Evidence map›Paper›PMID 19709421›Full record

ArticleCritical care (London, England)2009

Effects of inducible nitric oxide synthase inhibition or norepinephrine on the neurovascular coupling in an endotoxic rat shock model.

Bernhard Rosengarten, Stephanie Wolff, Sabine Klatt, Ralf T Schermuly

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-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

20 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Prolonged systemic inflammation worsens impairments to astrocyte CabioRxiv : the preprint server for biology · 2025
    Article
  3. Disturbed microcirculation and hyperaemic response in a murine model of systemic inflammation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment.Oxidative medicine and cellular longevity · 2022
    Review
  8. Seizures and Sepsis: A Narrative Review.Journal of clinical medicine · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Neuro-oxidative-nitrosative stress in sepsis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011
    Review
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Bernhard RosengartenDepartment of Neurology, Justus Liebig University Giessen, Am Steg 14, 35392 Giessen, Germany. bernhard.rosengarten@neuro.med.uni-giessen.de
Stephanie Wolff
Sabine Klatt
Ralf T Schermuly
University of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe inducible nitric oxide synthase (iNOS) plays a crucial role in early sepsis-related microcirculatory dysfunction. Compared to a catecholamine therapy we tested effects of a specific iNOS-inhibitor (1400W) on the microcirculatory function in the brain.

methodsSeventy SD-rats (280-310 g) were divided into 1 control and 6 sepsis groups. Sepsis groups received 1 or 5 mg/kg lipopolysaccharide (LPS) intravenously to induce a moderate or severe sepsis syndrome. Thirty minutes later rats were further randomized into subgroups receiving moderate volume therapy alone or additionally continuous norepinephrine (NE) or 1400W infusion. Separately, effects of 1400W on neurofunctional parameters were investigated in 3 rats without sepsis induction. Performing electric forepaw-stimulation evoked potentials (N2-P1 amplitude, P1-latency) and local hemodynamic responses were recorded with surface electrodes and laser Doppler over the somatosensory cortex at baseline and repeatedly after LPS administration. Cytokine levels (tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL6), interferon-gamma (IFNgamma)) and cell destruction markers (neuron-specific enolase (NSE), S-100 calcium binding protein B (S100B)) were obtained at the end of experiments.

resultsDuring sepsis progression resting cerebral blood flow increased and functionally activated hemodynamic responses decreased in a dose-dependent manner. Whereas 1400W and NE improved blood pressure, only 1400W stabilized resting flow levels. However, both regimens were ineffective on the functionally coupled flow responses and destruction markers were similar between groups.

conclusionsNE and 1400W appeared to be ineffective in mitigating the effects of sepsis on the neurovascular coupling. Other regimens are needed to protect the cerebral microcirculation under septic conditions.

Indexed as

AnimalsCerebrovascular CirculationCytokinesDose-Response Relationship, DrugEnzyme InhibitorsMaleMicrocirculationModels, AnimalNitric Oxide Synthase Type IINorepinephrineRandom AllocationRatsRats, Sprague-DawleyShock, SepticVasoconstrictor AgentsCytokinesEnzyme InhibitorsNitric Oxide Synthase Type IINorepinephrineVasoconstrictor Agents

Identifiers

PMID19709421
PMCPMC2750197
OpenAlexW1966063614

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.