Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/11884
Title: Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO)
Authors: Milicic, Vesna
Zivkovic V.
Jeremić N.
Arsenijevic, Nebojsa
Djuric, Dragan M.
Jakovljevic V.
Journal: Molecular and Cellular Biochemistry
Issue Date: 1-Jan-2016
Abstract: © 2015, Springer Science+Business Media New York. 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 (Formula presented.), superoxide anion radical (Formula presented.), 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 (Formula presented.) 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.
URI: https://scidar.kg.ac.rs/handle/123456789/11884
Type: Article
DOI: 10.1007/s11010-015-2628-3
ISSN: 03008177
SCOPUS: 84958915280
Appears in Collections:Faculty of Medical Sciences, Kragujevac
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