ReviewThe Western journal of medicine1998
Nitric oxide and septic shock. From bench to bedside.
Review in The Western journal of medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Nitric Oxide as a Central Molecule in Hypertension: Focus on the Vasorelaxant Activity of New Nitric Oxide Donors.Biology · 2021Review
- Reevaluation of Lung Injury in TNF-Induced Shock: The Role of the Acid Sphingomyelinase.Mediators of inflammation · 2020Article
- Relationship between inducible NOS single-nucleotide polymorphisms and hypertension in Han Chinese.Herz · 2018Article
- Influence of the CCR-5/MIP-1 α axis in the pathogenesis of Rocio virus encephalitis in a mouse model.The American journal of tropical medicine and hygiene · 2013Article
- Chorioamnionitis with or without funisitis increases the risk of hypotension in very low birthweight infants on the first postnatal day but not later.Archives of disease in childhood. Fetal and neonatal edition · 2006Article
- Human endothelial cell activation and mediator release in response to Listeria monocytogenes virulence factors.Infection and immunity · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Refractory hypotension with end-organ hypoperfusion is an ominous feature of inflammatory shock. In the past fifteen years, nitric oxide (a diffusible, short-lived product of arginine metabolism) has been found to be an important regulatory molecule in several areas of metabolism, including vascular tone control. Vascular endothelial cells constitutively produce low levels of nitric oxide that regulate blood pressure by mediating adjacent smooth-muscle relaxation. In an inflammatory shock state, cytokines, like interleukin-1 and tumor necrosis factor-alpha, induce a separate, high-output form of the enzyme that synthesizes nitric oxide in both endothelial and smooth-muscle cells. The ensuing high rates of nitric oxide formation result in extensive smooth-muscle relaxation, pressor refractory vasodilation, and--ultimately--shock. The concept of the pathogenesis of inflammatory shock explains many limitations of current therapies and may foster the development of new interventions to mitigate the effects of nitric oxide overproduction in this syndrome.
Indexed as
Identifiers
9549416PMC1304857W1594902056What OpenQuestion holds
Registered trials
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.