ArticleExperimental and clinical cardiology2005
The role of nitric oxide in endotoxin-induced cardiodepression.
Article in Experimental and clinical cardiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Low-Dose Endotoxin Induces Late Preconditioning, Increases Peroxynitrite Formation, and Activates STAT3 in the Rat Heart.Molecules (Basel, Switzerland) · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo determine the participation of inducible nitric oxide synthase (iNOS) in cardiodepressive phenomena during late preconditioning caused by subtoxic doses of lipopolysaccharide (LPS).
methodsSpontaneously beating hearts isolated from male Wistar rats (350 g to 400 g), intact or preconditioned with LPS (0.25 mg/kg given intraperitoneally 18 h before heart excision), were used to measure contractile performance during 30 min of ischemia and 40 min of reperfusion in the Langendorff mode. For selective iNOS blockade, hearts were perfused with phenylene-1,3-bis(ethane-2-isothiourea) (50 nmol/L). Expression of iNOS (determined using Western blotting) and NOS activities were determined in frozen myocardial tissues.
resultsSubtoxic doses of LPS caused iNOS induction in the heart and depression of contractile function, but improved heart postischemic recovery. In all groups of animals, expression of iNOS was higher in the right than left ventricles. Ischemia and postischemic reperfusion of intact heart intensified production of nitric oxide (NO), predominantly by iNOS. The preconditioning led to iNOS activation during ischemia in the left ventricle and iNOS depression in the right ventricle, owing to feedback caused by the initially higher iNOS expression and activity in the right ventricle. Postischemic reperfusion diminished NOS activities in preconditioned myocardial tissues. Blockade of iNOS significantly slowed preconditioned heart recovery and partially restored left ventricular developed pressure, but only after 20 min of reperfusion.
conclusionsiNOS-produced NO plays a role in the development of delayed cardioprotection and cardiodepressive effects (in part) after extravasal administration of a minimal dose of endotoxin.
Indexed as
Identifiers
19641673PMC2716236W259109566What OpenQuestion holds
Registered trials
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