Evidence map›Paper›PMID 10562304›Full record

ArticleThe Journal of clinical investigation1999

Hypoxic pulmonary blood flow redistribution and arterial oxygenation in endotoxin-challenged NOS2-deficient mice.

R Ullrich, K D Bloch, F Ichinose, W Steudel, W M Zapol

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Impairment of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012
    Review
  10. Article
  11. Nitric oxide synthase 3 contributes to ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2010
    Article
  12. Article
  13. Review
  14. Article
  15. Leukotrienes in acute lung injury: a potential therapeutic target?American journal of respiratory and critical care medicine · 2005
    Article
  16. Article
  17. 5-Lipoxygenase deficiency prevents respiratory failure during ventilator-induced lung injury.American journal of respiratory and critical care medicine · 2005
    Article
  18. Article
  19. Article
  20. Cytosolic phospholipase A(2) in hypoxic pulmonary vasoconstriction.The Journal of clinical investigation · 2002
    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 2 institutions in 1 country.

R UllrichDepartment of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
K D Bloch
F Ichinose
W Steudel
W M Zapol
Harvard University · USMassachusetts General Hospital · US

Funding

INHALED NITRIC OXIDER01HL042397 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ZAPOL, WARREN MYRON · 1990 to 2007
$2.8M
NO/CGMP SIGNAL TRANSDUCTION IN ACUTE PULMONARY INJURYR01HL055377 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BLOCH, KENNETH D · 1996 to 1999
–
NHLBI NIH HHS HL42397NHLBI NIH HHS HL55377NHLBI NIH HHS R01 HL042397
6 · The paper itself

Abstract

Sepsis and endotoxemia impair hypoxic pulmonary vasoconstriction (HPV), thereby reducing arterial oxygenation and enhancing hypoxemia. Endotoxin induces nitric oxide (NO) production by NO synthase 2 (NOS2). To assess the role of NO and NOS2 in the impairment of HPV during endotoxemia, we measured in vivo the distribution of total pulmonary blood flow (QPA) between the right (QRPA) and left (QLPA) pulmonary arteries before and after left mainstem bronchus occlusion (LMBO) in mice with and without a congenital deficiency of NOS2. LMBO reduced QLPA/QPA equally in saline-treated wild-type and NOS2-deficient mice. However, prior challenge with Escherichia coli endotoxin markedly impaired the ability of LMBO to reduce QLPA/QPA in wild-type, but not in NOS2-deficient, mice. After endotoxin challenge and LMBO, systemic oxygenation was impaired to a greater extent in wild-type than in NOS2-deficient mice. When administered shortly after endotoxin treatment, the selective NOS2 inhibitor L-NIL preserved HPV in wild-type mice. High concentrations of inhaled NO attenuated HPV in NOS2-deficient mice challenged with endotoxin. These findings demonstrate that increased pulmonary NO levels (produced by NOS2 or inhaled at high levels from exogenous sources) are necessary during the septic process to impair HPV, ventilation/perfusion matching and arterial oxygenation in a murine sepsis model.

Indexed as

AnimalsBlood PressureBronchiCrosses, GeneticEndotoxinsEscherichia coliFemaleHeart RateHypoxiaMaleMiceMice, Inbred C57BLMice, Inbred StrainsMice, Mutant StrainsNitric Oxide SynthaseNitric Oxide Synthase Type IIEndotoxinsNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseOxygen

Identifiers

PMID10562304
PMCPMC409836
OpenAlexW2022684234

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.