ArticleBMC cardiovascular disorders2002
Organ culture: a new model for vascular endothelium dysfunction.
Article in BMC cardiovascular disorders, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 36 citations in OpenAlex.
- Ticagrelor Prevents Endothelial Cell Apoptosis through the Adenosine Signalling Pathway in the Early Stages of Hypoxia.Biomolecules · 2020Article
- Complementary Role of P2 and Adenosine Receptors in ATP Induced-Anti-Apoptotic Effects Against Hypoxic Injury of HUVECs.International journal of molecular sciences · 2019Article
- Article
- Disruption of actin cytoskeleton mediates loss of tensile stress induced early phenotypic modulation of vascular smooth muscle cells in organ culture.Experimental and molecular pathology · 2010Article
- Cigarette smoking leads to reduced relaxant responses of the cutaneous microcirculation.Vascular health and risk management · 2008Article
- The enhanced endothelin-1-induced contraction in cultured coronary arteries from mature female pigs is not antagonized by 17beta-estradiol.Vascular pharmacology · 2007Article
- Smoking particles enhance endothelin A and endothelin B receptor-mediated contractions by enhancing translation in rat bronchi.BMC pulmonary medicine · 2006Article
- Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man.BMC cardiovascular disorders · 2006Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelium dysfunction is believed to play a role in the development of cardiovascular disease. The aim of the present study was to evaluate the suitability of organ culture as a model for endothelium dysfunction.
methodsThe isometric tension was recorded in isolated segments of the rat mesenteric artery branch, before and after organ culture for 20 h. Vasodilatation was expressed as % of preconstriction with U46619. The acetylcholine (ACh) induced nitric oxide (NO) mediated dilatation was studied in the presence of 10 microM indomethacin, 50 nM charybdotoxin and 1 microM apamin. Endothelium-derived hyperpolarising factor (EDHF) was studied in the presence of 0.1 mM L-NOARG and indomethacin. Prostaglandins were studied in the presence of L-NOARG, charybdotoxin and apamin.
resultsThe ACh-induced NO and prostaglandin-mediated dilatations decreased significantly during organ culture (NO: 84% in control and 36% in cultured; prostaglandins: 48% in control and 16% in cultured). Notably, the total ACh-dilatation was not changed. This might be explained by the finding that EDHF alone stimulated a full dilatation even after organ culture (83% in control and 80% in cultured). EDHF may thereby compensate for the loss in NO and prostaglandin-mediated dilatation. Dilatations induced by forskolin or sodium nitroprusside did not change after organ culture, indicating intact smooth muscle cell function.
conclusionsOrgan culture induces a loss in NO and prostaglandin-mediated dilatation, which is compensated for by EDHF. This shift in mediator profile resembles that in endothelium dysfunction. Organ culture provides an easily accessible model where the molecular changes that take place, when endothelium dysfunction is developed, can be examined over time.
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