{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T03:47:42Z","timestamp":1791085662934,"version":"4.1.0"},"reference-count":23,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2000,2,4]]},"abstract":"<jats:p>\n                    <jats:italic>Abstract<\/jats:italic>\n                    \u2014Experimental and clinical studies have suggested an increased production of reactive oxygen species (ROS) in the failing myocardium. The present study aimed to obtain direct evidence for increased ROS and to determine the contribution of superoxide anion (\u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    ), H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    , and hydroxy radical (\u00b7OH) in failing myocardial tissue. Heart failure was produced in adult mongrel dogs by rapid ventricular pacing at 240 bpm for 4 weeks. To assess the production of ROS directly, freeze-clamped myocardial tissue homogenates were reacted with the nitroxide radical, 4-hydroxy-2,2,6,6,-tetramethyl-piperidine-\n                    <jats:italic>N<\/jats:italic>\n                    -oxyl, and its spin signals were detected by electron spin resonance spectroscopy. The rate of electron spin resonance signal decay, proportional to \u00b7OH level, was significantly increased in heart failure, which was inhibited by the addition of dimethylthiourea (\u00b7OH scavenger) into the reaction mixture. Increased \u00b7OH in the failing heart was abolished to the same extent in the presence of desferrioxamine (iron chelator), catalase (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    scavenger), and 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron; LaMotte) (\u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    scavenger), indicating that \u00b7OH originated from H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    and \u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    . Further, \u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    produced in normal myocardium in the presence of antimycin A (mitochondrial complex III inhibitor) could reproduce the increase of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    and \u00b7OH seen in the failing tissue. There was a significant positive relation between myocardial ROS level and left ventricular contractile dysfunction. In conclusion, in the failing myocardium, \u00b7OH was produced as a reactive product of \u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    , which might play an important role in left ventricular failure.\n                  <\/jats:p>","DOI":"10.1161\/01.res.86.2.152","type":"journal-article","created":{"date-parts":[[2012,6,11]],"date-time":"2012-06-11T20:52:16Z","timestamp":1339447936000},"page":"152-157","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":325,"title":["Direct Evidence for Increased Hydroxyl Radicals Originating From Superoxide in the Failing Myocardium"],"prefix":"10.1161","volume":"86","author":[{"given":"Tomomi","family":"Ide","sequence":"first","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyuki","family":"Tsutsui","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shintaro","family":"Kinugawa","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuhiro","family":"Suematsu","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shunji","family":"Hayashidani","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuhiro","family":"Ichikawa","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideo","family":"Utsumi","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youji","family":"Machida","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kensuke","family":"Egashira","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Takeshita","sequence":"additional","affiliation":[{"name":"From Cardiovascular Medicine (T.I., H.T., S.K., N.S., S.H., Y.M., K.E., A.T.), Graduate School of Medical Sciences, and Department of Biophysics, Faculty of Pharmaceutical Sciences (K.I., H.U.), Kyushu University, Fukuoka, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.65.5.245"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.97.16.1536"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.266.4.H1280"},{"key":"e_1_3_2_4_2","first-page":"291","volume":"148","year":"1996","unstructured":"Hill MF, Singal PK. 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