Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO)
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 h...
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creator | Milicic, Vesna Zivkovic, Vladimir Jeremic, Nevena Arsenijevic, Nebojsa Djuric, Dragan Jakovljevic, Vladimir Lj |
description | 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 H
2
O). 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 (
NO
2
-
), superoxide anion radical (
O
2
-
), and hydrogen peroxide (H
2
O
2
) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H
2
O
2
release were significantly higher in iNOS
−/−
mice group. TBARS and
O
2
-
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. |
doi_str_mv | 10.1007/s11010-015-2628-3 |
format | Article |
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−/−
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 H
2
O). 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 (
NO
2
-
), superoxide anion radical (
O
2
-
), and hydrogen peroxide (H
2
O
2
) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H
2
O
2
release were significantly higher in iNOS
−/−
mice group. TBARS and
O
2
-
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.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-015-2628-3</identifier><identifier>PMID: 26708221</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Anaphylaxis ; Anaphylaxis - metabolism ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cardiovascular disease ; Coronary Circulation ; Heart ; Hydrogen peroxide ; Hydrogen Peroxide - metabolism ; In Vitro Techniques ; Life Sciences ; Male ; Medical Biochemistry ; Mice ; Mice, Knockout ; Nitric oxide ; Nitric Oxide - physiology ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Nitrites ; Oncology ; Oxidative Stress ; Peroxidation ; Rodents ; Superoxide ; Superoxides - metabolism ; Thiobarbituric Acid Reactive Substances - metabolism</subject><ispartof>Molecular and cellular biochemistry, 2016-01, Vol.412 (1-2), p.221-227</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>COPYRIGHT 2016 Springer</rights><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-cbe710d900e43b87ef0e3faaff070f1a82c09fcf127f3e8aa7870f0721f6cf213</citedby><cites>FETCH-LOGICAL-c509t-cbe710d900e43b87ef0e3faaff070f1a82c09fcf127f3e8aa7870f0721f6cf213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-015-2628-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-015-2628-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26708221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Milicic, Vesna</creatorcontrib><creatorcontrib>Zivkovic, Vladimir</creatorcontrib><creatorcontrib>Jeremic, Nevena</creatorcontrib><creatorcontrib>Arsenijevic, Nebojsa</creatorcontrib><creatorcontrib>Djuric, Dragan</creatorcontrib><creatorcontrib>Jakovljevic, Vladimir Lj</creatorcontrib><title>Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO)</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>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 H
2
O). 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 (
NO
2
-
), superoxide anion radical (
O
2
-
), and hydrogen peroxide (H
2
O
2
) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H
2
O
2
release were significantly higher in iNOS
−/−
mice group. TBARS and
O
2
-
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.</description><subject>Anaphylaxis</subject><subject>Anaphylaxis - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Coronary Circulation</subject><subject>Heart</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>In Vitro Techniques</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitrites</subject><subject>Oncology</subject><subject>Oxidative Stress</subject><subject>Peroxidation</subject><subject>Rodents</subject><subject>Superoxide</subject><subject>Superoxides - metabolism</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kd1rFDEUxYModq3-Ab5IwJf6MPXezEcyvpVFq1Dsiz6HbOamm5KdrMlMtfjPm2Fbv1ASuHD5ncNJDmPPEU4RQL7OiIBQAbaV6ISq6gdsha2sq6bH_iFbQQ1QKZTyiD3J-RoKDIiP2ZHoJCghcMW-r2OKo0m33IX4lZtx4PGbH8zkb4jnKVHOfJiTH694iNaEQpj99jYYO3nLEy0zjtyXm2MwEw185y3xLZk0veHTlniKgXh0fPRTKprFnvjJx8tXT9kjZ0KmZ3fzmH1-9_bT-n11cXn-YX12UdkW-qmyG5IIQw9ATb1RkhxQ7YxxDiQ4NEpY6J11KKSrSRkjVdmDFOg66wTWx-zk4LtP8ctMedI7ny2FYEaKc9YoO1Bdh6ou6Mu_0Os4p7GkK1SroK-7pv9FXZlA2o8uTsnYxVSfNY1QPbS4UKf_oMoZqHxRHMn5sv9DgAeBTTHnRE7vk9-VbjSCXgrXh8J1KVwvhesl8Iu7wPNmR8NPxX3DBRAHIO-XFin99qL_uv4ADVG0tQ</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Milicic, Vesna</creator><creator>Zivkovic, Vladimir</creator><creator>Jeremic, Nevena</creator><creator>Arsenijevic, Nebojsa</creator><creator>Djuric, Dragan</creator><creator>Jakovljevic, Vladimir Lj</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20160101</creationdate><title>Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO)</title><author>Milicic, Vesna ; Zivkovic, Vladimir ; Jeremic, Nevena ; Arsenijevic, Nebojsa ; Djuric, Dragan ; Jakovljevic, Vladimir Lj</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-cbe710d900e43b87ef0e3faaff070f1a82c09fcf127f3e8aa7870f0721f6cf213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Anaphylaxis</topic><topic>Anaphylaxis - metabolism</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Coronary Circulation</topic><topic>Heart</topic><topic>Hydrogen peroxide</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>In Vitro Techniques</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitrites</topic><topic>Oncology</topic><topic>Oxidative Stress</topic><topic>Peroxidation</topic><topic>Rodents</topic><topic>Superoxide</topic><topic>Superoxides - metabolism</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Milicic, Vesna</creatorcontrib><creatorcontrib>Zivkovic, Vladimir</creatorcontrib><creatorcontrib>Jeremic, Nevena</creatorcontrib><creatorcontrib>Arsenijevic, Nebojsa</creatorcontrib><creatorcontrib>Djuric, Dragan</creatorcontrib><creatorcontrib>Jakovljevic, Vladimir Lj</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Milicic, Vesna</au><au>Zivkovic, Vladimir</au><au>Jeremic, Nevena</au><au>Arsenijevic, Nebojsa</au><au>Djuric, Dragan</au><au>Jakovljevic, Vladimir Lj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO)</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>412</volume><issue>1-2</issue><spage>221</spage><epage>227</epage><pages>221-227</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><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 H
2
O). 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 (
NO
2
-
), superoxide anion radical (
O
2
-
), and hydrogen peroxide (H
2
O
2
) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H
2
O
2
release were significantly higher in iNOS
−/−
mice group. TBARS and
O
2
-
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.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26708221</pmid><doi>10.1007/s11010-015-2628-3</doi><tpages>7</tpages></addata></record> |
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subjects | Anaphylaxis Anaphylaxis - metabolism Animals Biochemistry Biomedical and Life Sciences Cardiology Cardiovascular disease Coronary Circulation Heart Hydrogen peroxide Hydrogen Peroxide - metabolism In Vitro Techniques Life Sciences Male Medical Biochemistry Mice Mice, Knockout Nitric oxide Nitric Oxide - physiology Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Nitrites Oncology Oxidative Stress Peroxidation Rodents Superoxide Superoxides - metabolism Thiobarbituric Acid Reactive Substances - metabolism |
title | Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO) |
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