Evidence map›Paper›PMID 19666847›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Transfer of nitric oxide by blood from upstream to downstream resistance vessels causes microvascular dilation.

H G Bohlen, X Zhou, J L Unthank, S J Miller, R Bills

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Nitric oxide formation by lymphatic bulb and valves is a major regulatory component of lymphatic pumping.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  12. Article
  13. Article
  14. Nitric oxide signaling in the microcirculation.Critical reviews in biomedical engineering · 2011
    Review
  15. Article
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

5 authors at 1 institution in 1 country.

H G BohlenDepartment of Cellular and Integrative Physiology, Indiana University Medical School, Indianapolis, Indiana 46202, USA. gbohlen@iupui.edu
X Zhou
J L Unthank
S J Miller
R Bills
Indiana University – Purdue University Indianapolis · US

Funding

Microvascular Regulation During Intestinal AbsorptionR01HL020605 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BOHLEN, HAROLD G · 1985 to 2010
$1.6M
VASCULAR ADAPTATION IN PATHOPHYSIOLOGYR01HL042898 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI UNTHANK, JOSEPH L · 1997 to 2007
$882k
VASCULAR ADAPTATION IN PATHOPHYSIOLOGYR29HL042898 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI UNTHANK, JOSEPH L · 1991 to 1995
–
NHLBI NIH HHS HL-20605NHLBI NIH HHS HL-42898
6 · The paper itself

Abstract

The discovery that hemoglobin, albumin, and glutathione carry and release nitric oxide (NO) may have consequences for movement of NO by blood within microvessels. We hypothesize that NO in plasma or bound to proteins likely survives to downstream locations. To confirm this hypothesis, there must be a finite NO concentration ([NO]) in arteriolar blood, and upstream resistance vessels must be able to increase the vessel wall [NO] of downstream arterioles. Arteriolar blood NO was measured with NO-sensitive microelectrodes, and vessel wall [NO] was consistently 25-40% higher than blood [NO]. Localized suppression of NO production in large arterioles over 500-1,000 microm with L-nitroarginine reduced the [NO] approximately 40%, indicating as much as 60% of the wall NO was from blood transfer. Flow in mesenteric arteries was elevated by occlusion of adjacent arteries to induce a flow-mediated increase in arterial NO production. Both arterial wall and downstream arteriolar [NO] increased and the arterioles dilated as the blood [NO] was increased. To study receptor-mediated NO generation, bradykinin was locally applied to upstream large arterioles and NO measured there and in downstream arterioles. At both sites, [NO] increased and both sets of vessels dilated. When isoproterenol was applied to the upstream vessels, they dilated, but neither the [NO] or diameter downstream arterioles increased. These observations indicate that NO can move in blood from upstream to downstream resistance vessels. This mechanism allows larger vessels that generate large [NO] to influence vascular tone in downstream vessels in response to both flow and receptor stimuli.

Indexed as

Splanchnic CirculationVascular ResistanceVasodilationAnimalsArteriolesBradykininCollateral CirculationEnzyme InhibitorsIntestinesIon-Selective ElectrodesIsoproterenolMaleMesenteric ArteriesMicroelectrodesNitric OxideNitric Oxide Synthase Type IIIBradykininEnzyme InhibitorsIsoproterenolNitric OxideNitric Oxide Synthase Type IIINitroarginineNos3 protein, ratS-NitrosoglutathioneVasodilator Agents

Identifiers

PMID19666847
PMCPMC2770775
OpenAlexW2086006222

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.