ArticleMolecular and cellular biochemistry2016
Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO).
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Oxidative Stress and Mitochondria Are Involved in Anaphylaxis and Mast Cell Degranulation: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Circulating serum profile of small non-coding RNAs in patients with anaphylaxis beyond microRNAs.Frontiers in allergy · 2024Article
- Anaphylactic cardiovascular collapse and Kounis syndrome: systemic vasodilation or coronary vasoconstriction?Annals of translational medicine · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to assess the role of nitric oxide (NO) in cardiac anaphylaxis regarding changes in coronary reactivity and oxidative status of the mice heart. The animals were divided into two groups: experimental group (CBA, iNOS(-/-) mice) and control group: wild-type mice (CBA/H). The hearts of male mice (n = 24; 6-8 weeks old, body mass 20-25 g, 12 in each experimental group) were excised and retrogradely perfused according to the Langendorff technique at a constant perfusion pressure (70 cm H2O). Cardiac anaphylaxis was elicited by injection of solution (1 mg/1 ml) of ovalbumin into the aortic cannula. For the next 10 min, in intervals of 2 min (0-2, 2-4, 4-6, 6-8, 8-10 min) coronary flow (CF) rates were measured and samples of coronary effluent were collected. Markers of oxidative stress including index of lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS), NO measured in the form of nitrites (NO2(-)), superoxide anion radical (O2(-)), and hydrogen peroxide (H2O2) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H2O2 release were significantly higher in iNOS(-/-) mice group. TBARS and O2(-) values did not vary significantly between wild and iNOS(-/-) mice groups. Our results indicate that coronary vasoconstriction during cardiac anaphylaxis does not necessarily depend on inducible nitric oxide synthase (iNOS)/NO activity and that iNOS/NO pathway may not be an only influential mediator of redox changes in this model of cardiac anaphylaxis.
Indexed as
Identifiers
26708221What 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.