ArticleIntensive care medicine2007
Neuronal nitric oxide synthase deficiency decreases survival in bacterial peritonitis and sepsis.
Article in Intensive care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- From Insight to Impact: Spotlight on the Potential Implications of the Neuronal Nitric Oxide Synthase Isoenzyme (nNOS) in Experimental Chronic Toxoplasmosis.Diseases (Basel, Switzerland) · 2026Article
- A Historical Review of Vasoactive Intestinal Peptide and Pituitary Adenylate Cyclase-Activating Polypeptide in Sepsis.Biology · 2026Review
- Effects of the glucagon-like peptide-1 receptor agonist liraglutide on retinal endothelial function and oxidative stress during sepsis.Frontiers in pharmacology · 2026Article
- Gases in Sepsis: Novel Mediators and Therapeutic Targets.International journal of molecular sciences · 2022Review
- Review
- Modulation of oxidative and nitrosative stress attenuates microvascular hyperpermeability in ovine model of Pseudomonas aeruginosa sepsis.Scientific reports · 2021Article
- Local anaesthetics upregulate nitric oxide generation in cord blood and adult human neutrophils.Scientific reports · 2019Article
- SERCA Cys674 sulphonylation and inhibition of L-type Ca2+ influx contribute to cardiac dysfunction in endotoxemic mice, independent of cGMP synthesis.American journal of physiology. Heart and circulatory physiology · 2013Article
- Review
- The three isoforms of nitric oxide synthase distinctively affect mouse nocifensive behavior.Nitric oxide : biology and chemistry · 2012Article
- Disruption of the transient receptor potential vanilloid 1 can affect survival, bacterial clearance, and cytokine gene expression during murine sepsis.Anesthesiology · 2011Article
- The heart is an early target of anthrax lethal toxin in mice: a protective role for neuronal nitric oxide synthase (nNOS).PLoS pathogens · 2009Article
- Differential protection against oxidative stress and nitric oxide overproduction in cardiovascular and pulmonary systems by propofol during endotoxemia.Journal of biomedical science · 2009Article
- Bench-to-bedside review: nitric oxide in critical illness--update 2008.Critical care (London, England) · 2009Review
- Year in review in Intensive Care Medicine, 2007. I. Experimental studies. Clinical studies: brain injury and neurology, renal failure and endocrinology.Intensive care medicine · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo investigate the role of neuronal nitric oxide synthase (NOS1) in murine polymicrobial peritonitis and sepsis.
designRandomized experimental trial.
settingAnimal research facility. SUBJECTS: B6129S NOS1+/+ and B6;129S4 NOS-/- mice.
interventionsNOS1+/+ and NOS1-/- animals underwent cecal ligation and puncture (CLP) or sham surgery and received the NOS1 inhibitor 7-nitroindazole (7-NI) or vehicle. MEASUREMENTS AND MAIN
resultsAfter CLP, genetic deficiency and pharmacologic inhibition of NOS1 significantly increased risk of mortality [8.69 (3.27, 23.1), p<0.0001 and 1.71 (1.00, 2.92) p=0.05, hazard ratio of death (95% confidence interval) for NOS1-/- and 7-NI-treated NOS1+/+ respectively] compared with NOS1+/+ animals. In 7-NI-treated NOS1+/+ animals, there were increases (6 h) and then decreases (24 h), whereas in NOS-/- animals persistent increases in blood bacteria counts (p=0.04 for differing effects of 7-NI and NOS1-/-) were seen compared with NOS1(+/+) animals. After CLP, NOS1(-/-) had upregulation of inducible NOS and proinflammatory cytokines and greater increases in serum tumor necrosis factor-alpha and interleukin-6 levels compared with NOS1+/+ mice (all p<0.05). Following CLP, there were similar significant decreases in circulating leukocytes and lung lavage cells (p<or=0.0008) and significant increases in peritoneal lavage cells (p=0.0045) in all groups. Over 6 h and 24 h following CLP, compared with NOS1+/+, NOS-/- mice had significantly higher peritoneal cell concentrations {respectively 0.40+/-0.09 vs 0.79+/-0.15 [log(x10(4)cells/ml)] averaged over both times p=0.038}.
conclusionsDeficiency and inhibition of NOS1 increases mortality, possibly by increasing proinflammatory cytokine response and impairing bacterial clearance after CLP. These data suggest that NOS1 is important for survival, bacterial clearance, and regulation of cytokine response during infection and sepsis.
Indexed as
Identifiers
What 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.