/local heating units. T(loc) initially was held at 34 degrees C and then increased to 41.5 degrees C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34 degrees C T(loc) did not differ between l-NAA-treated and untreated sites (P > 0.05). Local skin warming to 41.5 degrees C T(loc) increased CVC at both sites. This response was attenuated at l-NAA-treated sites (P < 0.05). In protocol 2, during normothermia, CVC did not differ between l-NAA-treated and untreated sites (P > 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites (P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased T(loc), but not during reflex responses to whole body heat stress.

Indexed as

Skin TemperatureAdministration, CutaneousAdultArginineBlood PressureEndothelium, VascularEnzyme InhibitorsFemaleForearmHeat Stress DisordersHumansLaser-Doppler FlowmetryMaleMicrodialysisNitric OxideNitric Oxide Synthase Type IIIArginineEnzyme InhibitorsN(G)-aminoarginineNitric OxideNitric Oxide Synthase Type IIINitroprussideNOS3 protein, humanVasodilator Agents

Identifiers

PMID18469149
PMCPMC2494770

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.